Ruptured popliteal artery aneurysm. Case report

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 4(comme la Mosaic ou l'Epic) devrait être encoreplus marqué: ces dernières valves bénéficientd'un traitement anti-calcification trèsprometteur.Dans le même temps, peu de progrès ontété réalisés dans le domaine des valvesmécaniques et du traitement anticoagulantqu'elles imposent. Le design des prothèses àailettes a peu évolué. Les tentatives detraitement de la surface de carbone (ForceFieldde ATS) ne sont pas disponibles cliniquement. Leseul vrai progrès dans l'attente des anticoagulantsanti X oraux, est le self monitoring del'INR par le patient lui-même: le taux deprothrombine est plus stable, l'INR peut êtreabaissé modérément réduisant d'autant le risquehémorragique.La comparaison des performancescliniques des deux catégories de valve à longterme est intéressante: le taux de survie de lapopulation tout âge confondu est égal dans legroupe des patients porteurs de valvesmécaniques et dans celui des patients porteursdes valves biologiques de première génération.Le taux d'évènements liés à la valve est sur 20ans équivalent. La seule différence est la naturede ces évènements: accident hémorragiquechez les porteurs de valves mécaniques,dysfonction de la prothèse en cas debioprothése. Rappelons la gravité totalementdifférente des deux complications: la premièrepeut être rapidement létale, la seconde étantfacilement corrigée par une ré-intervention aurisque faible. Le résultat de ces étudescomparatives doit être pris avec une granderéserve: les bioprothèses utilisées aujourd'huiprésentent des performances très supérieures àcelles qui ont permis l'étude entreprise il y a plusde vingt ans. Une bonne êtude comparative desprothèses actuellement utilisées reste donc àfaire!Cette étude comparative desperformances respectives de chaque prothèsea convaincu les grandes sociétés savantes:qu'elles soient américaines ou européennes, lessociétés savantes ont émis desrecommandations précises. Au-delà d'un âgede 65 ans, les patients reçoivent une prothèsebiologique, sachant que la durée de vie de laprothèse dépasse à cet âge l'espérance de viedu patient. Chez les patients de moins de 65 ans,l'utilisation des bioprothèses est raisonnable chezles patients en rythme sinusal et larecommandation est double: le médecin doitparler au malade des risques de l'anticoagulationet de la ré-intervention; il doitprendre en compte dans ses recommandationsau patient du mode de vie de celui-ci.Il est intéressant de noter à cet égardque les aspirations des patients les plus jeunesont évolué. Au sacro saint allongement à toutprix de la durée de vie, les malades préfèrentaujourd'hui la qualité de vie. Il est peu discutableque la qualité de vie des patients porteurs debioprothèse est très supérieure à celle despatients porteurs de prothèses mécaniques.Silencieuses, les bioprothèses se font totalementoublier d'autant plus que le patient ne connaitpas la contrainte de l'anti-coagulation. Cetteobservation explique que de nombreux patientspréfèrent aujourd'hui le confort de la valvebiologique.Un élément nouveau est apparurécemment: la ré-intervention aprésdysfonctionnement d'une valve biologique n'estplus synonyme d'opération chirurgicale.L'avènement des prothèses implantables parvoie percutanée change ainsi le raisonnementlors du choix de la première prothèse. Il y a toutlieu de penser que les progrès très rapidesobservés au cours des cinq dernières annéesvont s'amplifier et que dans les dix ans quiviennent ce nouveau concept de la valve dansla valve sera largement validé.Au total, l'avenir est indiscutablement auxvalves biologiques. Les observations scientifiquesfaites jusqu'à ce jour, qui donnent un certainavantage aux bio-prothèses, l'evolution de lademande des malades pour plus de confort, lesperspectives de développement des valvestrans-catheter concourent à amplifier letendance actuelle.BibliographieHammermeister MK, Sethi GK, Henderson WG, Grover FL, Oprian C, Rahimtoola SH - Outcomes 15years after valve replacement with a mechanical versus a bioprosthesic valve: final report of theVeterans Affairs randomized trial. J. Am. Coll. Cardiol. 2000, 36, 1152-8.Ruel M, Chan V, Bedart P, et al - Very long term survival implications of heart valve replacementwith tissue vs mechanical prosthesis in adults < 60 years of age. Circulation 2007, 116 (11 suppl)1294-300.2008 Focused update incorporated into ACC/AHA 2006 guidelines for the management ofpatients with heart valvular heart disease. J. Am. J. Cardiol. 2008, 52, 1-1424

ISSN 1583-3534, Boudiaf EH, Amrane MO ■ 2009, vol. 8, no. 1-2, pp. 6-10Facteurs pronostiques de morbi-mortalite de la ChirurgieValvulaire ReduxPr. Boudiaf EH.*, Pr. Amrane MO**Service de chirurgie cardio-vasculaire, E.H.S MAOUCHE MA. - ALGER, ALGERIE*Professeur Agrégé à la Faculté de Médecine d’Alger**Professeur à la Faculté de Médecine d’Alger, Chef de serviceResumeObjectifs: la chirurgie valvulaire rédux est de plus en plus fréquente en Algérie. Le but de cetteétude était d’identifier les facteurs de risque de morbi-mortalité hospitalière de ce type de chirurgie.Methode: 49 patients d’un âge moyen de 51 ans (20-67ans) et avec un sex-ratio de 0.88 ontbénéficié de chirurgie valvulaire rédux entre janvier 2006 et janvier 2009; il s’agissait de chirurgieprogrammée dans la majorité des cas (89.79%), et dans prés de la moitié des cas (46%) la primointerventiona été effectuée dans notre service; les causes de ré interventions les plus fréquentes sontles dysfonctions de plastie mitrale, l’expression d’une nouvelle atteinte valvulaire et les désintertions deprothèses mécaniques sur endocardite infectieuse. L’Euroscore a été utilisé pour prédire le risqueopératoire.Resultats: 80% de nos patients, sont classés dans le groupe dit à risque modéré (score 3-5) avecune mortalité attendue comprise entre 2.90 et 2.94%, nos résultats retrouvent pour ces patients unemortalité à 2.56%. L’étude des résultats post opératoires a objectivé un certain nombre decomplications cardiaques (28.5% de bas débit et 37% de troubles du rythme), de complicationsinfectieuses (8% de médiastinites) et de complications neurologiques (6%). Les facteurs de risque demortalité opératoire retrouvés sont: un geste valvulaire multiple (p = 0.03), une fibrillation auriculairepersistante ou apparue en postopératoire (p = 0.05) et enfin un âge supérieur à 70 ans (p = 0.04).Conclusion: La chirurgie de rédux valvulaire avec geste mono-valvulaire présente une morbimortalitéopératoire, une survie actuarielle et un bénéfice fonctionnel post-opératoire tout à faitcomparables à ceux d’une primo-intervention; Alors que dans la chirurgie de rédux avec geste plurivalvulaire,la morbi-mortalité opératoire est nettement supérieure, mais la survie actuarielle et lebénéfice fonctionnel sont comparables à ceux d’une primo-intervention.Mots-clés: chirurgie valvulaire, réintervention, morbi-mortalitéIntroductionLa pathologie valvulaire rédux, cad la réintervention portant sur un geste valvulaire chez unpatient déjà opéré une ou plusieurs fois auparavant pour une pathologie valvulaire, est enaugmentation constante; elle représente 10% à 15% des patients opérés dans le service.Ce qui reste vrai c’est que c’est une chirurgie à haut risque de morbi-mortalité (sup. à 5%) nonseulement à cause du terrain (multiples tares), mais aussi à cause de la pathologie cardiaque valvulaire(resténose valvulaire, dysfonction de prothèse, désintertion de prothèse sur endocardite, thrombose...).Ce qui change par contre, c’est l’épidémiologie des patients, en effet nous avons affaire à despatients de plus en plus âgés et qui présentent le plus souvent une ou plusieurs tares (diabète, HTA,troubles du rythme, IRF…).6

Boudiaf EH., Amrane MO ■ 2009, vol. 8, no. 1-2, pp. 7Matériel et méthodeIl s’agit d’une étude rétrospective portant sur une série de 49 patients opérés de janvier 2006 àjanvier 2009 dans le service de chirurgie cardio-vasculaire de l’EHS MA.MAOUCHE.Le sex-ratio est de 0.88 avec une légère prédominance féminine (23 hommes / 26 femmes),l’âge moyen est de 51 ans (extrêmes 20-67 ans), pour le type de chirurgie il s’agit de chirurgieprogrammée dans 89.79% (seul 05 patients ont été opérés en urgence); enfin pour ce qui est de laprovenance des patients il s’agit pour 46% de primo-interventions effectuées dans le service et pour 54%primo-interventions effectuées dans d’autres services en Algérie ou à l’étranger.Dans cette étude, le critère d’inclusion est de retenir toute réintervention après primointerventionvalvulaire; il s’agit surtout d’une réintervention, mais nous avons recensé néanmoins 04 casde réinterventions mutiples; le délai de réintervention moyen est de 12 ans (extrêmes 21 jours/26ans).chgie AAchgievalvulreduxvalvulP ACLes patients présentent de plus en plus souvent une ou plusieurs tares qui peuvent être à l’originede complications dans les suites post-opératoires et qui allongent la durée d’hospitalisation; en effet présdu tiers des patients présentent une HTA (28%) et/ou un DID (26%), et a présenté un ou plusieurs épisodesd’insuffisance cardiaque gauche, d’OAP, ou d’insuffisance rénale fonctionnelle; plus de la moitié despatients opérés présentait en pré-opératoire des troubles du rythme à type de FA (56%); enfin pour cettesérie de patients le stade NYHA moyen est de 3.2 ± 0.9.Pour ce qui est des explorations pré-opératoires, l’indice cardio-thoracique moyen est à 58 ± 5%,l’étude de l’ECG a objectivé 12% de blocs de branche gauche, enfin les donnéeséchocardiographiques pré-opératoires ont relevé une fraction d’éjection moyenne à 56 ± 20%, et unepression artérielle pulmonaire systolique moyenne élevée puisqu’elle est à 58 ± 15 mm Hg.ResultatsPour ce qui est des causes de réinterventions, nous avons relevé par ordre de fréquencedécroissante, les dysfonctions de plastie (qui concernent le plus souvent la valve mitrale), l’expressiond’une nouvelle atteinte valvulaire (il s’agit surtout des insuffisances tricuspides négligées lors de la primointervention),puis viennent les désintertions de prothèse (dont prés de la moitié sur endocarditesinfectieuses), les thromboses de prothèses (surtout mitrales) et enfin les dysfonctions de prothèses (surtoutaortiques).L’étude dans le détail des causes de dysfonction de plastie mitrale objective que le gesteeffectué lors de la primo-intervention consistait par ordre décroissant en une commissurotomie à cœurouvert, une plastie mitrale avec mise en place d’un anneau de CARPENTIER, et enfin d’unecommissurotomie à cœur fermé; nous avons par ailleurs remarqué que les délais moyens deréintervention (pour chacun des gestes effectués en primo-intervention) sont intéressants puisqu’ils sonttous supérieurs à 10 ans.L’étude des causes de thrombose de valve prothétique mitrale a retrouvé une thromboseprécoce à J19 post-opératoire par défaut d’anti-coagulation (patient opéré en urgence dans untableau d’OAP et de bas débit sévère), deux thromboses sur grossesses de 8 semaines et enfin deuxthromboses partielles sur valves prothètiques mécaniques.7

■ 季 刊 中 国 資 本 市 場 研 究 2007 Autumn図 表 5 債 券 市 場 の 発 行 状 況年国 債記 帳 式 貯 蓄 国 債 合 計( う ち 短 期国 債 )政 策 金 融債短 期 融 資債 券中 央 銀 行手 形非 政 策 性金 融 債企 業 債( 億 元 )2000 2,692 1,900 4,592 200 1,645 0 0 0 75 6,3122001 3,084 1,800 4,884 0 2,590 0 0 0 140 7,6142002 4,461 1,473 5,934 265 3,175 0 1,938 0 325 11,3722003 5,439 2,505 7,944 595 4,520 0 7,850 0 324 20,6382004 4,414 2,510 6,924 1,398 4,348 0 15,072 749 307 27,3992005 5,042 2,000 7,042 4,190 6,032 1,454 27,882 1,129 654 44,1922006 6,533 2,350 8,883 6,365 8,650 2,920 36,574 695 995 59,1162007 10,327 1,100 11,427 3,986 6,635 2,119 34,091 - 536 -( 注 ) 2007 年 は 8 月 時 点 。 貯 蓄 国 債 は 個 人 向 けであり、 記 帳 式 国 債 が 公 開 市 場 操 作 に 関 係 する。 短 期 国 債 は満 期 1 年 以 下 。 非 政 策 性 金 融 債 は 商 業 銀 行 債 券 ・ 劣 後 債 、 国 際 開 発 機 関 の 債 券 を 含 む。( 出 所 ) 中 国 人 民 銀 行 (2007)、 中 国 債 券 信 息 網 より 作 成合 計発 に 利 用 できるように 改 定 作 業 が 進 められている 14 。 具 体 的 には、2007 年 8 月 14 日 に、「 会 社債 発 行 試 験 弁 法 」が 施 行 された。これは、 会 社 法 で 規 定 される 株 式 会 社 と 有 限 会 社 の 中 国 国 内 における 社 債 発 行 についての 規 定 である。これまでは、 社 債 発 行 に 国 家 発 展 改 革 委 員 会 の 認 可 が 必要 であったが、 新 制 度 では、 株 主 会 ・ 株 主 総 会 での 決 議 を 経 て、 証 監 会 の 認 可 を 受 ければ 良 く、また、 発 行 価 格 はブックビルディングを 通 じて 決 定 されることになっており、 発 行 量 、 金 利 とも規 制 からの 脱 却 が 図 られている。第 五 に、 市 場 流 動 性 の 点 で、2006 年 7 月 に、 銀 行 間 市 場 におけるマネーブローカー 業 務 が 正式 に 開 始 した。また、 人 民 銀 行 は 2007 年 1 月 に「 全 国 銀 行 間 債 券 市 場 債 券 マーケットメイカー管 理 規 定 」を 発 表 した。これは、 銀 行 間 債 券 市 場 の 債 券 マーケットメイカーの 参 入 基 準 の 引 下 げなどを 含 むものである。2. 特 別 国 債人 民 銀 行 の 保 有 債 券 不 足 の 問 題 は、2007 年 8 月 に 発 行 され 始 めた 特 別 国 債 により 多 少 緩 和 されると 見 られる。これは、 外 貨 準 備 の 運 用 のために 今 年 中 に 設 立 される「 中 国 投 資 有 限 公 司 」の資 金 源 として 財 政 部 が 発 行 する 国 債 である。まず、6000 億 元 の 特 別 国 債 が 2007 年 8 月 29 日 に発 行 された。この 6000 億 元 により、 人 民 銀 行 から 6000 億 元 相 当 分 の 外 貨 準 備 を 買 い 取 って 運 用する。8 月 の 発 行 の 際 は、 国 債 を 人 民 銀 行 が 直 接 引 き 受 けることはできないので、 一 旦 、 財 政 部が 特 別 国 債 を 中 国 農 業 銀 行 に 向 けて 発 行 し、 人 民 銀 行 が 農 業 銀 行 から 買 い 取 る 形 をとった 15 。この 時 点 では、 農 業 銀 行 の 中 央 銀 行 預 金 (= 準 備 預 金 )に 変 化 はなく、 銀 行 システム 全 体 でも 準 備預 金 に 変 化 はない。1415中 国 では、 企 業 債 と 会 社 (「 公 司 」) 債 を 区 分 する 方 向 にある。 中 国 では 国 家 的 プロジェクトをファイナンスするために、 会 社 法 に 規 定 する 会 社 ではない 事 業 体 が 発 行 する 企 業 債 も 多 い。 企 業 債 については 従 来 通 り 国 家発 展 改 革 委 員 会 が 主 管 し、 会 社 債 については 機 動 的 な 発 行 を 可 能 にする。次 の 2000 億 元 の 特 別 国 債 は、 財 政 部 が 銀 行 間 市 場 で 直 接 売 却 する 予 定 であり、 発 行 の 際 、 準 備 が 吸 収 されるものと 思 われる。18

Boudiaf EH., Amrane MO ■ 2009, vol. 8, no. 1-2, pp. 93020100I II III IVNY HA pré-opNY HA pos t-Quant à l’amélioration de la FEVG, sur un délai moyen de 18 mois nous avons revus tous lespatients survivants, et l’étude des résultats a pu objectivé une amélioration moyenne de la FEVG de 18 ±13%; la FEVG moyenne est passée de 56 ± 20% en pré-opératoire à 63 ± 12% en post-opératoire, celasignifie que 73% des patients survivants à l’issue de la période opératoire ont récupéré au moins 5 pointsde FEVG.L’étude de la courbe de survie actuarielle à 3 ans des patients qui ont subi une réinterventionavec geste mono-valvulaire et celle des patients qui ont bénéficié d’un geste mono-valvulaire en primointerventionsont tout à fait comparables.Alors que la comparaison de la courbe de survie actuarielle à 3 ans des patients qui ont subi uneréintervention avec geste pluri-valvulaire avec celle des patients qui ont bénéficiés d’un geste plurivalvulaireen primo-intervention montre des différences notables.9

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 10ConclusionsLa chirurgie de rédux valvulaire avec geste mono-valvulaire présente une morbi-mortalitéopératoire, une survie actuarielle et un bénéfice fonctionnel post-opératoire tout à fait comparables àceux d’une primo-intervention.Alors que dans la chirurgie de rédux avec geste pluri-valvulaire, la morbi-mortalité opératoire estnettement supérieure, mais la survie actuarielle et le bénéfice fonctionnel est comparable à ceux d’uneprimo-intervention.Enfin, pour améliorer les résultats en terme de morbi-mortalité opératoire, il faut impérativementque la prise en charge chirurgicale soit précoce avant la détérioration du status fonctionnel (NYHA) etde la fonction ventriculaire (FEVG), il faut évaluer les co-morbidités et déterminer les risques de mortalitépar l’utilisation des scores, et surtout, il faut améliorer le suivi médical des porteurs de prothèsesvalvulaires mécaniques.Bibliographie1. JEGADEN O. - BONNEFAY J.Y. - « Les réinterventions en chirurgie valvulaire, à propos de 194cas », Archives des maladies du cœur et des vaisseaux 1986 vol. 79, N°122. DOUZEAU GOUGE. P - BENOMAR. M. - « Les réinterventions sur bioprothèses valvulaires »Archives des maladies du cœur et des vaisseaux 1985 vol. 78, N°810

ISSN 1583-3534, R. Căpîlnă et al ■ 2009, vol. 8, no. 1-2, pp. 11-16Right ventricular outflow tract reconstruction using pericardicvalved conduit – a 3 year retrospective study in Mures Transplantand Cardiovascular Disease InstituteR. Căpîlna¹, H. Suciu², Brîndusa Căpîlna³, R. Bălau 5 , I. Tilea 4 ,Jerzicska E. 1 , Monica Suciu 5 , R. Deac²1. Clinica Chirurgie cardiovasculară II, Institutul de Urgenta Boli Cardiovasculare si Transplant Tg-Mureş2. Disciplina Chirurgie, Clinica Chirurgie Cardiovasculară, Facultatea de Medicină, U.M.F. Tg-Mureş3. Disciplina Pediatrie, Clinica Pediatrie I, Facultatea de Medicină, U.M.F. Tg-Mureş4. Disciplina Medicină Internă III, Clinica Medicală III, Facultatea de Medicină, U.M.F. Tg-Mureş5. Clinica Chirurgie Cardiovasculară II, IBCVT Tg-MureşAbstractObjective: To assess the performance of the valved conduit used for tract reconstruction inright ventricular (RV) outflow stenosis or athresia.Methods: A retrospective study of 7 consecutive right ventricular to pulmonary artery-conduitimplants patients between January 2006 and April 2009 was performed. The majority of cases 3 - werewith pulmonary atresia/VSD, one with Fallot’s tetralogy one with truncus arteriosus with ventricularseptal defect, one with single ventricle type right ventricle and one with complete atrioventricularseptal defect with double outlet left ventricle and great vessels transposition. At all the cases we haveperformed conduit implantation and supplementary repair techniques. Echocardiography wasperformed for a median follow-up of 14 months.Results: Median age at implantation was 13 months and median weight was 7.8 kg. Six patientswere

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 12IntroductionIt is 40 years since Ross and Somerville reported the successful use of human tissue graft valves,which broadened the scope for a possible durable conduit for right ventricular outflow tractreconstruction. A variety of prosthetic conduits have since developed, although homografts continue tobe regarded as the most reliable option. The most used conduit is heterologus pericardial conduit,because it is made with low costs. The alternative possibility is to use homologous conduit or jugularbovine conduit (Contegra) [4]. However, the pericardial conduit is a conduit with good pliability, butthey have an important inconvenience – early/medium calcification and degeneration, particularly invery young patients [6]. The objective of this study was to assess the performance of pericardial valvedconduit particularly reffering to younger age at time of implantation.Material and MethodThis is a prospective study of 7 cases of valved conduits used in right ventricle outflow tractreconstruction between January 2006 and April 2009 at Transplant and Cardiovascular Disease Institute.The majority of cases 3 were with diagnosed pulmonary atresia/VSD (43%), one with Fallot’s Tetralogy(14%), one with truncus arteriosus with ventricular septal defect, one with single ventricle type rightventricle and one with complete atrioventricular septal defect with double outlet left ventricle andtransposed great vessels. (Table 1)Table 1All the children presented patent ductus arteriosus. The most common diagnosed method wasechocardiography, only the patient with Truncus arteriosus needed cardiac catheterization forpulmonary hypertension evaluation. New techniques are figured by 3D tomography reconstruction(Figure 1), (Figure 2), (Figure 3).12

R. Căpîlnă et al ■ 2009, vol. 8, no. 1-2, pp. 15The proximal suture line (at theventriculotomy site) was performed with alayer of continuous 5/0 or 6/0 polypropylenesuture (depending on the conduit size)reinforced with interrupted pledgettedsutures at the heel of the anastomosis.(Figure 7)Figure 7: Intraoperator aspect – final resultafter valved conduit implantationAll the children were left with the sternum open, with a pericardial membrane, for 24-48 few days,to avoid sternal conduit compression. Early mortality was 14% (n = 1).The recovery in cardiac intensive room had a mean value of 7, 6 days with a range between 5and 11 days. The children were discharged from the hospital at a median time of 14 days after theoperation. Actuarial survival was 100% and all the children have freedom from reintervention at 4 yearsafter the operation. Some studies recommend anticoagulant or Aspirin utilization, to haste theendothelialisation of the graft in a low pressure system. In some cases, we used Aspirin therapy for a fewmonths after the operation.We follow the patients at 1, 3, 6, 12 month after the operation and annually thereafter. At thistime, all the children are free of unexpected evolution of the pericardial valved conduit. The valvedconduits are free of stenoses (only in 1 case have a moderate stenosis of distal suture line), conduitdilatation and/or valvular regurgitation, conduit endocardithis or trombosys.At ecocardiography of the children who was operated 3 and 4 years ago, we observe incipientcalcification and degeneration of the pericardial valved conduit. The international studies shown us thatthe pericardial conduit presents severe calcification after a mean time of 8 years (Figure 8), (Figure 9).Figure 8: Explanted valved conduitFigure 9: Radioscopic image of explanted valvedconduitShort and mid-term results showed minimal transvalvular pressure gradients and goodhemodynamic functional performance according to other available conduits. All the small children arein good clinical status and low clinical symptoms.15

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 16DiscussionsThe heterologous valved conduit could be an attractive option with small costs for rightventricular outflow tract reconstruction particularly in smaller patients. [3, 4, 5, 6] Excellent tissue handling,haemostasis, versatility and off-the-shelf availability are the main advantages [4, 6]. However, there is alow incidence of conduit-related complications, the commonest being the stenosis at the distal sutureline during follow-up only at the smaller-sized conduits (12 and 14 mm). High pressure in the conduit canlead to aneurismal dilatation and secondary valvar regurgitation [4]. However, there is also a smallunpredictable risk of conduit dilatation that is unrelated to pressure and also of thrombosis in the valvesinuses, neither of which appear to be clinically important but remain a cause for concern and will needfurther evaluation. The role of aspirin and antithrombotic therapy needs to be evaluated.It must be taken into account that a child is more sensitive than adults, and cardiac surgery hasa major psychological impact. It is necessary to choose always the most favorable surgical maneuver toprevent the reintervention and to ensure the comfort of a child's life at a high level. [1, 2]Bibliography1. Suciu H., Căpîlna R., Matei M. et all - Right Ventricle Outflow Tract. ReconstructiveOpportunities, 20082. Suciu H., Căpîlna R., Harpa M. – Particularity of surgical treatment in Fallot Tetralogy withpulmonary atresia, Congressus Marissiensis, 20093. Jonas A.R., DiNardo J., Laussen P.C. et all – Comprehensive Surgical Management ofCongenital Heart Surgery, Arnold-Hodder Headline Group, London, 2004; 413-429, 457-4704. Shebani S.O., McGuirk S., Baghai M., et all - Right ventricular outflow tract reconstruction usingContegra® valved conduit, European Journal of Cardiothoracic Surgery 2006; 29:397-4055. Rodriguez E., - Pulmonary Atresia with Ventricular Septal Defect, emedicine.com article, 20066. Ghanayem N. Jaquiss R.B.D., Cava R.J. et all - Right Ventricle–to–Pulmonary Artery ConduitVersus Blalock-Taussig Shunt, Forty-second Annual Meeting of The Society of Thoracic Surgeons,Chicago, IL, Jan 30–Feb 1, 2006 and Ann Thorac Surg 2006; 82:1603-1610.7. McMullan D.M., Oppido G., Alphonso N., et all - Evaluation of downsized homograft conduitsfor right ventricle–to–pulmonary artery reconstruction, Journal Thoracic and CardiovascularSurgery 2006; 132:66-7116

ISSN 1583-3534, Grigore Tinică et al ■ 2009, vol. 8, no. 1-2, pp. 17-20Off-pump bidirectional cavo-pulmonary (Glenn) shuntimproves the outcome in a functionally univentricular heartGrigore Tinica, Alexandru Ciucu, Dan Dascalescu,Liliana Ciucu, Mihail Enache, Diana Ciurescu, Victor PrisacariCardiovascular Surgery Department, IasiUniversity of Medicine and Pharmacy „Gr. T. Popa” IasiAbstractThe cavo-pulmonary shunt using a temporary external shunt in functionally univentricular heart hasbecome an alternative to the common bidirectional Glenn procedure performed undercardiopulmonary by-pass 1,2,3 . We present a patient with a single left ventricle, hypoplastic rightventricle, L malposition of the aorta, huge ventricular septal defect and severe pulmonary stenosis.Key Words: Bidirectional cavopulmonary shunt; Off-pump.IntroductionThe development of the cavo-pulmonary anastomosis is an important landmark in the surgicaltreatment of the congenital heart disease. This shunt was developed experimentally and introduced inclinical practice by many surgeons working independently and unaware of each other’saccomplishments and is now referred to as the Glenn procedure 4 . The bidirectional Glenn procedure asa palliative surgical management for children with functionally univentricular heart is now widelyaccepted 5 . Most frequently, this procedure is performed under cardiopulmonary by-pass 6 . Theavoidance of cardiopulmonary by-pass with the use of transient external shunt in selected patients offersa multitude of advantages 7,8,9 . Using this technique, the patient is early extubated, has less thoracic fluiddrainage and has a decreased need for inotropic support due to a better hemodinamic status with astable systemic circulation and an adequate pulmonary flow 10,11 . This technique improves efficiency ofgas exchange and increases pulmonary blood flow thus raising systemic arterial oxygen saturation(SaO2) without volume overload of the ventricle.Case reportA 7-year-old boy, weighing 17.5 kg who was diagnosed at birth with congenital heart disease isadmitted in our clinic with progressive cyanosis, clubbing, dyspnoea at rest and a transcutaneousoxygen saturation of 58-74%. Electrocardiogram showed sinus rhythm, a normal atrioventricularconduction, a right ventricular hypertrophy and a right deviated ORS axis. Cardiac catheterizationshowed right to left shunt at the ventricular level; an aortic saturation of 47%; right atrium connected toright sided, morphologic left ventricle. Ventriculography showed from the right side, morphologic leftventricle with a contrast that goes both into the aorta and the pulmonary artery; left malposition of theaorta with an asceding aorta of 22 mm, the main pulmonary artery of 10 mm with both left and rightbranches of 14 mm and a normal pulmonary vascular tree; severe pulmonary valvular stenosis; hugeventricular septal defect; small left sided right ventricle; left aortic arch and no aortic regurgitation; leftcircumflex artery emerges from right coronary artery; important bronho-pulmonary collaterals. Thetransthoracic echocardiography showed a huge ventricular septal defect of 25 mm in diameter,between right and anterior situated morphologic left ventricle and a left and posterior situatedmorphologic right ventricle. The morphologic left ventricle is considerably greater; the flow across theventricular septal defect is bidirectional; functionally single ventricle; both atrioventricular valves are17

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 18committed to the morphologic left ventricle (the right sided atrioventricular valve is tricuspid and the leftsided one is of mitral type); normal function of the atrioventricular valves; the ventriculoarterialconnection is of double outlet type with the main pulmonary artery situated posterior and to the rightand the aorta situated anterior and to the left; severe subvalvular pulmonary stenosis (with a gradient of85/70 mmHg) and a hypoplastic main pulmonary artery. LVDd 40 mm, LVDs 35 mm, LVWd 9 mm, EFvol40-50%, LVTDV 76 ml, LVTSV 33 ml, LA 28 mm, RA 23/21 mm. After this complete evaluation of the patientwe decided to conduct the bidirectional Glenn procedure without cardiopulmonary by-pass.The procedure was performed under general anesthesia with cannulation of the radial arteryand left internal jugular vein with a triple-lumen central venous catheter for administration of vasoactivedrugs and fluids. ECG, SaO2, EtCO2 and rectal temperature were continuosly monitored. Blood glucoselevels and arterial blood gases were analyzed at regular intervals. The ambiental temperature wascooled to 17 0 C and the patient was cooled to 35 0 C and we conducted the operation with the head ofthe table elevated for lowering the proximal caval pressure. After a median sternotomy, the pericardiumwas opened, systemic heparinization (1 mg/kg) was administrated and the superior vena cava (SVC)was dissected and isolated from the cardiac end to innominate vein junction and the right pulmonaryartery was dissected and isolated from the bifurcation to the hilar region. The azygous vein was ligatedand divided to allow proper mobilization. Purse-strings sutures were placed on the right atrium and theinnominate vein.Clamping the SVC withoutdecompression exposes thebrain to the effects of reducedcerebral perfusion pressure. Inorder to decompress the SVC toprevent neurological damageduring clamping, a shunt wasestablished between theinnominate vein and the rightatrium with a right-angled andstraight cannula, respectively.The SVC was temporarilyoccluded in order to fill up thecircuit with blood to prevent airembolism. After establishing thetemporary shunt and clampingthe SVC, the venous pressureincreased up to 30 mmHg.Then, we could safely proceedto clamp the SVC and divide itfrom the cavoatrial junction,taking care not to damage thesinus node.18

Grigore Tinică et al ■ 2009, vol. 8, no. 1-2, pp. 19The atrial end was oversewn and the right pulmonary artery was clamped with vascular clampsand a longitudinal arteriotomy of 1,5-2 cm was performed on the superior aspect, followed by the endto-sideanastomosis with the SVC using a running suture with 7/0 polypropylene and after that wereleased the clamps and the temporary shunt was disconnected in the middle and the blood in thecannulae was allowed to drain into the innominate vein and right atrium, respectively. Then, thecannulae were removed and the purse-string sutures tied.Basal arterial O2saturation were 60 2 mmHgand after operation increasedto 88 2 mmHg. Duringclampage, minimum arterialblood pressure was measured60 3 mmHg. Mean centralvenous pressure duringclampage of 22 2 mmHg,and post-operatively of 12 2mmHg. The duration of theanastomosis (clamping) was12 min and the duration of theoperation was 130 min. Thepatient had a good recovery,an immediate improvement inSaO2 and an excellentpostoperative response to theshunt, the hemodynamicstatus did not deteriorateduring the anastomosis. Noblood transfusion was requiredduring operation and in the postoperative period. The weaning off mechanical ventilator was within thefirst 2 hours of surgery. The patient received antiplatelet treatment in form of low doses of aspirin.Cyanosis was clearly relieved at discharge and SaO2 increased up to 84%. Postoperativeechocardiography demonstrated a functional cavopulmonary anastomosis. The patient hadneurological examination performed by the same phisician on the second postoperative day andbefore discharge and did not show any abnormality.DiscussionBidirectional Glenn shunt could be performed without using CPB if there is no need of correctingany other intracardiac malformations 12 . This bidirectional Glenn procedure diverts systemic venous returnfrom the superior vena cava to the both lungs through the right pulmonary artery, bypassing thehypoplastic right ventricle 13,14 .Since 1958, when Glenn 15 described the clinical use of an SVC-RPA shunt to a 7-year-old boy withtransposition of great vessels and decreased blood flow, who’s condition was improved significantlyafter the shunt, many variations have been performed for the palliation of children with cyanoticcongenital heart diseases, where the increased SaO2 may be enough to reduce cyanosis, and theadditional source of pulmonary blood flow may modestly improve exercise tolerance. Glenn’s clinicalreport was followed shortly by a successful operation reported by Sanger, Robicsek and Taylor 16 .The first to describe the use of the transient shunts for caval drainage during clampage ofsuperior vena cava was Lamberti 17 et al. because the ineffective caval drainage may lead to an acuteincrease in intracranial pressure. In their experience of seven cases, they could decrease caval pressureabout 15 mmHg using an external shunt. Cherian et al. 9 performed bidirectional Glenn shunt operationby using different types of transient external shunt. Mohan Reddy 18 et al. demonstrated a post-operativeincrease in pulmonary vascular resistance and hypoxia after cardiopulmonary bypass and reported thattransient external shunt approach must be indicated on a wider basis. Further studies need to be done inorder to establish the best type of shunt to use. Tireli 19 et al. demonstrated the best hemodynamicalcondition and arterial O2 levels were achieved with the shunt placed between superior vena cava andleft pulmonary artery.19

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 20Jahanghiri 20 et al. reported seven bidirectional Glenn procedures without using cardiopulmonarybypass or transient external shunts, through a toracotomy. They encountered no neurologicalcomplications and reported that establishing an intraoperative shunt was not necessary.In conclusion, the technique used provides a good venous drainage, a good-long-termprognosisand eliminates the problems related to cardiopulmonary by-pass known to activate theinflammatory mediators, increase lung water, and decrease right ventricular compliance which canincrease pulmonary vascular resistance and decrease pulmonary blood flow after the cavopulmonaryconnection. That is the reason that we try to perform this procedure without the CPB, whenever ispossible. This approach is only possible to selected patients. The bidirectional cavopulmonary shuntperformed without cardiopulmonary bypass and using different types of transient external shuntsimproves systemic arterial oxygen saturation without increasing ventricular work or pulmonary vascularresistance. Our technique is a safe and easy to perform procedure in the early management of patientswith univentricular heart.References1. Mazzera E, Corno A, Picardo S, Di Donato R, Marino B, Costa D, Marcelletti C. Bidirectional cavopulmonaryshunts: clinical applications as staged or definitive palliation. Ann Thorac Surg 1989; 47:415–420.2. Trusler GA, MacGregor D, Mustard WT. Cavopulmonary anastomosis for cyanotic congenital heart disease. JThorac Cardiovasc Surg 1971; 62:803–809.3. Hopkins RA, Armstrong BE, Serwer GA, Peterson RJ, Oldham HN Jr. Physiological rationale for a bidirectionalcavopulmonary shunt. A versatile complement to the Fontan principle. J Thorac Cardiovasc Surg 1985; 90:391–398.4. Konstantinov IE, Alexi-Meskishvili V. Cavo-pulmonary shunt: From the first experiments to clinical practice. Ann.Thorac Surg 1999; 68:1100-6.5. Glenn WWL. Circulatory bypass of the right side of the heart. IV. Shunt between superior vena cava and distalright pulmonary artery – report of clinical application. N Engl J Med 1958; 259:117–120.6. Liu J, Lu Y, Chen H, Shi Z, Su Z, Ding W. Bidirectional Glenn procedure without cardiopulmonary bypass. AnnThorac Surg 2004; 77:1349–1352.7. Villagra F, Gomez R, Ignacio HJ, Larraya FG, Moreno L, Sar P. The bidirectional cavopulmonary (Glenn) shuntwithout cardiopulmonary bypass: a safe and advisable technique. Rev Esp Cardiol 2000; 53:1406–1409.8. Luo X, Yan J, Wu Q, Yang K, Xu J, Liu Y. Clinical application of bidirectional Glenn shunt with off-pumptechnique. Asian Cardiovasc Thorac Ann 2004; 12:103–1069. Murthy KS, Coelho R, Naik SK, Punnoose SK, Thomas W, Cherian KM. Novel technique of bidirectional Glennshunt without cardiopulmonary bypass. Ann Thorac Surg 1999; 67:1771–1774.10. Burke RP, Jacobs JP, Ashraf MH, Aldousany A, Chang AC. Extracardiac Fontan operation withoutcardiopulmonary bypass. Ann Thorac Surg 1997;63:1175-711. Uemura H, Yagihara T, Yamashita K, Ishizaka T, Yoshizumi K, Kawahira Y. Establishment of total cavopulmonaryconnection without use of cardiopulmonary bypass. Eur J Cardiothorac Surg 1998; 13:504-7.12. Xie Bin MD, Zhang Jin Fang MD, Devi Prasad Shetti MS. Bidirectional Glenn shunt: 170 cases. Asian CardiovascThorac Ann 2001; 9:196-9.13. Freedom RM, Nykanen D, Benson LN. The physiology of the bidirectional cavopulmonary connection. AnnThorac Surg 1998; 66:664-7.14. McElhinney DB, Marianeschi SM, Reddy VM. Additional pulmonary blood flow with the bidirectional Glennanastomosis: does it make a difference? Ann Thorac Surg 1998; 66:668-72.15. Glenn WWL. Circulatory bypass of the right side of the heart. IV. Shunt between superior vena cava and distalright pulmonary artery – report of clinical application. N Engl J Med 1958; 259:117–120.16. Sanger PW, Robicsek F, Taylor FH. Vena cava-pulmonary artery anastomosis:III. Successful operation in case ofcomplete transposition of the great vessels with intra-atrial septal defect and pulmonary stenosis. J ThoracCardiovasc Surg 1959; 38:166-71.17. Lamberti JJ, Spicer RL, Waldman JD, Grehl TM, Thomson D, George L, Kirkpatrick SE, Mathewson JW. Thebidirectional cavopulmonary shunt. J Thorac Cardiovasc Surg 1990; 100:22–30.18. Reddy VM, Liddicoat JR, Hanley Fl. Primary bidirectional superior cavopulmonary shunt in infants between 1 and4 months of age. Ann Thorac Surg 1995; 59:1120-5.19. Tireli E, Basaran M, Kafali E, Harmandar B, Camei E, Dayioglu E, Onursal E. Peri-operative comparison of differenttransient external shunt techniques in bidirectional cavo-pulmonary shunt. Eur J Cardiothoracic Surg 2003;23:518–524.20. Jahangiri M, Keogh B, Shinebourne EA, Lincoln C. Should the bidirectional Glenn procedure be performedthrough a thoracotomy without cardiopulmonary bypass? J Thorac Cardiovasc Surg 1999; 118:367–368.20

ISSN 1583-3534, Boudiaf EH, Dr. Benkelfat C ■ 2009, vol. 8, no. 1-2, pp. 21-26Revascularisation myocardique par pontages artérielsRésuméPr. Boudiaf EH, Dr. Benkelfat C,Clinique CHIFFA – ALGER, ALGERIEDepuis les grandes études (CASS, Européenne, Vétérans), le pontage mammaire interne s'estimposé comme la technique de référence en chirurgie coronaire. Le pontage mammaire bilatéral aété très controversé; actuellement il est admis qu'il a un effet additionnel sur le pronostic vital etfonctionnel des patients lorsqu'il revascularise le réseau coronaire gauche. L'artère radiale et l'artèregastro-épiploïque droite sont souvent utilisées en complément pour une revascularisation artérielleexclusive, sans que leur impact positif sur les résultats de la chirurgie coronaire n'ait été montré. Unestratégie chirurgicale qui intègre le matériel disponible, la spécificité des patients et les perspectivesde résultats à moyen et long terme, est proposée.Mots-clés: pontage coronaire, artère mammaire interne, artère radiale, artère gastro-épiploïqueLe principe de l'utilisation de greffons artériels en chirurgie coronaire repose avant tout sur ladégradation inéluctable et continue des pontages veineux avec un taux de perméabilité à 10 ansinférieur à 60% [1]; les greffons perméables présentant le plus souvent des anomalies intra-luminalessusceptibles de progresser. Cette altération des pontages veineux s'accélère après la 5 e année postopératoireet est significativement corrélée au recul post-opératoire, à l'existence de maladiesmétaboliques: diabète ou dyslipidémie, et à la survenue d'événements cardiaques post-opératoires:récidive angineuse ou infarctus du myocarde [2]. En revanche, le bénéfice pour les patients de larevascularisation de l'interventriculaire antérieure par un pontage artériel mammaire interne gauche aété clairement montré: comparé à l'utilisation d'un pontage veineux, à 10 ans le risque de décès estdiminué 1,6 fois, le risque d'infarctus 1,4 fois, le risque de réintervention deux fois et le risque de toutévénement cardiaque post-opératoire de 1,3 fois [3]; du fait de l'excellente longévité des pontagesmammaires internes avec un taux de perméabilité à 10 ans de 90% [4]. Ces résultats ont imposé lepontage mammaire interne comme la technique de référence pour revasculariser l'interventriculaireantérieure, devant être réalisé chaque fois qu'il est possible d'autant que son utilisation n'augmente pasle risque opératoire.Le bénéfice démontré du pontage mammaire interne-IVA a incité de nombreuses équipes àutiliser le deuxième pédicule mammaire interne pour revasculariser le réseau circonflexe ou coronairedroit, en association au pontage mammaire interne-IVA. Le concept du double pontage mammaireinterne repose donc sur l'hypothèse d'un effet additionnel d'un deuxième pédicule artériel sur lesrésultats de la chirurgie de revascularisation myocardique, avec un bénéfice cumulé des pontagesmammaires internes. L'intérêt des deux pédicules mammaires internes en chirurgie coronaire a étécontroversé du fait de l'absence d'étude randomisée ou multicentrique. Néanmoins, se dégage unconsensus pour admettre que le risque opératoire des doubles pontages est peu différent de celuiobservé pour les procédures utilisant un seul pédicule mammaire interne [5-7]. En cas de pontagemammaire interne bilatéral, les facteurs pronostiques habituels de la chirurgie coronaire sont trouvés;l'utilisation des deux pédicules mammaires internes n'augmente pas la morbidité péri-opératoire despatients à l'exception du risque de médiastinite qui semble accrue en cas d'obésité ou de diabète [8].De même, cette technique n'augmente pas le risque opératoire chez les patients de plus de 65 ans ouen cas de réopération [6]. L'excellence des pédicules mammaires internes droit ou gauche en termesde perméabilité et de débit est la même [9, 10].21

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 22Figure 1 A. Implantation de l'artère thoraciqueinterne gauche (ATIG), pédiculée squelettisée, surune interventriculaire antérieure (IVA)Figure 1 B. Implantation de l'artère thoraciqueinterne gauche, pédiculée squelettisée, surune branche latéro-circonflexe.Le pontage mammaire interne bilatéral assure une suppléance coronaire satisfaisante à l'effortet représente une réserve coronaire suffisante pour le réseau coronaire gauche même en cas degreffon séquentiel avec deux ou trois anastomoses par pédicule [11]. L'utilisation des greffonsmammaires internes séquentiels permet d'augmenter le nombre d'anastomoses artérielles par patientsans compromettre leur excellente perméabilité [12].Bien qu'il existe un certain consensus pour préconiser l'utilisation des artères mammaires internesen greffons pédiculés, certains auteurs ont développé l'utilisation de l'artère mammaire interne droite engreffon libre aorto-coronaire associé au pontage classique mammaire interne gauche-IVA afind'augmenter la longueur du greffon mammaire disponible et donc d'optimiser les possibilités derevascularisation myocardique artérielle complète [13]. Cette technique est controversée car elles'accompagne d'une altération de la perméabilité à long terme du greffon mammaire libre [4, 12]. Uncompromis technique a été proposé par Tector [14] avec un greffon mammaire interne droit libremammaire-coronaire, c'est-à-dire réimplanter latéralement sur le pédicule mammaire interne gaucheréalisant ainsi un greffon en T. Bien que cette technique semble préserver la perméabilité mammaire àlong terme, elle est controversée du fait de sa difficulté technique et de la dépendance de la totalitéde la revascularisation coronaire à partir du seul pédicule mammaire interne gauche avec un risqued'hypoperfusion coronaire [4].La réalité d'un effet additionnel du deuxième pédicule mammaire interne sur les résultats àmoyen terme de la chirurgie coronaire a été difficile à mettre en évidence; le bénéfice du pontagemammaire interne bilatéral semblait tardif [6], vraisemblablement parce que l'impact de larevascularisation du réseau circonflexe ou coronaire droit est moindre que celui de la revascularisationde l'IVA; sans doute également du fait des grandes variations d'utilisation du deuxième pédiculemammaire interne: revascularisation du réseau circonflexe ou coronaire droit, greffon séquentiel ou non,greffon libre ou pédiculé, pontage veineux associé ou non. Cependant, Pick [15] a montré dans uneétude comparative non randomisée que par rapport au pontage mammaire interne unique associé àdes pontages veineux, le pontage mammaire interne bilatéral revascularisant de façon préférentielle leréseau coronaire gauche, améliorait de façon significative à 10 ans le pronostic vital et fonctionnel despatients.22

Boudiaf EH, Dr. Benkelfat C ■ 2009, vol. 8, no. 1-2, pp. 23Figure 2. Contrôle d'une implantation en Y del'artère thoracique interne droite à destinée latérocirconflexe,sur l'artère thoracique interne gaucheà destinée interventriculaire antérieure.Figure 3. À la partie supérieure: implantation d'uneartère thoracique interne droite en greffon libre eten séquentiel sur deux branches du réseaucirconflexe. À la partie inférieure: implantationséquentielle en saphène sur l'interventriculairepostérieure et la rétroventriculaire gaucheDe même Schmitt [16] dans une étude comparative non randomisée a montré que l'utilisationpréférentielle des deux artères mammaires internes pour revasculariser le réseau coronaire gauchepermettait d'améliorer de façon significative le pronostic vital des patients à partir de la cinquièmeannée post-opératoire par rapport à une revascularisation mammaire bilatérale intéressant l'IVA et leréseau coronaire droit. Cet impact positif du pontage mammaire interne bilatéral sur le pronosticfonctionnel et vital à long terme des patients a été confirmé de façon indiscutable par deux étudescomparatives importantes portant sur plusieurs milliers de patients: selon Buxton [17] le pontage internebilatéral est un facteur prédictif indépendant des taux de mortalité tardive, d'infarctus myocardiquesecondaire et de réopération; selon Lytle [18] le pontage mammaire interne bilatéral diminue de façonsignificative le risque à long terme de décès, de réopération et d'angioplastie coronaire; dans ces deuxétudes, le pontage mammaire interne bilatéral a été réalisé de façon préférentielle pour revasculariserle réseau coronaire gauche.Ces résultats ont incité de nombreuses équipes à considérer le pontage mammaire internebilatéral comme la technique de référence optimale en chirurgie coronaire et à rechercher un troisièmepédicule ou greffon artériel susceptible d'être associé aux pédicules mammaires internes afin de réaliserdes revascularisations myocardiques artérielles exclusives. L'artère épigastrique a été peu utilisée; sastructure histologique favorise le spasme et le développement de lésions athéromateuses [19]. L'artèreradiale connaît un regain d'intérêt important bien que son prélèvement nécessite un deuxième siteopératoire. Sa longueur et sa structure sont adaptées à des pontages coronaires multiples et elle estutilisée en greffon libre soit aorto-coronaire, soit mammaire-coronaire [20]. L'utilisation technique est peudifférente de celle d'un pontage veineux classique et sa perméabilité à 5 ans est satisfaisante, enmoyenne 85% [21]; ces deux critères ont beaucoup contribué au développement de son utilisationparfois bilatérale [22]. Le prélèvement de l'artèreradiale n'a pas de conséquence fonctionnelle sur lemembre supérieur après vérification pré-opératoire dela perméabilité des anastomoses palmaires par testd'Allen. L'utilisation de l'artère radiale commealternative à une deuxième mammaire semblediminuer l'incidence des infections sternales postopératoires[23], mais risque de compromettre lesrésultats à moyen et à long terme compte tenu de ladifférence de perméabilité de ces deux greffonsartériels.Figure 4. Contrôle d'un pontage séquentiel artèrethoracique interne gauche, diagonaleinterventriculaire antérieure23

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 24Figure 5 A. Contrôle d'un pontage artèrethoracique interne gauche interventriculaireantérieureFigure 5 B. Contrôle d'un pontage artèrethoracique interne droite pédiculéeinterventriculaire antérieure (passage antérieur)L'artère gastro-épiploïque droite est également très utilisée [24]; son prélèvement ne nécessitepas un autre site opératoire, sa structure histologique est peu différente de celle de l'artère mammaireinterne [19], sa perméabilité à 5 ans est satisfaisante, en moyenne 92% [25, 26] et elle assure unesuppléance coronaire satisfaisante à l'effort [24]. Son utilisation n'augmente pas le risque opératoire etn'induit pas de morbidité spécifique. Elle est utilisée pédiculée, le plus souvent pour revasculariser leréseau coronaire droit en alternative à un pontage veineux ou à un pontage artériel libre.La combinaison de ces différents greffons artériels permet de réaliser des revascularisationsmyocardiques artérielles exclusives, techniques qui s'imposent progressivement comme le gold standarden chirurgie coronaire [27, 28]. Sa réalisation n'augmente pas le risque péri-opératoire et les résultats àmoyen terme sont actuellement très encourageants avec une survie à 5 ans supérieure à 90% pour destaux de récidive angineuse faibles, inférieurs à 15% à 7 ans [29].On peut ainsi définir une stratégie chirurgicale en chirurgie coronaire qui intègre le matérieldisponible, la spécificité des patients et les perspectives de résultats à moyen et à long terme. Lepédicule mammaire interne reste de façon indiscutable le matériel de choix et de référence et il nesemble pas licite d'utiliser un autre greffon artériel en alternative à un pédicule mammaire interne.L'absence de pontage mammaire interne-IVA doit être exceptionnel et fortement justifié. Les deuxpédicules mammaires internes sont utilisés de façon préférentielle pour revasculariser le réseau coronairegauche avec une large utilisation des pontages mammaires internes séquentiels pour desrevascularisations myocardiques les plus complètes possibles. La limite du pontage mammaire internebilatéral est la dilatation des cavités ventriculaires lorsque la longueur des pédicules mammaires internesest insuffisante; le deuxième greffon artériel est alors utilisé en greffon libre: mammaire interne enpremière intention, artère radiale en deuxième intention et pontage veineux en troisième intention. Pourdes raisons anatomiques, la revascularisation du réseau coronaire droit est l'apanage de l'artère gastroépiploïquedroite lorsqu'on en a l'expérience. Ses limites d'utilisation sont des antécédents de chirurgieabdominale, une pathologie digestive ou un diamètre insuffisant de l'artère; les alternatives sont ungreffon radial libre ou un pontage veineux.La revascularisation myocardique artérielle est techniquement plus exigeante et nécessite uneprotection myocardique optimale. En fin de procédure, le débit dans les greffons artériels doit êtremaximal et la prévention des bas débits post-opératoires est essentielle afin d'éviter le cercle vicieux: basdébit cardiaque, bas débit dans les greffons artériels, ischémie myocardique, bas débit cardiaque.Le bénéfice de la revascularisation myocardique artérielle n'étant pas encore validé par desétudes comparatives randomisées, le contrôle du risque opératoire est capital. L'indication derevascularisation myocardique artérielle doit être adaptée. Elle est fortement recommandée en cas deréopération, chez les patients jeunes de moins de 65 ans, lorsque l'espérance de vie du patient estsupérieure à l'espérance de vie des greffons veineux, et lorsqu'il existe une probabilité importante dedégradation rapide des pontages veineux: dans les maladies métaboliques (diabète, dyslipidémie,insuffisance rénale chronique) et lorsque le réseau coronaire est grêle ou de mauvaise qualité.L'indication peut être discutée lorsque l'espérance de vie des patients à moyen terme est faible: chez lespatients de plus de 75 ans, en cas de pathologie associée évolutive. L'indication doit être enfin24

Boudiaf EH, Dr. Benkelfat C ■ 2009, vol. 8, no. 1-2, pp. 25prudente lorsque le risque opératoire est susceptible d'être augmenté par une procédure artérielle encas d'insuffisance respiratoire sévère ou en cas de dysfonction ventriculaire gauche sévère où il existe unrisque élevé de bas débit cardiaque post-opératoire.ConclusionsLa revascularisation myocardique artérielle est certainement à ce jour une technique deréférence en pathologie coronaire, dont les résultats à long terme dépendront davantage de ladégradation du réseau coronaire que de l'altération des pontages artériels multiples. Il faut cependantgarder à l'esprit qu'il n'existe pas une technique et des patients, mais des techniques et un patient.References1. Grondin CM, Campeau L, Lesperance J, Enjalbert M, Bourassa M., Comparison of later changes ininternal mammary artery and saphenous vein grafts in two consecutive series of patients 10 years afteroperation. Circulation 1984; 70 (suppl. 1): 208-21.2. Lytle BW, Loop FD, Cosgrove DM, Ratliff NB, Easley K, Taylor PC., Long-term (5 to 12 years) serial studiesof internal mammary artery and saphenous vein coronary bypass grafts. J Thorac Cardiovasc Surg 1985;89: 248-58.3. Loop FD, Lytle BW, Cosgrove DM, et al. Influence of the internal mammary artery graft on 10-yearsurvival and other cardiac events. N Engl J Med 1986; 314: 1-6.4. Barner HB, Standeven JW, Reese J., Twelve- year experience with internal mammary artery forcoronary bypass. J Thorac Cardiovasc Surg 1985; 90: 668-75.5. Edwards FH, Clark RE, Schwartz M., Impact of internal mammary artery conduits on operative mortalityin coronary revascularization. Ann Thorac Surg 1994; 57: 27-32.6. Galbut DL, Traad EA, Dorman MJ, et al. Seventeen-year experience with bilateral internal mammaryartery grafts. Ann Thorac Surg 1990; 49: 195-201.7. Kouchoukos NT, Wareing TH, Murphy SF, Cheryl P, Marshall WG. Risks of bilateral internal mammaryartery bypass grafting. Ann Thorac Surg 1990; 49: 201-9.8. He GW, Ryan WH, Acuff et al. Risk factors for operative mortality and sternal wound infection inbilateral internal mammary artery grafting. J Thorac Cardiovasc Surg 1994; 107: 196-202.9. Ramstrom J, Lund O, Cadavid E, Oxelbark S, Thuren JB, Henze AC. Right internal mammary artery formyocardial revascularization: early results and indications. Ann Thorac Surg 1993; 55: 1485-91.10. Hendrick BB. The continuing evolution of arterial conduits. Ann Thorac Surg 1999; 68: S1-8.11. Mortia R, Kltamura S, Kawachi K, et al. Exercise coronary flow reserve of bilateral internal thoracicartery bypass grafts. Ann Thorac Surg 1993; 55: 883-7.12. Dion R, Glineur D, Derouch D, et al. Long-term clinical and angiographic follow-up of sequentialinternal thoracic artery grafting. Eur J Cardio-Thoracic Surg 2000; 17: 407-14.13. Tatoulis J, Buxton BF, Fuller AJ. Results of 1,454 free right internal thoracic artery to coronary arterygrafts. Ann Thorac Surg 1997; 64: 1263-9.14. Tector AJ, Amundsen S, Schmahl TM, Kress DC, Peter M. Total revascularization with T grafts. AnnThorac Surg 1994; 57: 33-9.15. Pick AW, Orszulak TA, Anderson BJ, Schaff HV. Single versus bilateral internal mammary artery grafts:10-year outcome analysis. Ann Thorac Surg 1997; 64: 599-605.16. Schmidt SE, Jones JW, Thornby JI, Miller III CC, Beall AC. Improved survival with multiple left-sidedbilateral internal thoracic artery grafts. Ann Thorac Surg 1997; 64: 9-15.17. Buxton BF, Komeda M, Fuller JA, Gordon I. Bilateral internal thoracic artery grafting may improveoutcome of coronary artery surgery. Risk-adjusted survival. Circulation 1998; 98: II-1-II-6.18. Lytle BW, Blackstone EH, Loop FD, et al. Two internal thoracic artery grafts are better than one. JThoracic Cardiovasc Surg 1999; 117: 855-72.25

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 2619. He GW. Arterial grafts for coronary artery bypass grafting: biological characteristics, functionalclassification, and clinical choice. Ann Thorac Surg 1999; 67: 277-84.20. Parolari A, Rubini P, Alamanni F, et al. The radial artery: which place in coronary operation? AnnThorac Surg 2000; 69: 1288-94.21. Acar C, Ramsheyi A, Pagny JY, et al. The radial artery for coronary artery bypass grafting: clinical andangiographic results at five years. J Thorac Cardiovasc Surg 1998; 116: 981-9.22. Tatoulis J, Buxton BF, Fuller JA. Bilateral radial artery grafts in coronary reconstruction: technique andearly results in 261 patients. Ann Thorac Surg 1998; 66: 714-20.23. Borger MA, Cohen G, Buth KJ, et al. Multiple arterial grafts. Radial versus right internal thoracicarteries. Circulation 1998; 98: II-7-II-14.24. Jegaden O, Eker A, Montagna P, et al. Technical aspects and late functional resultats ofgastroepiploic bypass grafting (400 cases). Eur J Cardio-Thorac Surg 1995; 9: 575-81.25. Suma H, Wanibuchi Y, Terada, et al. The right gastroepiploic artery graft. Clinical and angiographicmidterm results in 200 patients. J Thorac Cardiovasc Surg 1993; 105: 615-23.26. Voutilainen S, Verkkala K, Jarvinen A, Keto P. Angiographic 5-year follow-up study of rightgastroepiploic artery grafts. Ann Thorac Surg 1996; 62: 501-5.27. Sundt III TM, Barner HB, Camillo CJ, Gay WA. Total arterial revascularization with an internal thoracicartery and radial artery T graft. Ann Thorac Surg 1999; 68: 399-405.28. Tatoulis J, Buxton BF, Fuller JA, Royse A. Total arterial coronary revascularization: techniques andresults in 3,220 patients. Ann Thorac Surg 1999; 68: 2093-9.29. Bergsma TM, Granjean JG, Voors AA, Boonstra PW, den Heyer P, Ebels T. Low recurrence of anginapectoris after coronary artery bypass graft surgery with bilateral internal thoracic and right gastroepiploicarteries. Circulation 1998; 97: 2402-526

ISSN 1583-3534, Aniversary ■ 2009, vol. 8, no. 1-2, pp. 27-29Professor Dr. Marian Gasparat the age of 50Marian Gaspar, university professor, headchief of "The II Cardiovascular Surgery Clinic ofCardiovascular Disease Institute", Timişoara(România), turned 50 on 16 th of July 2009. Half thisperiod has passionately dedicated himself tosurgery, beginning as a medical assistant, andprobationer at the Surgery Clinics, universityassistant.Not just the Iove for surgery, but also theskills has proven, the perseverance, the studyand assiduous work have brought him to hisactual state.This is stated by a member of the InternationalSociety of Medicine History, member of theRomanian Surgery Society and of the RomanianCardiac Surgery Society, doctor in MedicalSciences, primary surgeon, who practicedsurgery for 50 years, and 7 years as an Anatomyand Surgery professor at the Sanitarium School,but the most important thing-dates back from 24September 2008 when the author of these lineswas subject to open cardiac surgery performedby Prof. Marian Gaspar, in charge with theanesthetics being Prof. Dr. Petre Deutsch, helpedby Dr. Calin Jusca, primary medical doctor, Dr.Daniel Nica, secondary doctor in the Vllth yearand Nurse / Assistant Alina Danciu -instrumentary. Extra corporal circulation wasprovided by, Adi Ardelean - assistant.Being a surgeon who has encouragedthousands of ill people to operate themselves,27being an ill person who solely went to thesurgeon to operate, this was my destiny entrustedto Mister Marian Gaspar. He asked me whether Iwanted him to be helped by the Austrianprofessor Gunther Laufer, question to which Ianswered that in an operation there has to beonly one command, one mind to do the thinkingthisis the trust and the great responsibility I took.Marian Gaspar is born on 16.07.1959, inDragsinesti, Timiş, from parents Iuliu andValentina. He is married to Victoria, office workerat a bank. They have two girls, Adina, student inGreece and Andreea, high-school student.Attached by Medicine, he graduatedfrom Sanitarium High in Timişoara (1979) andstudied at the University of Medicine andPharmacy "Victor Babes" Timişoara (1980-1986).During this period he worked as a medicalassistant in the County Hospital Timişoara (1984-1986) and after graduation he was designated aprobationer medic in Surgery Clinics of the sameHospital (1986-1989). During 1989-1990 he workedas a General Medicine medic in a health unitCrisan - Tulcea. He had the ambition to becomea cardio - vasculary surgeon, followed byresidency in vascular surgery (1991-1995).Three residents: Marian Gaspar andOvidiu Nutu-Surgery and Lucian Petrescu inCardiology have promoted in 1990 the contestfor university assistants at the university clinic ofCardiovascular surgery within "Victor Babes"Hospital, which was working together withThoracic Surgery, Viorel Ene chief of department,and Prof. Dr. Ilie Pavelescu, from the FundeniClinic, was appointed head of the clinic.In 1990-1993, the Cardiac Surgery Clinicoperated together with the Thoracic SurgeryClinic, each unit occupying a storey with 50beds, 2 operation halls and Intensive Therapywith 8 beds.On 26 of April 1991, Prof. Dr. Ilie Pavelescuand Marian Gaspar made the first open Cardiacsurgery in Timisoara-replacement of the mitralvalve with a mechanical prosthesis.In 1993 Marian Gaspar does aspecialization in Cardiac Surgery at Nice(France).The Cardiology Centre is founded inTimişoara, under the leadership of Prof. Dr. ŞtefanDragulescu, specialized activity beingreorganized by bringing the Cardiology Clinicfrom the County Timişoara Hospital in thestructure and organization of the "Victor Babes"

_______________________ UNIVERSITY OF WASHINGTON • APPLIED PHYSICS LABORATORY _________________Energy: Hydrophone and SeismometerSpectrograms plot energy versus frequency and time corresponding to the two events. The fourplots (left to right) show the hydrophone and seismic vertical, radial, and tangential componentsof motion, respectively, all at the same scale for a given event. At frequencies below about 5 Hz,the total energy on the seismic components in the seafloor sediment is greater than on thehydrophone located in the water only 0.5 m above the seafloor. However, at higher frequencies,the power in the hydrophone signal is greater. The banded structure in the seismic traces isindicative of modal coupling to the seafloor sediments. The hydrophone shows both modalstructure and scattered energy.Polarization AngleThe polarization (radial-vertical) angles of individual Ti modes are shown as a function offrequency for four earthquakes. Positive angle is down and radially away from the source. Thesecond event near Kamchatka (Mw=6.4) occurred 6 minutes after the first and at the samelocation (distance and azimuth within 0.02% of first event from H2O). The Blanco FractureZone earthquake (Mw=6.2) on June 2, 2000, occurred at a distance of 2130 km northeast ofH2O. Low-frequency modes (5 Hz) show increasingly steeper angles and greater scatter. Symbols are plotted at thepolarization of the maximum energy; lines indicate range of polarization of modal frequencies.Small variations in frequencies of individual modes are observed between events. Notepolarization variation of Ti mode at 10.7 Hz between the first and second earthquakes nearKamchatka, which have almost identical paths.Ti Wave Propagation and Seamount ScatteringThe great circle paths (yellow) from the Guatemalan earthquake to the OSN1 site and HawaiianIslands seismic stations are shown. The apparent great circle to OSN1 is blocked by the bigIsland of Hawaii. Ti is observed on both on the OSN1B seafloor-buried sensor as well as theOSN1 borehole seismometer 245 m below the seafloor. The apparent propagation direction of Tiderived from polarization analysis on the seafloor buried seismometer is shown as the red line.The green lines indicate propagation delays for paths scattered from seamounts to the southeast.Seismoacoustic T• < ~5 Hz• Propagates dominantly in thesediments, observed in borehole inbasalt• Coupled higher-mode surface wave• Propagation from earthquake sourceor regionally scattered?• Seamount scattering• > ~5 Hz• Propagates dominantly in the water• Scattered to seafloor, but no clearsingle mechanism: Internal waves,spice, bio-scatter (large marineanimals), sea surface• Multiple scattering?TR 0406 24

Aniversary ■ 2009, vol. 8, no. 1-2, pp. 294. "Aortic Root Pathology-surgical management"- in collaboration with several countries (Austria,Czech Republic, France, England)5. Cardiovascular Surgery (volume edited byProf. Dr. Radu Deac) from The Surgery Treatise -edited by Prof. Dr. Irinel Popescu - in presscurrently.6. Marian Gaspar, Gunther Laufer, Radu Deac,Martin Grabenwoger - Aortic Root Pathology -Remodeling or Replacement Aortic ValveSparing Procedure using a new Sinus ValsalvaVascutek Prosthesis. "Update in CardiovascularMedicine", April, 4-6, 2002, Timisoara România7. I. Socoteanu, M. Gaspar, C. Streian, L. Falnita,G. Taranu - Ascending aorta reconstruction -optimizing the therapeutical management. TheDanubian Forum of Cardiac Surgery, Palie, June2004.8. Marian Gaspar, Horea Feier, Gunther Laufer,Adina Ionac, Petre Deutsch, Ştefan I. Dragulescu.Chronic aortic dissection with right leg ischemia:to operate or not to operate?4 th WienInterdisciplinary Symposium On Aortic RepairVisar - october 6-8 th, 2005.9. Gaspar M., H. Feier, C. Jusca, P. Deutsch, St.I.Dragulescu. Spontaneous aortic arch rupturewith pseudoaneurysm and chronic Cardiactamponade. 10 th Danubian Forum for CardiacSurgeiy, May 26-27 2006, Visegrad, Hungary.10. Mihaela Dumitrasciuc, Silvia Mancas, MăriaRada, M. Gaspar, St.I. Dragulescu. Prognosisfactors for the outcome pulmonary hypertensionafter mitral valve replacement. Il th DanubianForum for Cardiac Surgery, Timişoara, June l-2 nd ,2007.11. M. Gaspar, W. Klepetko, G. Marta, P. Deutsch,B. Mut, Adina Ionac, C. Jusca, G. Dumitrasiuc, H.Feier, St.I. Dragulescu. Pulmonarythrombendarterectomy for chronic pulmonarythromboembolism and severe pulmonaryhypertension. ll th Danubian Forum for CardiacSurgery, Timişoara, l-2 nd June 2007.12. C. Jusca, M. Gaspar, G. Laufer, D. Cioata, G.Dumitrasciuc, D. Nica, St.I. Dragulescu. Ourexperience in using aortic allografts. Early andmid-term results. ll th Danubian Forum for CardiacSurgery, Timişoara, l-2nb June 2007.13. Marian Gaspar - Cardiovasculare Surgery -"Vasile Goldis" University Press. Arad 2009.Today, Ranko Szuhanek runs TheCardiology Institute Timişoara and thecompartment for operating diseases on childrenis under construction.The performance of Prof. Dr. Marian Gaspar hasreached under 1% postoperatory death rate.But what is worth noticing is the kindnessof Mr. Gaspar, the way he speaks/talks to illpersons in different places, with random tradesand occupations, the way he supervises theapplication of the smallest details in moderntreatments before and after the operation,alongside his crew from Intensive Care, aparamount collaboration, thing experienced byme, as a patient.Now, turning 50, 1 wish him all the best,real achievements in his family and many yearsfrom now on, to still posses the surgical skill he hasbeen gifted with, and I am talking about that artof passing hold needle symmetrically in sutures,using the famous glasses and the perfecttightening of the Knots, fine gestures and artconsidering the size of the vessels and thethickness of the suture string. Watching him on adaily basis, during his visits to ill persons, longoperations, as well as his didactic activity, werealize the complexity, but especially the passionhe proves, being recognized nationally andinternationally.Happy Birthday, Professor!Bibliography:1. Prof. Dr. Marian Gaspar - "Who's who Medical in România" (editor – Panayiotis Vassos) -Pegasus Press publishing, Bucharest, 2006, page 154.2. Nicolae Ursea (in press) - "A Romanian Encyclopedia from the Origins to the Present Day" - TIV,"Carol Davila" University Press, Bucharest 2009, p. 2748, 2756.3. Gh. Dinu, M.D. Ph.D., Member of the International Society of Medicine History - Personalconversations. Internet data.29

ISSN 1583-3534, A. Molnar et al ■ 2009, vol. 8, no. 1-2, pp. 30-36Factors influencing the outcome among 38 consecutive caseswith ruptured infrarenal aortic aneurysms.Experience in one single center from RomaniaA. Molnar, Diana Sacui, T. Scridon, M. BârsanCardiovascular Surgical Clinic, Heart Institute, Cluj-Napoca, RomaniaAbstractAAA represents a common pathologic condition, with an estimated incidence between 30‰and 66‰ in various studies, increasing in the last three decades. Unfortunately, the mortality rate inruptured AAAs had also increase. Therefore it is important to identify and treat them before theybecome a surgical emergency. The aim of this study was to determine the variables that couldinterfere with the surgical outcome of patients with AAA and with the perioperative morbidity andmortality rates.Material and Method: In this study were included 94 consecutive patients with AAA, whounderwent elective repair or emergency repair for ruptured AAA, in the Cluj-Napoca CardiovascularSurgery Clinic between January 2003 and December 2008. The mean age of the studied patients was68.64 ± 6.27 years (range: 49 - 84 years), of which 11 (12%) were females and 83 (88%) were males. Themean hospital stay was 14.36 ± 7.63 days (range: 0.3 - 39 days). The mean aneurysm diametermeasured intraoperatively, was 7.4 ± 1.85 cm (range: 4 - 13 cm). The symptoms and clinical findings atadmission were as it follows: in the case of ruptured AAAs, the main findings were low arterial bloodpressure in 22 patients (78.6%) and abdominal pain in 18 patients (64.3%), the lumbar pain and thepulsatile abdominal mass were found in 14 patients (50%), while in the patients who underwentelective surgery the predominant signs were the pulsatile abdominal mass in 38 patients (67.8%) andabdominal pain in 34 patients (60.7%).Results: Three types of interventions were performed: tubular graft interposition, aorto-biliacbypass and aorto-bifemoral bypass. The perioperative mortality in the elective repair group was 8.93%(5 / 56), while the perioperative mortality in the emergency repair group was 39.47% (15 / 38).Conclusions: Ruptured AAA or AAA in imminence of rupture continues to represent a conditionassociated with substantial risks and high mortality, however its rate is decreasing in the last decades,mainly due to an increase in professional performances. It is therefore necessary the selectivescreening and the elective repair for the improvement of infrarenal AAA patients’ survival rate.IntroductionThe infrarenal AAAs represent the most frequent arterial aneurysms, with a multifactorial etiologyin which the degenerative alterations of the arterial wall seem to have the predominant role. They affectmostly the male patients with a history of smoking and hypertension. Although the prevalence of AAA ishigh, the risk of rupture and the consequent mortality rate is underestimated.Our aim was to determine the factors that influence the postoperative outcomes in AAAs andthe perioperative morbidity and mortality rates: the demographics of the patients, the associateddiseases (hypertension, COPD, renal dysfunction, peripheral arterial disease), the clinical signs atpresentation (abdominal or lumbar pain, hypovolemic shock, pulsatile abdominal mass), the AAAdiameter, and the serum creatinine levels at presentation. The preoperative imaging studies were theabdominal US, CT scanning, and angiography (in elective cases associated with renal disease orperipheral occlusive arterial disease). The operative treatment (tubular graft interposition, aorto-biiliacbypass or aorto-bifemoral bypass) was evaluated by the operatory moment, the approach of the aorta(transabdominally or through the retroperitoneal space), and the perioperative complications andmortality causes.30

A. Molnar et al ■ 2009, vol. 8, no. 1-2, pp. 31Patient Population and MethodsA retrospective study was undertaken of all the 94 patients with infrarenal AAA, who underwentelective repair or emergency repair for ruptured AAA, in the Cluj-Napoca Cardiovascular Surgery Clinicbetween January 2003 and December 2008. The data were collected from the hospital inpatient inquirysystem and the operative registers.The main objective was to quantify the connection degree between the comorbidities and thepostoperative complications respectively, with the perioperative mortality risk. We also compared thepostoperative outcomes and mortality rates in patients who underwent elective repair with those thatunderwent emergency repair.Elective RepairFifty-nine percent (n=56) of the study population had elective AAA repair. The mean age was 68± 4.46 years (range 49-84 years), by which 87.5% (49/56) were males and 12.5% (7/56) were females. Themean hospital stay was 16.5 ± 4.3 days (range 6-38 days). The serum creatinine level at presentationvaried between 0.6 and 2.35 mg/dl, with a mean of 1.18 mg/dl, and the mean AAA diameter was 6.9 ±1.26 cm (range 4-13 cm). The clinical signs at presentation most frequently encountered were thepulsatile abdominal mass (67.8%) and abdominal pain (60.7%), while the most frequent comorbiditieswere hypertension (78.57%), other cardiac diseases (55.35%), and peripheral arterial disease (35.71%).The operative management was by conventional open repair, using the transabdominal method.Postoperatively most patients have had no complications (35/56), but in the others 21 patients the maincomplications were at the surgical wound level (11/56), and only 1.8% of patients presented cardiac orrespiratory failure. The most frequent cause of perioperative mortality in this populational group wascardiac failure (3/56), followed by renal failure and mesenteric ischemia, each encountered in 1 case.The perioperative mortality rate was almost nine percent of the patients (5/56).Surgical TechniquesPacientsPostoperative ComplicationsPacientsNo%Elective repairNo% Postoperative ComplicationsAorto-bifemural bypass 15 27% cardiac complications 1 1,79%Aorto-biliac bypass 9 16% surgical wound 11 19,65%Tubular graft interposition 32 57% renal complications 2 3,57%56 100% respiratory complications 1 1,79%no complications 35 62,50%mesenteric ischemia 2 3,57%peripheral ischemia 3 5,34%sepsis 1 1,79%56 100,00%POSTOPERATIVE COMPLICATIONSELECTIVE REPAIR15; 27%40353025201510501112 135231cardiac complicationssurgical woundrenal complicationsrespiratory complicationsno complicationsmesenteric ischemiaperipheral ischemiasepsis32; 57%9; 16%Aorto-bifemural bypassAorto-biliac bypassTubular graft interpositioncardiac com plicatio nssurgical w oundre nal complicationsrespiratory com plicationsno complicationsmesenteric ischemiaperipheral ischem iasepsis31

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 32Perioperative Mortality:4Emergency RepairD e c ea se d P atie n ts3Forty-one percent (n=38) of thestudy population patients hademergency repair. Only 7 of these 2patients (18.42%) were previously knownand followed up for AAA, and all had1 1initial emergent presentation. Their1mean age was 68.5 ± 5.58 years (range52 - 83 years), by which 89.57% (34/38)were males and 10.53% (4/38) werefemales. The mean hospital stay was 011.2 ± 5.8 days (range 0.3 - 39 days). Thecardiac causes renal causes mesenteric ischemiaserum creatinine level at presentationvaried between 0.73 and 8.78 mg/dl,with a mean of 2.30 mg/dl, and the mean AAA diameter was 8.2 ± 1.37 cm (range 4.5 - 13 cm). The mostfrequent clinical signs at presentation were the hypovlemic shock (hypotension) (78.6%) and abdominalpain (64.3%), the abdominal pulsatile mass being detected in 50% of patients, while the most frequentcomorbidities were hypertension (60.52%), other cardiac diseases (55.26%), and peripheral arterialdisease (18.42%). The operative management was by conventional open repair, using thetransabdominal method. Postoperatively the main complications were at the surgical wound level(6/38), cardiac complications (6/38) and mesenteric ischemia (6/38) and only 4 patients presented renaldysfunction; also the sepsis and respiratory failure appeared in 2.6% of patients. The most frequentcauses of perioperative mortality in this populational group were renal failure (5/38) and mesentericischemia (5/38), followed by MSOF (3/38) and cardiac failure in 2 cases. The perioperative mortality ratewas almost forty percent (15/38).Surgical TechniquesRuptured AneurysmPacientsNo3Postoperative Complications% Postoperative ComplicationsPacientsNoAorto-bifemural bypass 7 18% cardiac complications 6 15,79Tubular graft interposition 31 82% surgical wound 6 15,7938 100% renal complications 4 10,51respiratory complications 1 2,63no complications 12 31,60mesenteric ischemia 6 15,79peripheral ischemia 2 5,26sepsis 1 2,6338 100,00%Ruptured Aneurysm%7; 18%Aorto-bifemural bypassTubular graft interposition31; 82%32

A. Molnar et al ■ 2009, vol. 8, no. 1-2, pp. 33Postoperative complications141210864206 64112621cardiac complicationssurgical woundrenal complicationsrespiratory complicationsno complicationsmesenteric ischemiaperipheral ischemiasepsiscardiac complicationssurgical woundrenal complicationsrespiratory complicationsno complicationsmesenteric ischemiaperipheral ischemiasepsisOperatory Moment:1614121086< 12 hA tP r e se nt a t i on420< 2 4 h> 2 4 hPerioperative Mortality:655 5Deceased Patients4321230cardiac causes renal causes mesentericischemiaMSOF33

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 34Statistical AnalysisStatistical analysis was done using the Chi-square and the Student t-test for qualitative variables,and the correlation coefficient between numerical data. Statistical significance was taken as p < 0.05.ResultsPatient CharacteristicsCharacteristic Elective Repair (n=56) Emergency Repair (n=38)Mean Age (years) 68 ± 4.46 68.5 ± 5.58Males 49 (87.5%) 34 (89.47%)Mean Hospital Stay (days) 16.5 ± 4.3 11.2 ± 5.8Mean AAA Diameter (cm) 6.9 ± 1.26 8.2 ± 1.37Mean Serum Creatinine (mg/dl) 1.18 2.30Comorbidities 44 (78.57%) 23 (60.52%)Postoperative Complications 21 (37.50%) 26 (68.42%)Perioperative Mortality 5 (08.93%) 15 (39.47%)The mean hospital stay for emergency repair was statistically significant lower than for the elective repairgroup (t-Test), with a p value of 0.001. In the emergency repair group of patients the mean serumcreatinine level at admission was significantly higher than in the elective group (t-Test: p = 0.0003).t-Test: Two-Sample Assuming Unequal VariancesHospital Stay Elective Repair Emergency RepairMean 16.517857 11.192105Variance 35.563312 76.245612Observations 56 38Hypothesized Mean Difference 0df 60t Stat 3.2768289P(T ≤ t) one-tail 0.0008739t Critical one-tail 1.6706489P(T ≤ t) two-tail 0.0017478t Critical two-tail 2.0002978t-Test: Two-Sample Assuming Unequal VariancesSerum Creatinine Elective Repair Emergency RepairMean 1.18 2.30526316Variance 0.15471273 3.06330669Observations 56 38Hypothesized Mean Difference 0df 40t Stat -3.897027P(T ≤ t) one-tail 0.00018106t Critical one-tail 1.68385101P(T ≤ t) two-tail 0.00036212t Critical two-tail 2.02107537t-Test: Two-Sample Assuming Equal VariancesAneurysm Size Elective Repair Emergency RepairMean 6.892857143 8.171052632Variance 3.106493506 2.990220484Observations 56 38Pooled Variance 3.05973153Hypothesized Mean Difference 0df 92t Stat -3.476782352P(T ≤ t) one-tail 0.000388304t Critical one-tail 1.661585397P(T ≤ t) two-tail 0.000776609t Critical two-tail 1.98608627234

A. Molnar et al ■ 2009, vol. 8, no. 1-2, pp. 35There was a significant statistical difference in mean aneurysm diameter between the electiverepair and the emergency repair group (p = 0.0007).ComorbiditiesThe connection between the frequency of comorbidities and the postoperative complicationsand the mortality rate respectively (Chi-square test) in the emergency repair group showed no statisticaldifference (p = 0.563 and 0.443 respectively).Postoperative ComplicationsIn the emergency repair group there was a significant statistical difference in the correlationbetween the perioperative mortality rate and the presence of associated diseases (Chi-square test),with a p value of 0.0096.Also the correlation between the frequency of postoperative complications and patient age orhospital stay respectively was statistically moderate, with Cs = 0.5 and 0.44 respectively; there was nosignifficant correlation between the hospital stay and the patients age, in the emergency repair group(Cp = 0.12).Perioperative (30-Day) MortalityThe 30-day mortality in the emergency operative group (39%) was almost four-times higher thanin the elective operative group (9%) (p = 0.0003), showing a significant difference between the twopatient populations.DiscussionMany studies have determined that some preoperative, intraoperative, and postoperativepatient variables could predict mortality for the AAA open repair. Some of the most commonly citedvariables include age, gender, elevated serum creatinine, congestive heart failure, chronic pulmonaryobstructive disease, hypotension, cardiac arrest, and syncope (1) . Elderly patients with AAA in emergencypresentation with hipovolemic shock status or cardiorespiratory arrest present an increased risc forperioperative morbidity and mortality and should be evaluated in order to establish the indication forendovascular repair. The endovascular repair has been widely accepted for the elective treatment ofAAA. There is also a growing body of evidence supporting the successful application of this technique topatients with ruptured AAA (1) , but our center has very little experience in applying it, especially topatients with ruptured AAA. This is due to numerous reasons, including surgeon preference and thespeed of open repair with acceptable results.Between the two groups of patients we found significant difference in serum creatinine levels atadmission (higher for emergency repair group - p = 0.0003); also the mean hospital stay was lower for thepatients presenting with ruptured AAA, maybe due to the higher frequency of major postoperativecomplications which lead to higher mortality rates.The study showed an increased incidence of associated cardiac diseases and hypertension bothin the elective repair group (55.35% and 78.57%) and in the emergency repair group (55.26% and60.52%); still there was no evidence of a significant correlation with the frequency of perioperativecomorbidities or 30-day mortality rate (p = 0.563 and 0.443).Postoperative complications were predominantly cardiac (15.78%), renal (10.52%) and ischemic– especially mesenteric ischemia (21.05%) in the emergency repair group while in the elective repairgroup the most frequent complication was at the surgical wound level (19.64%). There is a statisticallymoderate correlation between the postoperative complications frequency and the patients’ age andhospital stay respectively (0.5 and 0.44).Although relatively high, the overall perioperative mortality rate in elective repair group wassignificantly lower (8.93 %) than in the emergency repair group (39.47%) (p = 0.0003), with a statisticallysignificant connection with the presence of postoperative complications in the emergency repair forruptured AAA (p value = 0.009). In light of decreasing elective operative mortality rates, early recognitionof likely rupture might further identify those patients for whom the surgical management of AAA wouldbe beneficial. Among the variables potentially linked with rupture are gender, aneurysm size, andpreexisting cardiovascular disease (especially hypertension) (13) . The conventional thinking is that the riskof rupture is most related with the maximum AAA diameter. Comparing the average aneurysm size in theelective group with that of the aneurysms of the emergency group we found that there is a significantdifference in the average size (p = 0.0007). Thus, selective screening and elective surgical repair isnecessary in order to improve the survival rate for the patients with infrarenal AAA.In conclusion, we believe that the ruptured AAA continues to represent a condition associatedwith considerable risks and high mortality rates, even if those are decreasing in the past decades,35

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 36especially due to an increase in professional performances. The decision of when, or whether toelectively operate on high-risk patients will ultimately depend on the risk of surgery compared with therisk of nonoperative management or alternative procedures (13) . However, to estimate the risk of electiveAAA repair it is necessary not only to identify what constitutes "high risk" but also to understand thenatural postoperative history with short- and long-term outcomes.References and Bibliography1. Ali Azizzadeh; Charles C. Miller III; Martin A. Villa; Anthony L. Estrera; Sheila M. Coogan; Sean T. Meiner;Hazim J. Safi: Effect of Patient Transfer on Outcomes after Open Repair of Ruptured Abdominal AorticAneurysms. Vascular. 2009; 17(1):9-14.2. Ali Azizzadeh; Martin A. Villa; Charles C. Miller III; Anthony L. Estrera; Sheila M. Coogan; Hazim J. Safi:Endovascular Repair of Ruptured Abdominal Aortic Aneurysms: Systematic Literature Review. FromVascular Published: 11/07/2008.3. Brady AR, Fowkes FG, Greenhalgh RM, Powell JT, Ruckley CV, Thompson SG: Risk factors forpostoperative death following elective surgical repair of abdominal aortic aneurysm: results from the UKSmall Aneurysm Trial. On behalf of the UK Small Aneurysm Trial participants. Br J Surg. Jun 2000; 87(6):742-9.4. Brewster DC, Cronenwett JL, Hallett JW Jr, Johnston KW, Krupski WC, Matsumura JS: Guidelines for thetreatment of abdominal aortic aneurysms. Report of a subcommittee of the Joint Council of theAmerican Association for Vascular Surgery and Society for Vascular Surgery. J Vasc Surg. May 2003;37(5):1106-17. [Medline].5. Jerry C. Chen, Henry D. Hildebrand, Anthony J. Salvian, David C. Taylor, Sandy Strandberg, Terence M.Myckatyn, York N. Hsiang: Predictors of death in nonruptured and ruptured abdominal aortic aneurysmsJournal of Vascular Surgery, Volume 24, Issue 4, October 1996, Pages 614-623.6. Gloviczki P, Ricotta JJ II: Aneurysmal vascular disease. In: Townsend CM, Beauchamp RD, Evers BM,Mattox KL, eds. Sabiston Textbook of Surgery. 18th ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 65.7. Greenhalgh RM, Powell JT: Endovascular repair of abdominal aortic aneurysm. N Engl J Med. 2008;358:494-501.8. Isselbacher EM: Diseases of the aorta. In: Libby P, Bonow RO, mann DL, Zipes DP. Braunwald's HeartDisease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap56.9. Lederle FA, Kane RL, MacDonald R, Wilt TJ: Systematic review: repair of unruptured abdominal aorticaneurysm. Ann Intern Med. 2007; 146:735-741.10. Lederle FA, Johnson GR, Wilson SE, Chute EP, Littooy FN, Bandyk D: Prevalence and associations ofabdominal aortic aneurysm detected through screening. Aneurysm Detection and Management(ADAM) Veterans Affairs Cooperative Study Group. Ann Intern Med. Mar 15 1997; 126(6):441-9 [Medline].11. Lederle FA, Wilson SE, Johnson GR, Reinke DB, Littooy FN, Acher CW: Immediate repair compared withsurveillance of small abdominal aortic aneurysms. N Engl J Med. May 9 2002; 346(19):1437-44. [Medline].12. Majumder PP, St Jean PL, Ferrell RE, Webster MW, Steed DL: On the inheritance of abdominal aorticaneurysm. Am J Hum Genet. Jan 1991;48(1):164-70 [Medline].13. Niamh Hynes, Nik Kok, Brian Manning, Bhasakarapandin Mahendran, Sherif Sultan: Abdominal AorticAneurysm Repair in Octogenarians versus Younger Patients in a Tertiary Referral Center. Vascular. 2005;13(5):275-285.14. Rutherford RB, Krupski WC: Current status of open versus endovascular stent-graft repair of abdominalaortic aneurysm. J. Vasc. Surg. May 2004; 39(5):1129-39 [Medline].15. The UK Small Aneurysm Trial Participants. Mortality results for randomized controlled trial of earlyelective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet. 1998;353:1649-55.36

ISSN 1583-3534, E. Jerzicska et al ■ 2009, vol. 8, no. 1-2, pp. 37-43Cerebral hyperperfusion syndrome – a complication of carotidrevascularizationAbstractJerzicska E., H. Suciu, Kovacs Judith*, R. Mitre, R. Capilna, R. DeacTg. Mures, Emergency Institute for Cardiovascular Diseases and Transplantation,Cardiovascular Surgery Clinic*Anaesthesia and Intensive Care ClinicThe cerebral hyperperfusion syndrome (CHS) is a relatively new clinical entity, several itsmanifestations being integrated in other pathology categories over the past years. It is specific forcerebral revascularization and has a unique pathophysiological mechanism.We studied the actual literature, in a review intended to clarify this chapter of carotidrevascularization complications. Our experience in this field is presented and compared, summarizedin a prospective study, conducted over a period of 4 years, from 2005-2008, which included thepostoperative clinical evaluation of 247 patients with carotid revascularization.As a result of this literature review, we defined the CHS, underlined its causative pathologicalmechanisms, contoured the clinical manifestations and proposed therapeutic maneuvers, bothpreventive and curative. We also presented the reported risk factors for the development of CHS,adding our own observations, and described the imagistic diagnostic possibilities. In our series, theincidence of this complication is lower than reported in literature, so we emphasize our treatmentprotocol which allowed us to reach this level of complications. Prophylaxis is the most efficienttreatment, and it is achievable through an adequate education of the medical personal with minimalfinancial implications in order to assure a faster recovery in carotid postrevascularization.Keywords: cerebral hyperperfusion, carotid surgery, revascularizationSindromul de hiperperfuzie cerebrala – complicaţie a revascularizării carotidieneJerzicska E., H. Suciu, Kovács Judit, R. Mitre, R. Capilna, R. Deac1Clinica Chirurgie Cardiovasculară, Institutul de Urgenţă de Boli Cardiovasculare si Transplant TârguMureş2 Clinica ATI Cardiovascular, Institutul de Urgenţă de Boli Cardiovasculare şi Transplant Târgu MureşSindromul de hiperperfuzie cerebrală (SHC) este o entitate clinică relativ nouă conceptual,diferitele manifestări ale sale fiind integrate de-a lungul timpului în alte categorii de patologie. Estespecific pentru revascularizarea cerebrală şi are mecanism fiziopatologic unic. Am studiat literaturacurentă cu intenţia de a clarifica acest capitol al complicaţiilor revascularizării carotidiene. Experienţanoastră în acest domeniu este reprezentată şi comparată, sumarizată într-un studiu prospectiv,cuprinzând o perioadă de 4 ani, din 2005-2008, bazată pe evaluarea clinică postoperatorie a 247pacienţi cu revascularizare carotidiană.Ca şi rezultat al acestei evaluări, am definit SHC, subliniind mecanismul patogen, am conturatmanifestările clinice, respectiv am propus manevre terapeutice, atât preventive, cât şi curative. Ammai prezentat factorii de risc în SHC, adăugând observaţiile noastre, respectiv am descris posibilităţilediagnosticii imagistice. În lotul nostru incidenţa acestei complicaţii este mai mică faţă de datele dinliteratura de specialitate, subliniind eficienţa protocolului nostru de tratament care ne-a permisatingerea acestei rate a complicaţiei. Profilaxia este cel mai eficient tratament, este posibilă prineducarea adecvată a personalului sanitar cu implicaţii financiare minime, în scopul asigurării uneirecuperări postrevascularizaţie carotidiană cât mai rapide.Cuvinte cheie: hiperperfuzie cerebrală, chirurgie carotidiană, revascularizare37

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 38The cerebral hyperperfusion syndrome (CHS) is a relatively new clinical entity, several itsmanifestations being integrated in other pathology categories over the past years. Its commondenominator which led to the description of this particular syndrome are represented byphysiopathological mechanisms that competed to accomplish a fairly heterogeneous clinical image.CHS is typical for both for surgical (carotid endarterectomy CEA) and endovascular (carotidstenting CAS) carotid revascularization.For the first time Sundt described this syndrome, dated from 1981 (7). He characterized thissyndrome in the association of an increased cerebral perfusion with a clinical triad represented by:ipsilateral migraine headache, seizures, focal neurological deficits in the lack of cerebral ischemia afterCEA.The specific phisiopathological element of this syndrome is represented by the alteration ofvascular self-regulation at the level of the revascularized territory, situation which based on elevatedpressure of cerebral perfusion is capable to determine a wide variety of symptoms. Whether in the mildcases local metabolic disturbance, the alteration of the hematoencefalic barrier occur, the gravityincrease assumes more severe injuries, starting from the primarily cerebral edema becoming generalizedtill a more complex and infaust event, conferring exceptional gravity to the case, meaning intracerebralhemorrhage.The definition of cerebral hyperperfusion syndrome is difficult, forasmuch from a clinical point ofview it is characterized by an extremely varietal image. Due to this reason we consider as relevant thedefinition based on the determinant physiopathological mechanism. CHS represents the clinical contextulterior of a carotid revascularization intervention (CEA or CAS) characterized by the alteration of thehematoencefalic barrier at the revascularized territory without any other known pre-existent orconcomitant detectable cause.The physiopathology of CHS is based on the exhaustion of the self-regulating vascular capacity inthe cerebral circulation on the affected territory. This self-regulation system represents the maincompensating mechanism in balancing the modifications of the cranial blood debit, accomplished bythe reactivation of the local arterioles, especially by humoral regulation. This exhaustion is due to a longterm vasodilatation, necessary for the circulatory compensation in case of a cerebral perfusion deficit(carotid stenosis), in a linear ratio with the grade of the deficit (15). The ascendant factors on thecerebral micro vascular self-regulation are dominated by the grading of the deficit of the cerebralblood debit. The duration of this deficit is as well as important, however in the carotid atheroscleroticpathology we might consider as an irrelevant factor, as in most of the cases it is about a long period oftime, ages in developing carotid stenosis. The duration factor is only important in rare cases when anacute occlusion or stenosis develops (non-stenotic atherosclerotic plaque complicated by thrombosis,trauma).The cranian blood flow deficit is influenced by the degree of the ipsilateral carotid stenosis, thecontrolateral occlusion or stenosis, the frail collateral debit, vertebrobasilar circulatory failure (1, 13, 16-19). Any significant stenosis hemodynamic (>50%) on an extra cranial axe produces compensatorymodifications in the cranial microcirculation (19).The main molecular mechanisms that generate alteration are represented by the increase innitric oxide during the decrease of cerebral blood flow, respective the increase of free radicals duringreperfusion. These humoral mediators aggress the self-regulating capacity in different moments, on theother hand determining an extreme vasodilatation, respective directly affecting the vascular endothelia(12). There are studies (20,21) which demonstrate the increase of lipid degradation products due toinduced peroxides by free radicals (malon dialdehyde, diene conjugates, lipoperoxides) in jugular veinsafter declamping the internal carotid artery during CEA. It also has been concomitant observed anexistence of an increase of biomarkers with neuronal affectation (neuron-specific enolase = NSE and S-100B) after CEA in the jugular torrent (37).Other factors that contribute at the appearance of this syndrome are represented by: systemichypoperfusion, intra- and postprocedural cerebral microemboli, the stimulation or interruption of carotidglomus efferents.Systemic hypoperfusion determines an implicit decrease of cerebral blood flow. This systemichypoperfusion might install after CEA or CAS as well. During CEA in general anesthesia, the anestheticinduction represents a critical moment. Also, the instrumental handling of the carotid glomus mightinduce bradicardia respective hypotension. According to this, the surgeon must thwart thesemanifestations, mainly by strongly cooperating with the anesthetist, respective through simple andconcrete actions at the right time. Infiltrating the intercarotid space with 3-5 ml 1% lidocaine during theprocedure represents a classic solution. The exclusively instrumental maneuvers, the less “palpation” ofthe carotids are some other techniques. Similarly with the “no touch” concept described by Turnbull foroncologic surgery, we propose avoiding maneuvering the carotid, bypassing excessive vagal stimuli,38

E. Jerzicska et al ■ 2009, vol. 8, no. 1-2, pp. 39respectively avoiding mobilization of emboli from the level of the atherosclerotic plaque. The exactanatomic diagnosis of the lesion preoperatively, early heparinization, sectioning the efferents of carotidglomus (Hering nerve) are amongst other adjuvant maneuvers.During CAS, using dilatation balloons influences mechanically the baroreceptors at the level ofthe internal carotid artery and carotid glomus, able to determine an immediate vagal reaction, leadingto bradicardia and hypotension.Cerebral microemboli are frequent; especially din case of CAS (30). Their existence is alsodocumented postprocedure by transcranial Doppler. This is an important monitoring procedure in orderto improve and control the quality of cerebral revascularization through CEA or CAS. Although severaltimes clinically mute, these microemboli can generate a CHS, explaining intracerebral hemorrhage afterCAS.Sectioning the efferents of the carotid glomus or carotid glomectomy associated with eversionCEA might generate an intra- or postoperative instability, usually marked by arterial hypertension,situation which obviously increases cerebral hyperperfusion, becoming an adjuvant factor of CHS. Inextreme cases, with high blood pressure values, it might become a trigger factor for CHS. For this reason,monitoring the perioperatory blood pressure is a key element for a successful carotid revascularization.The clinical manifestations of CHS are extremely various. Understanding the phisiopathologycalmechanisms at the base of this syndrome is essential to identify the symptoms at patients with carotidrevascularization. The symptomatology is widely various, due to localization, extension and severity ofhemodynamic disturbances in cerebral circulation. The most frequent symptoms summoned in literatureare (1):- Temporal-spatial disorientation- Confusion- Migraine type headache- Focal seizures- Motor disturbances (hemiparesis, hemiplegia)- Aphasia- Nausea- Intracerebral hemorraghe- Physiological disturbances- Hemianopsy- AtaxyBased on our experience the most frequent symptoms were (following the incidence):- Persistent headache- Temporo-spatial disorientation- Physiological agitation- Nausea, vomiting- Troubled consciousness (torpor, obnubilation)In our case study no senzorial or motor disturbances were described.The debut of this symptomatology is relative, from a few hours till several weeks. Seemingly CAS isassociated with the symptomatology of CHS much earlier than CEA, the first 12 hours vs. the 6 th daypostop (apex) (23). The migraine type ipsilateral headache, confusion, temporo-spatial disorientationare the most frequent symptoms (2, 4, 5, 8, 16, 22).The imagistic diagnosis is important to sustain cerebral hyperperfusion, respective for thedifferential diagnosis with other perioperatory complications of the revascularizating procedures.Although hyperperfusion is not a synonym of CHS, it represents an important factor in the genesis of thissyndrome. The available imagistic techniques today allow the evaluation of the degree of cerebralperfusion (marking hyper/hypoperfusion), cerebral vascular reactivity, respective the positive/differentialdiagnosis of cerebral lesions.Highlighting cerebral hyperperfusion is possible through SPECT (single photon emission CT),multislice dynamic susceptibility contrast MRI or PWI (perfusion weighted MRI)(17,18,24,57,67). Due totheir high cost there is a lack of substantial data.Cerebral vascular reactivity might be evaluated through SPECT after administratingacetazolamide, however the usage of this substance at a transcranial Doppler examination is more costefficient. In order to achieve vasodilatation inhalation of CO2 might be useful or the apnea test,followed by measuring the velocity and blood flow in the middle cerebral artery, we might detect anexhausted microvascular system. The disadvantages of the transcranial Doppler examination are due tothe characteristic subjectivism of the exploration, the difficulty to obtain an echographic window, themultiple anatomic variations (the standard anatomy of the poligone of Willis at the maximum of 54% of39

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 40the population) and controlateral stenosis with a significant redistribution of the cerebral debit(9,30,31,26-29).The incidence of CHS in literature is different for CEA respective CAS, however, without statisticalsignificance. Moulakakis et al. publishes a metaanalysis of the existent data in literature regarding theincidence of CHS post CEA, respective post CS (2003-2008)(1).CHSIntracerebral hemorrhageEAC 0.40%-14.0%, average 4.53% 0 – 1.0%, average 0.48%CAS 0.44%-11.7%, average 3.65% 0 – 4.5%, average 2.08%The incidence at our institution, prospectively evaluated on 247 patients, exclusively with CEA ingeneral anaesthesia with different surgical approach, was represented by 7 patients, meaning 2.83%.The patients were evaluated in days 1 and 2 postop. regarding the complaints, consciousness andpossible neurological manifestations. 5 of these patients (2.02%) presented postop. headaches of highintensity, ipsilaterally the surgical intervention, not responding to specific pain management, howeverwith propitious reaction to cerebral depletive drugs (diuretics), respectively to the dropping of arterialblood pressure. The other two patients (0.81%) presented a more complex symptomatology, associatingtemporo-spatial disorientation to the headaches, respective troubled consciousness, nausea andvomiting. None of the patients presented motor disturbance (hemiparesis, hemiplegia).CHS risk factorsPreoperative Perioperative PostoperativeHypertensivemicroangiopathyDiabetes mellitusAge > 80 yearsRecent contralateral EAC (

E. Jerzicska et al ■ 2009, vol. 8, no. 1-2, pp. 41at a normal or mild low range (6, 13, 35, 36). Transcranial Doppler monitoring of cerebral blood flow isalso a useful technique (3, 5).Sedation, hyperventilation (general anesthesia), mannitol, hypertone saline are all to be useful intreating cerebral edema (9, 24, 33, 34). Corticotherapy was utilized in treatment of CHS (9, 24, 33, 34).The curative treatment of CHS is actually the treatment of the generated complication, mainlycerebral edema, intracerebral hemorrhage, epileptic seizures, and so on. A subservient algorhytm indiagnosis and treatment in case of unfavorable neurological evolution of a patient after surgical orendovascular carotid revascularization is presented as it follows:After Moulakakis et al. (1)The prevention protocol in our institution is based on the concepts represented above. Althoughthere are limitations due restricted financial resources, by using judgematical the available materials andinvestigations leads to a very good cost-efficient ratio regarding prevention in CHS:- The correct indication of revascularization (CEA vs. CAS)- A complete and correct preoperatory diagnosis- A possibly exact anatomic-lesion diagnosis- Highlighting the risk factors for CHS- Avoiding bilateral CEA- Using intravascular shunt- “no touch” surgery before carotid clamping- Using pharmacological protection: preoperatory antiagregation and statins, intraoperatoryanticoagulation (heparin 1 mg/kg, without postoperator antagonisation)- Avoiding intra- and postoperator blood pressure variations, prompt and energetic treatmentof hypertension- Continuous postop monitorization of the patients in the first 3 days- Ambulatory reevaluation of the patient after 14 days postop.- The notification of the attending physician about the possible postoperative complications.Conclusions:CHS is a redoubtable complication of carotid revascularization. Its manifestations are various, butthe base is the same phisiopathological concept. It is essential to distinguish the risk factors and incipientsymptoms. Prophilaxis is the most efficient treatment, and it is achievable through an adequateeducation of the medical personal with minimal financial implications in order to assure a faster recoveryin carotid postrevascularisation.41

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ISSN 1583-3534, H. Suciu et al ■ 2009, vol. 8, no. 1-2, pp. 44-48Particular methods of carotid revascularizationSuciu H., Jerzicska E., Mitre R., Judit Kovacs 1 , Capilna R., Deac R.Cardiovascular Surgical Hospital – Institute of Cardiovascular Diseases and Transplant, Targu Mures1Cardiovascular ICU – Institute of Cardiovascular Diseases and Transplant, Targu MuresAbstractIntroduction. Carotid revascularization is standardly represented by the endarterectomy of the internaland/or common carotid arteries associated or not with several other vascular surgical techniques (resections,angioplasties). This situation is obviously possible in case of localized lesion at the level of the carotid bifurcation,which by the way represents the most frequent localization.Objective. We would like to present the existent surgical treatment options for stenotic carotid affectionslocalized downstream from the carotid bifurcation (aortic arch, brahiocephalic trunk, common carotid arteries).The atherosclerotic stenosis from this teritorry are frequently represented by stenosis or occlusion of the commoncarotid artery, respective stenosis of the brahiocephalic trunk. The pathology affecting the aortic arch and whichcan determine alterations of the brain circulation is represented by dissection of the aortic arch. Seldom situationsare represented by aortic arch aneurysms (saccular) and intraluminal thrombosis of the aortic arch. A relativelyfrequent situation is represented by common carotid lesions which appear in open or closed cervical trauma.Material and method. The study material was represented casuistry of Cardiovascular Surgical HospitalTargu Mures, all chosen cases being treated at this facility.Results. We present cases of common carotid arterial reconstruction, aortocarotidian bypass, aorticsubclavian-carotidbypass, subclavian-carotid bypass and indirect reconstruction of brahiocephalic trunkdissection.Conclusions. The pathology of supraaortic arterial systems is clearly dominated by internal carotidstenosis. Although referred rarely, cases about lesions of brahiocephalic trunk or common carotid arteries aresevere and their treatment is sometimes about difficult and complex abordations, marked by features dependingon the patient.Tehnici particulare de revascularizare carotidianăSuciu H., Jerzicska E., Mitre R., Judit Kovacs 1 , Capilna R., Deac R.Clinica Chirurgie Cardiovasculară – Insitutul de Urgenţă de Boli Cardiovasculare şi Transplant Târgu Mureş1Clinica ATI Cardiovascular - Insitutul de Urgenţă de Boli Cardiovasculare şi Transplant Târgu MureşRezumatIntroducere. Revascularizarea carotidiană este reprezentată în mod standard de endarterectomiaarterei carotidei interne şi/sau comune asociată sau nu cu diverse alte tehnici de chirurgie vasculară (rezecţii,angioplastii, etc). Această situaţie este evident posibilă în cazul localizării leziunii la nivelul bifurcaţiei carotidiene,care reprezintă de altfel cea mai frecventă localizare.Obiective. În lucrarea de faţă dorim să prezentăm opţiunile chirurgicale existente pentru tratamentulafecţiunilor stenotice carotidiene situate în amonte de bifurcaţia carotidiană (arc aortic, trunchi brahiocefalic,artera carotidă comună). Stenozele aterosclerotice din acest teritoriu sunt reprezentate frecvent de stenozelesau ocluziile de artere carotide comune, respectiv stenoze de trunchi brahiocefalic. Patologia care afecteazăarcul aortic şi care poate determina afectări ale circulaţiei cerebrale este reprezentată de disecţia de crosăaortică. Situaţii mai rar întâlnite sunt reprezentate de anevrismele de crosă aortică (saculare) şi trombozaintraluminală de crosă aortică. O situaţie relativ frecventă o reprezintă leziunile arterei carotide comune careapar în cazul traumatismelor cervicale deschise sau închise.Material şi metodă. Materialul de studiu a fost reprezentat de cazuistica Clinicii Chirurgie CardiovascularaTargu Mures, toate cazurile alese pentru exemplificare fiind tratate chirurgical in acest serviciu.Rezultate. În lucrarea de fata prezentam cazuri de reconstuctia arteriala carotidiana comuna, by-passaorto-carotidian, by-pass aorto-subclavio-carotidian, by-pass subclavio-carotidian respectiv reconstructieindirecta a unei disectii de trunchi brahiocefalic.Concluzii. Patologia sistemelor arteriale supraaortice este dominata net de stenozele de artera carotidainterna. Desi referite rar, cazurile care prezinta leziuni ale arcului aortic trunchiului brahiocefalic sau arterelorcarotide comune sunt grave iar tratamentul lor necesita de multe ori abordari dificile sau complexe, grevate departicularitati in functie de pacient.44

H. Suciu et al ■ 2009, vol. 8, no. 1-2, pp. 45IntroductionCarotid revascularization is standardly represented by the endarterectomy of the internal and/orcommon carotid arteries associated or not with several other vascular surgical techniques (resections,angioplasties). This situation is obviously possible in case of localized lesion at the level of the carotidbifurcation, which by the way represents the most frequent localization.ObjectiveWe would like to present the existent surgical treatment options for stenotic carotid affectionslocalized downstream from the carotid bifurcation (aortic arch, brahiocephalic trunk, common carotidarteries). The atherosclerotic stenosis from this teritorry are frequently represented by stenosis or occlusionof the common carotid artery, respective stenosis of the brahiocephalic trunk. The pathology affectingthe aortic arch and which can determine alterations of the brain circulation is represented by dissectionof the aortic arch, frequently cointeressed in type A aortic dissections. Seldom situations are representedby aortic arch aneurysms (saccular) and intraluminal thrombosis of the aortic arch. A relatively frequentsituation is represented by common carotid lesions which appear in open or closed cervical trauma.Material and methodThe study material was represented casuistry of Cardiovascular Surgical Hospital Targu Mures, allchosen cases being treated at this facility.Results and discussionSurgical tehniques are standardly divided in reconstructive and arterial bypass interventions.Exceptionally indirect methods may also be used. Arterial bypass techniques can be anatomical orextraanatomical. For the described region, anatomic techniques assumpt aortocarotid bypass, whilstthe extraanatomical ones surmise subclavian-carotid bypass.The etiology of the described lesions is in the great majority represented by atheroslerosis, but wemay notice other rare causes like aortic dissection, open or closed cervical trauma, localizedintravascular thrombosis at the level of the aortic arch.1. Common carotid arterial reconstructionThe present etiology in our casuistry was represented by closed cervical trauma. As localfavorizing factor we highlight the atheromatous plaque.The benefits of this procedure are represented by the simple laterocervical abordation, arelatively simple surgical method, the facile use of intravascular shunt.Indications of the procedure are represented by focal lesions of the common carotid, mediumand distal portion (aneurysm, pseudoaneurysm, stenosis).Fig. 1: Posstrauamtic pseudoaneurysm, rightcommon carotid.Fig. 2: Reconstruction of the right common carotidwith Gore-Tex patch associated with localendarterectomy (at local endovascular inspectiona localized atheromatous plaque is shownperilesional – favorizing factor for posttraumaticformation of pseudoaneurysm).45

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 462. Aortocarotidian bypassIt is a complex surgical method. Its benefits are represented by: anatomic by-pass, possible forboth common carotid, with possible association or not - carotid endarterectomy. The disadvantages ofthe procedure are the need of a complex abordation, cervical and thoracic (median or partialsternotomy superior till the IV intercostal space), reason why it is indicated in situations when theprocedure is contemporaneous with cardiac surgical interventions. Its indications: common carotidstenosis, common carotid occlusions with permeable intern carotid in context with associated cardiacinterventions (ex. aortocoronary bypass) or in case of indisponibility of other supraaortic branches forextraanatomic bypasses.Fig. 3: Distal anastomosis of an aortocarotidbypass with Gore-Tex prothesis of 6 mm indiamether.Fig. 4: Proximal anastomosis of aortocarotidbypass on the ascendent aorta.Fig. 5: Associated intervention (OPCAB –anastomosis of the left internal mammary with thedescendent anterior on beating heart).Fig. 6: Aortocarotid bypass and anastomosis ofthe internal mammary with the anteriordescendent – final intrapericardic aspect.3. Aortic-subclavian-carotid bypassRepresents a precise surgical intervention, using bifurcated “Y” prothesis anatomically disposed,representing as an advantage of the method. It is useful in brahiocephalic trunk stenosis (on the right) orin combined lesions of common left carotid with left subclavia (on the left). It may be associated withadjuvant interventions, like carotid endarterectomy, vertebral artery enlargement plasty, segment V1.46

H. Suciu et al ■ 2009, vol. 8, no. 1-2, pp. 47Fig. 7: Aorto-subclavian-carotid by pass –tunelizing the bifurcated prothesis.Fig. 8: Aorto-subclavian-carotid bypass– proximalanastomosis.4. Subclavian-carotid bypassIt is a surgical intervention indicated in common carotid stenosis. The distal carotid bypass maybe done on several segments of the common carotid artery, meaning right after the emergence, on theproximal segment (short subclavian-carotid bypass). Another possible solution is the common carotidbypass on the medium segment, situation when the bypass is intermediar. The feature is used in caseswhen the lesion extends more then the initial portion. The last variant is represented by the distalsubclavian-carotid bypass, on the bifurcation of the common carotid artery. It is a long bypass, usefulwhen the lesions include the whole common carotid artery.The proximal subclavian-carotid bypass assumes a unique supraclavicular abordation.Fig. 9: Short subclavian-carotid bypass (proximalcommon carotid artery) – final aspectFig. 10: Intermediar subclavian-carotid bypass(medial segment, common carotid artery) – finalaspect.Fig. 11: Subclavian-carotid byapss (intermediar segment of thecommon carotid artery). With Gore-Tex prothesis of 6 mm diamether.The distal subclavian-carotid bypass assumes mixt abordation,supraclavicular fossa and carotic trigonum. The proximal anastomosisis on the subclavian artery, the distal one being on the bifurcation ofthe ipsilateral common carotid. It might be associated with carotidendarterectomy.47

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 485. Solving a brahiocephalic trunk dissectionAscendent aortic and arch dissections might involve or interest the emergence of the greatsupraaortic vessels. Reconstruction techniques are represented by the above represented bypasses or inselect cases, indirect methods, which do not adress the brahiocephalic trunk or the left commoncarotid, but the acctual dissection, eliminating the false lumen. Biological adhesives and reinforcementprocedures might be used in order to eliminate the false lumen from the circulation.Fig. 12: Brahiocephalic artery dissection (incontext of a dissection of the ascendent aortaStanford A Debakey II).Fig. 13: Ascendent aortic dissection Stanford ADebakey II – dissection fold continuing on thebrahiocephalic artery.Fig. 14: Dissection of ascendent aorta (afterreplacing the aortic valve).ConclusionsFig. 15: Indirect reconstructuion of thebrahiocephalic trunk through elimination of thefalse lumen (unifying by using biologic adhesive,respective the reinforcement of the aortic crossblunt with internal and external bandelets).The pathology of supraaortic arterial systems is clearly dominated by internal carotid stenosis.Although referred rarely, cases about lesions of brahiocephalic trunk or common carotid arteriesare severe and their treatment is sometimes about difficult and complex abordations, marked byfeatures depending on the patient.48

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 50The aim of this article is to present the specific characteristics of the vertebro-basilar arterialsystem together with the author’s experience in treating the vascular lesions by using various surgicalmethods, and to draw attention on the particularities of the diagnostic workup and therapeuticapproaches.Special features of the vertebro-basilar systemThe two vertebral arteries frequently depict an asymmetric outline, with one being “dominant”.The first part of the subclavian arteries giving origin to the vertebral arteries must also be included in thegeneral picture of the vertebro-basilar system both in normal and in disease. Not infrequently, the leftvertebral artery may originate directly from the aortic arch, between the left carotid and the leftsubclavian artery respectively 3 . Hence an angiographically “absent” left vertebral artery must be soughteither by direct catheterization or by performing an arch aortography.A practical classification of the segments of the vertebral arteries is reported here 4,5 .Figure 1V0 = origin. The very origin of thevertebral artery is called the V0segment. The purpose of assigning aseparate name to this portion of thevertebral artery assists in drawing theattention toward the adjacent parts ofthe subclavian artery (or of the aorticarch); lesions of these closely-relatedarterial segments may limit, modify oreven contraindicate surgical (orpercutaneous) approaches.V1 = pre-transversal extraosseous. This isthe portion of the vertebral artery mostaccessed in surgery. With older age oratherosclerotic disease, the V1 portioncan show significant kinking. This is theportion of the vertebral artery that canbe mobilized most, allowing forexample, its re-implantation in thecommon carotid artery. This portion ofthe vertebral artery can be easilyconfused with the inferior thyroid artery.This latter structure lies however in amore superficial plane (anterior to thevertebral artery) and characteristically,gives off numerous cervical branches.Another important detail is that thevertebral artery represents the first (themost proximal) branch of thesubclavian artery.V2 = interosseous. Surgical access tothis part is more striving for the surgeondue to the need for partial boneresection. Lesions of this portion of thevertebral artery can be howevertreated more conveniently and morerapidly, by using the percutaneoustechniques. The vertebral artery is accompanied by a plexus of veins and by sympathetic nervesderived from the cervical ganglia, forming the vertebral nerve. This segment of the vertebral arterygives off branches to the cervical nerves, vertebrae, intervertebral joints, neck muscles and for thecervical spinal cord. A prominent branch at C5 level anastomoses with the anterior spinal artery. Theanastomoses with the deep cervical and with the ascending cervical artery can becomeconspicuous and offer parallel arterial pathways toward the distal vertebral artery (V3 segment).50

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 51Inversely, such well-developed anastomoses may promote the steal syndrome even in case ofocclusion of the vertebral artery at its origin (V0 and V1 segments).V3 = distal extracranial or the atlas loop. The artery runs laterally and then vertically toward thetransverse foramen of the atlas; after passing thorough the foramen, the artery winds medially alongthe lateral mass of the atlas, pierces the posterior atlanto-occipital membrane, entering the duramater and the arachnoid at the level of the foramen magnum. The suboccipital portion of thevertebral artery from the transverse foramen of the axis (C2), to the posterior atlanto-occipitalmembrane, is a relatively long segment, allowing a proper surgical exposure for a bypass at this level.Numerous muscular and articular branches must be identified and interrupted, at this level.V4 = intracranial. This segment of the vertebral artery lies entirely in the subarachnoid space. Beforethe confluence of the two vertebral arteries, each gives off some important branches in theintracranial portion: the posterior spinal artery, the posterior inferior cerebellar artery (PICA) and theanterior spinal artery. A lower (i.e. more proximal) origin of the PICA may impede surgicalmanoeuvres at the level of the intracranial vertebral artery.Numerous ANASTOMOSES exist between the carotid and the vertebro-basilar system of arteries:Cervical level. There are no direct communications between the common or internal carotid arterieswith the vertebral arteries. The only notable anastomoses are established between branches of theexternal carotid artery and subclavian arteries: superior thyroid (external carotid) with inferior thyroid(subclavian) or the deep and the superficial branch of the occipital artery (external carotid) with thedeep or ascending cervical arteries (subclavian) and with the muscular branches of the vertebralarteryIntracranial level. The arterial circle (Willis) represents the most important communication betweenthe basilar artery and the emerging posterior cerebral arteries, and the terminal portion of thecarotid arteries – by way of the posterior communicating artery.Figure 2: Anastomoses between the anterior and posterior circulation of the brainThe deep arterial branches from the arterial circle are terminal branches, but the cortical branches ofthe anterior, middle (carotid) and posterior (vertebro-basilar) cerebral arteries are connected throughthe leptomeningeal anastomoses. Such anastomoses may become conspicuous with occlusion of oneof the main trunks. Variations in the makeup of the arterial circle explain the different clinicalmanifestations or the individual variations during carotid or vertebral artery clamping 6 . Vestigial anastomoses between the two systems are represented by the proatlantal, hypoglossal,otic, trigeminal or stapedial arteries. The persistence of such arteries may explain atypical clinicalmanifestations or different tolerance to carotid clamping, in individual patients 7-15 .51

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 52THE TERRITORY OF VASCULARIZATION OF THE VERTEBRO-BASILAR SYSTEM is both wide and important. It comprisesthe brainstem, the cerebellum, a great portion of the cerebral cortex while the deep central branchesare distributed to the basal nuclei and thalamus 16 . The various syndromes described so far, reflect theseverity of the vascular lesions, the clinical significance and the dismal prognosis: medial medullarysyndrome (vertebral or proximal basilar artery occlusion), lateral medullary syndrome (vertebral, PICA ormedullary arteries occlusion), complete unilateral medullary syndrome (vertebral artery occlusion),medial inferior pontine syndrome (occlusion of paramedian branches of the basilar artery), lateralinferior pontine syndrome (anterior inferior cerebellar artery occlusion), lateral ponto-medullarysyndrome (vertebral artery occlusion), medial middle pontine syndrome (occlusion of paramedianmiddle branches of the basilar artery), lateral middle pontine syndrome (occlusion of shortcircumferential branches), medial superior pontine syndrome (occlusion of distal paramedian branchesof the basilar artery), lateral superior pontine syndrome (superior cerebellar artery occlusion), basilarartery syndrome (occlusion of basilar or of singular vertebral artery), temporal and occipital corticalsyndromes (occlusion of the cortical branches of the posterior cerebral artery: anterior temporal,posterior temporal, calcarine and parieto-occipital arteries), midbrain, subthalamic and thalamicsyndromes (occlusion of the deep branches of the posterior cerebral artery: peduncular, mesencephalicpostero-medial choroidal, hippocampal and splenial arteries).THE DIAGNOSTIC WORKUP comprises the following steps:History and physical examination. The clinical presentation in the individual patient is usually highlyvariable. The transient ischemic attack in the vertebro-basilar system includes vertigo, dizziness,ipsilateral facial numbness, contralateral limb numbness, diplopia, hoarseness, dysarthria, dysphagia,and rarely hemiparesis, while cerebral infarction may manifest with any of the numerous syndromespresented above. A particular mention must be made at this point regarding the lesions in thevertebro-basilar system, diagnosed during routine diagnostic interrogation for suspected lesions in thecarotid system of arteriesCardiologic clearance. Diseases representing a risk for the development of a stroke must beidentified if present. Higher-risk conditions include atrial fibrillation, mitral stenosis, mechanical valvarprosthesis, left ventricular dysfunction and intracavitary thrombi, recent myocardial infarction,infective endocarditis. Lower-risk conditions include: calcifications of the mitral annulus, mitral valveprolapse, patent foramen ovale, aneurysm of the atrial septum, aortic stenosis with valvarcalcification. Pre-operatively, the patient must be ideally in a stable condition especially regardingthe hemodynamic status, blood pressure levels, the presence of dysrhtythmia or heart failureDoppler examination. A complete ultrasound workup must be performed including the carotidsystem of arteries, the subclavian arteries, the vertebro-basilar system, and not least, the intracranialcirculation. Data regarding the diameter of the vertebral arteries and the direction of flow are veryimportant. A thorough staging of the arterial lesions is highly significant in view of the therapeuticplanning and for the choice of the proper surgical indication. There is no unanimous agreement andno comparative statistics regarding the data on the severity of stenotic lesions in the vertebro-basilarinsufficiency as compared with the carotid system of arteries. There is no accepted “stenoticthreshold” above which surgery or angioplasty should be employed, in the vertebro-basilar system.Severe kinking of the vertebral arteries may add further deleterious hemodynamic effects, which canbe revealed by means of the Doppler interrogation and not least, and specially while allowingvarious postures of the head and neck. Again, there is no unanimous agreement on the IMT indexvalues (intima/media thickness) in the case of the vertebro-basilar systemAngiographic interrogation. A 4-vessel angiogram (including extra- and intracranial exam)completed by aortic arch angiogram offers additional valuable data and is especially indicatedwith suspected “lower” lesions on the arch or on the origin of the cervical vessels. The intracranialdistribution of the main trunks allows a better planning of the surgical act and the order of vesselclamping. Angiogram adds more important details as compared with the carotid system, wherelesions are mostly located at the level of the bifurcations. The Doppler examination cannot offer butindirect data on the origin of the subclavian arteries or of the aortic arch, while a low-grade stenosisplus kinking of the vertebral artery appears as a severe stenosis on the echogram. Moreover, if arevascularization of the vertebral artery at suboccipital level is contemplated, the angiogram willoffer important additional details on the adjacent arteries that can be used as donor arteries(external carotid and its main branches for example). Angiography also offers data on the anatomicvariations of the basilar trunk, or of the origin of the PICA (posterior inferior cerebellar artery).52

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 53CT scan or MRI interrogation. These diagnostic tests offer details on the presence of infarctions orlacunae. An arterial stenosis or plaque can be defined as “symptomatic” in the presence ofpreviously unknown lacunae or cerebral infarctions in the very same vascular territory. Identificationof vulnerable, unstable, complicated plaques and details on the intimate composition of the plaque,are all best accomplished by the MRI interrogation, although rarely performed due to the costs andlonger examination timesMRA (magnetic resonance angiography) may substitute the classical angiogram, although itrepresents only a diagnostic tool with no therapeutic (e.g. percutaneous) possibilities. It mayrepresent a sound screening procedure and a useful test during follow upSpirometry with both static and dynamic lung volumes is mandatory in the planning of the surgicalact, and not least regarding the type of anesthesia envisaged.Endocrine evaluation especially for diabetes or even borderline glucose intoleranceThe risk stratification in the case of carotid lesions is usually well correlated with the initial symptomor sign, being higher with stroke, less with hemispheric TIAs and least with amaurosis 17 . However, thiscannot be accomplished in the vertebro-basilar system where such a staging of signs and symptoms isnot evident and where any delay can have dismal consequences.Although the diagnostic elements are all well known and established, THE SURGICAL THERAPY is lesscontemplated (as compared with the medical treatment and the percutaneous manoeuvres).However, surgery may offer a better alternative both on short and on long term and this aspect will beillustrated in this article. A number or 36 consecutive patients with lesions in the vertebro-basilar arterialsystem were surgically treated over a 4-year period.Patient DataTABLE 1: PATIENT DEMOGRAPHICSAGE (years) MALE (No) FEMALE (No)46-50 3 051-55 9 156-60 5 361-65 4 166-70 2 471-75 1 175-80 2 0Total / sex 26 10TOTAL 36Patient demographicsAs illustrated in TABLE 1 male patients wereyounger. Additionally, more of the malepatients presented with more severeneurologic symptoms and more had aprevious stroke.Clinical presentationPatients displayed the following signs and symptoms, upon admission in the hospital (TABLE 2)TABLE 2: CLINICAL PRESENTATIONCLINICAL SIGN / SYMPTOMNo of patientsStroke in the territory of the PCA* 1Vertigo, dizziness, unstable gait 4Previous stroke in the territory of the PCA + vertigo 2Neurologically instable: loss of consciousness when sitting up 3Stroke in the carotid territory + vertigo and dizziness 7TIA in the carotid territory + vertigo and dizziness 9Dizziness + upper limb ischemia 8Asymptomatic / minor unspecific symptoms 2* PCA = Posterior Cerebral ArteryTOTAL 36Noticeably, a large number of the patients presented with concomitant lesions in the carotidterritory and with a polymorphous symptomatology. Three of the patients were neurologically instable,53

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 54with loss of consciousness when sitting up or while performing Valsalva manoeuvres (sneezing orcoughing). Upper limb ischemia represented one of the major complaints in less than a quarter of thepatients. Two of the patients who had occlusion of the subclavian artery plus occlusion of the first andsecond portion of the ipsilateral vertebral artery (V1 and V2) presented with signs of upper limb ischemiaand vertebral steal syndrome, through enlarged cervical anastomoses, although clinically the distalpulse was palpable.ComorbiditiesThe patients presented numerous associated diseases. A significant number had 2 or morecomorbidities (TABLE 3)DISEASETABLE 3: COMORBIDITIESMALE (No)FEMALE(No)AHT 1 4 1COLD 2 2 0CRF 3 in haemodialysis 1 0Ischemic heart disease + AHT 2 1Diabetes + AHT 3 6AHT + COLD 7 0Diabetes +AHT + COLD 7 2Total / sex 26 10TOTAL 361 AHT = Arterial Hypertension2 COLD = Chronic Obstructive Lung Disease3 CRF = Chronic Renal FailureMale patients presented with morenumerous associated diseases andwith more severe forms of chronicobstructive lung disease. Ischemicheart disease included previousmyocardial infarction and/orangina. Peripheral vascular diseasewas present in 8 male patients andin 3 female patients (not illustrated inthe table). One male patientrequired simultaneous lower limbrevascularization for severeischemia.Arterial lesionsThe following types of arterial lesions were observed in this series of patients (TABLE 4):StenosisTABLE 4: ARTERIAL LESIONS IN THE CASE SERIESARTERIAL LESIONSkinking of the origin of the vertebral arteryNo3Vertebral steal syndrome: occlusion of the brachiocephalic trunkFigure 32Figure 4Vertebral steal syndrome: occlusion/severe stenosis of the subclavian artery 3

Vertebral steal syndrome: occlusion of the subclavian artery +bilateral carotid stenosisVertebral steal syndrome: occlusion of the subclavian artery +vertebral artery (V1-V2) – steal through collateralsFigure 532Vertebral steal syndrome: occlusion of the subclavian artery +stenosis of ipsilateral carotid bifurcationVertebral steal syndrome: occlusion of the subclavian artery +stenosis of contralateral carotid bifurcationVertebral artery stenosis +bilateral internal carotid occlusionVertebral artery stenosis +bilateral internal carotid stenosisFigure 68227A 7B57C 7DFigure 77E

Vertebral artery stenosis +ipsiteral internal carotid stenosis2Vertebral artery stenosis +contralateral internal carotid stenosisFigure 819A9BFigure 9Vertebral artery stenosis + internal carotid stenosis + subclavian artery occlusion 1Multiple neck vessel arterial disease: subclavian, carotid, vertebral + lower limbs10A10B1Vertebral artery occlusion (V1-V2) +internal carotid occlusion +subclavian artery occlusion10C10DFigure 101TOTAL 3656

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 57As illustrated in Table 4, only a small percentage of the patients presented with “pure” lesions ofthe vertebral artery (or of the first portion of the subclavian artery): most patients had diffuse arterialdisease either involving the supra-aortic trunks and branches, or the lower limbs. The diagnosticapproach and the surgical indication and technique – were hence more elaborated and morechallenging. A complete revascularization was envisaged every time while weighing the benefits of theoperation and the risks of a longer and a more complicated procedure on one hand and on the otherhand, the risks of non-treating all vascular lesions in a single operative moment (further details areoffered below).In this series, the diagnostic workup consisted in: Doppler examination (including the transcranialDoppler), 4-vessel angiogram, cardiologic and neurologic clearance, spirometry, cerebral CT of MRI.Surgical ProceduresThe patients underwent various surgical procedures. All operations requiring median sternotomywere performed under general anesthesia. Operations involving only the cervical approach wereperformed either under general anesthesia, or under loco-regional anesthesia (cervical block): TABLE 5and 6.TABLE 5: TYPES OF ANESTHESIA USEDGeneral anesthesia (with naso- or orotracheal intubation) 25Loco-regional (cervical plexus block interscalenic block) 11TOTAL 36TABLE 6: SURGICAL PROCEDURESType of procedureVertebral artery re-implantation in the common carotid arteryNo. ofpatientsNotes3 L-L or L-TFigure 11Common carotid-to-vertebral artery bypass 2 PTFE graftCommon carotid-to-subclavian artery bypass5 PTFE graftFigure 12Re-implantation of the subclavian artery into the common carotid artery 257

Carotid bifurcation endarterectomy +carotid-to-subclavian artery bypass6 PTFE graftCarotid bifurcation endarterectomy +re-implantation of the subclavian artery into the carotid arteryCarotid bifurcation endarterectomy +re-implantation of the vertebral artery into the common carotidCarotid bifurcation endarterectomy +carotid-to-subclavian artery bypass +carotid-to-suboccipital vertebral artery (V3) bypassFigure 13122Saphenousvein grafton thevertebralartery14AFigure 14Simultaneous bilateral carotid endarterectomy +carotid-to-subclavian artery bypassSimultaneous bilateral carotid endarterectomy +vertebral artery re-implantation into the common carotidSubclavian-to-contralateral subclavian and carotid artery bypass 1Ascending aorta-to-right subclavian and right carotid bypass 3Ascending aorta-to-carotid and bilateral subclavian artery bypass 1Brachiocephalic trunk-to-left subclavian, left carotid and left vertebral arterybypass1Ascending aorta-to-right subclavian, right carotid and left femoral arterybypass +left carotid endarterectomy +1left vertebral artery re-implantationTOTAL 3614B1 PTFE graft5DacrongraftMediansternotomy+cervicalapproachThe re-implantation of the vertebral artery in the common carotid artery 18 is performed eitherthrough a supraclavicular approach or through a single longitudinal cervical incision 19 . A combinedincision (longitudinal plus supraclavicular) for carotid and vertebral artery exposure was used in 4 of the58

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 59patients depicting shorter neck. In one of the 4 afore mentioned patients, the transversal canal at C6level was open, in order to obtain a longer segment of the vertebral artery.The common carotid-to-vertebral artery bypass represented an alternative of the formertechnique, used in 2 patients who depicted very frail vertebral arteries. A 6 mm. PTTFE graft was used forthe bypass.Common carotid-to-subclavian artery bypass was deployed in 5 patients with vertebral stealsyndrome due to severe stenosis or occlusion of the origin of the subclavian artery. The same 6 mm. PTFEreinforced graft was used. The prosthesis was tunnelled underneath the sternocleidomastoid muscle.An alternative of the technique mentioned above, is the (latero-terminal) re-implantation of thesubclavian artery in the common carotid artery (with the creation of “a neo-brachiocephalic trunk”).The procedure requires a more extensive mobilization of the origin of the subclavian artery, including theorigin of the vertebral artery. However, in none of the patients was necessary the ligature of the internalthoracic artery.With concomitant disease at the level of the ipsilateral carotid bifurcation, an additionalendarterectomy was initially performed, followed by the re-implantation of the subclavian artery in thecommon carotid artery (1 patient). However, the mostly used technique was endarterectomy andcarotid bifurcation-to-subclavian artery bypass with a 6 mm. PTFE graft. As previously mentioned, theprosthesis was tunnelled underneath the sternocleidomastoid muscle.When no significant lesions of the subclavian artery were present, the technique of carotidendarterectomy plus vertebral artery re-implantation in the common carotid artery, was used.In 2 patients, multiple arterial lesions were present: stenosis at the level of the carotid bifurcation,stenosis or occlusion of the first portion of the subclavian artery and occlusion of the first and second partof the vertebral artery (V1-V2). In spite of the vertebral artery occlusion at origin and intertransversalportion, the vertebral steal syndrome was present, through enlarged cervical collaterals, whichconnected the suboccipital vertebral artery (V3) to the second and third part of the subclavian artery.These patients had also palpable distal pulse in the upper limb. Such complex lesions required acomplete revascularization consisting of carotid-to-subclavian bypass, followed by carotidendarterectomy and eventually by carotid bifurcation-to-suboccipital vertebral artery venous bypass 20(with the creation of a carotid “trifurcation”.As bilateral carotid disease is frequently associated with subclavian or vertebral artery disease, inthe series of patients presented, 1 patient underwent simultaneous bilateral carotid endarterectomy pluscarotid-to-subclavian artery bypass, while the reminder 6 patients underwent simultaneous bilateralcarotid endarterectomy plus vertebral artery re-implantation in the common carotid artery. A specialnote is that all these patients were operated under loco-regional anesthesia.With extensive disease in the upper aortic system, involving almost if not all the cervical vessels, abroad and complex revascularization was achieved through a combined approach: mediansternotomy plus bilateral cervical incision. The donor vessel was the ascending (intra-pericardial) aortaand in only 1 case, the brachiocephalic trunk (this patient had a previously undiagnosed dilation of theascending aorta). The distal target vessels were the carotid bifurcations, the subclavian and thevertebral arteries.THE SHUNT was used only in 2 patients, of which one had occlusion of the brachiocephalic trunk(ascending aorta-to-common carotid shunt) and the other had a single vertebral artery patent butseverely stenosed at origin (both internal carotid arteries and the contralateral vertebral artery wereoccluded). In this latter case, a temporary shunt was used between the ipsilateral subclavian artery andthe vertebral artery.ResultsPatient follow-up ranged from 3 years to 1 month.All patients had an early Doppler interrogation at 2-3 weeks postoperatively, repeated at 6months interval. All patients who underwent complex surgical procedures had an additional earlypostoperative angiogram. All bypasses, conduits, etc. remained patent during follow-up.One patient with carotid endarterectomy plus common carotid-to-vertebral artery bypass had aminor (non-disabling) stroke in the carotid territory during his in-hospital stay. There were no deaths in thisseries. One female patient had a retractile cervical scar, after a combined longitudinal andsupraclavicular approach. Three of the patients had transitory Horner syndrome. The patients withrevascularization of the suboccipital part of the vertebral artery (V3) fared well with no neurologicalcomplications; one of these patients experienced left-sided headaches for about 3 weekspostoperatively.59

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 60DiscussionIn medical practice, when confronted with the patient with cerebrovascular disease, thephysician’s attention is mainly focused on the carotid system of arteries, less on the aortic arch andbranches, and in a much lesser degree on the vertebro-basilar system. Endarterectomy of the carotidbifurcation appears at first glance to be a relatively easy procedure, especially when performed underloco-regional anesthesia or when deploying time-saving procedures such as the eversion technique orthe direct closure of the arteriotomy. The area of the carotid bifurcation is consequently the preferredarea for many categories of specialists in spite of the fact that the phenomenon of cerebral arterialinsufficiency represents the consequence of numerous factors acting at various levels, either insequence or concomitantly. The long vascular pathway between the heart and the brain is monitoredand approached by various specialists, having different conceptions, skills and preferences. It is in thisvery context that the vertebro-basilar system is generally less investigated and even less approachedtherapeutically. As compared with the carotid system of arteries, in the case of the vertebro-basilarsystem, larger studies and statistics on the degree of stenosis and on the patient outcome and risks arelacking.Moreover, as previously stated, the atheroembolic mechanism of stroke in the vertebro-basilarsystem is less contemplated, while it is well known, both in the case of the carotid arteries, as well as inthe case of the coronary arteries, that moderate stenoses and instable plaques constitute the maincause of cerebral or coronary infarction 21-The aim of this article and the purpose of presenting this series of patients is to draw attention onthis particular vascular territory that can be pathologically involved either singularly, or in concomitancewith the carotid arterial system. Out of the numerous and sometimes ambiguous diagnostic data andparticulars, the emerging therapeutic indication and associated procedure, rarely represent astraightforward process.The series of patients presented, form a heterogeneous group. The arterial lesions ranged widely,from no vertebral lesion at all (occlusion of the subclavian artery with vertebral steal syndrome) tocomplex multi-vessel disease including the carotid, subclavian, vertebral, and iliac arteries. It is thusdifficult to compare different therapeutic approaches, indications and not least, results – in such aprotean group.In spite of this detail, it is noteworthy mentioning the following aspects: Cerebrovascular arterial disease includes lesions at various levels, depicting different degrees ofseverity existing either as separate entities, or adding up their potential deleterious effects. Athorough stratification of severity of the disease and of the potential consequences is notstraightforward and usually requires a multispecialist approach (surgeon, neurologist, andcardiologist). Attention is mainly focused on the carotid system of arteries, the vertebro-basilar system beingoften overlooked, especially because the symptomatology is less characteristic. Due to theimportant territory of vascularization, the vertebro-basilar system must be carefully and fullyexplored and the lesions must be efficiently treated Decision on which lesions and when to treat such lesions in the vertebro-basilar system is not asclearly settled as compared with the carotid arteries. Moreover, ASYMPTOMATIC vertebro-basilarlesions pose both technical and ethic problems The surgery for vertebro-basilar insufficiency is much more technically demanding (including bothanesthesia and surgery) Individual anatomic variations must be thoroughly sought as the therapeutic planning andmethods vary accordingly, especially in case of highly asymmetric vertebral arteries or withincomplete arterial circle (of Willis) In patients with extensive and severe carotid disease, the vertebral arteries might represent theonly remaining direct source of vascularization of the brain and both the diagnostician and thesurgeon must be familiarized with treating stenotic lesions in the vertebro-basilar system The long cervical tract of the vertebral arteries is amenable to various surgical and percutaneousprocedures reducing thus the need for transcranial revascularization procedures Performing operations under loco-regional anesthesia, offers a better comfort to the surgeon andallows the use of selective shunting only – a procedure more difficult to apply in the case of thevertebral artery.60

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 61Final RemarksThe vertebro-basilar system has an important territory of vascularization, asking for a thoroughdiagnostic workup and for a more complex and for more elaborate surgical techniques. Suchtechniques, gain wider acceptance among surgeons, although a unanimous opinion regarding whenand how to treat such arterial lesions, is still lacking. The case series presented, in spite of itsheterogeneity, draws the attention toward less expected but otherwise highly-present diseases,affecting either the vertebro-basilar system, or both the vertebro-basilar system and the carotid system ofarteries.Figure LegendsFigure 1: THE SEGMENTS OF THE VERTEBRAL ARTERYAngiogrphic aspect of the left vertebral artery in an antero-posterior view. The vertebral arteryoriginates from the first part of the subclavian artery. The very origin in sometimes called the V0 segment.The extraosseous pre-transversal segment V1 comprises the portion between the origin and thetransversal foramen of the C6 vertebra (although variations are described, with the vertebral arterytravelling as far as C2 in an extraosseous tract. This portion of the artery is most accessible surgically. Theinterosseous segment V2 defines the part of the vertebral artery running through the transverse foraminaof the cervical vertebrae from C6 through C2. The cervical cranial nerves lie on a more posterior planewith respect to the artery. The atlas loop forms the V3 segment of the artery, readily reachable through asuboccipital approach. The intracranial V4 segment is sometimes subdivided into two parts, extra- andintradural. A particular detail regards the origin of the posterior inferior cerebellar artery (PICA), as earlyorigin of the PICA might impede surgical manoeuvres on the intracranial portion of the vertebral artery.Figure 2: ANASTOMOSES BETWEEN THE ANTERIOR AND POSTERIOR CIRCULATION OF THE BRAINImage illustrating the angiographic aspect in the case of a patient with bilateral internal carotidartery occlusion, occlusion of the contralateral vertebral artery and stenosis of the single patentvertebral artery (VA) - antero-posterior in the left panel, and lateral view, in the right panel. The basilartrunk (BT) is hence fed by the single vertebral artery. Efficient anastomoses between the posterior andrespectively, the anterior circulation, allow the filling of the anterior portion of the arterial circle (Willis), ofwhich the anterior cerebral artery (ACA) and the middle cerebral artery are well visible. Note also thatall the important branches of the arterial circle – anterior, posterior as well as contralateral – are all fedby the single vertebral artery. Such cases however reflect both a good compensatory circulation and aslower evolution of the occlusive lesions. Another compensatory mechanism is provided by theanastomoses between the external and internal carotid artery (not shown in this figure).Figure 3: STENOSIS ± KINKING OF THEORIGIN OF THE VERTEBRAL ARTERYAngiographic aspect of the origin ofthe left vertebral artery depicting bothstenosis and kinking. In this patient, thesubclavian artery has no apparentstenotic lesions; consequently, thevertebral artery can be re-implantedeither into the subclavian artery or intothe carotid artery (the latter techniquewas eventually chosen). Thedeployment of a stent is limited orimpossible, due to the kinking of the V1segment of the vertebral artery. Thekinking itself, with a relative excess inlength of the vertebral artery,facilitates the re-implantation into thecarotid artery and allowing a moregentle curve of the re-implantedvertebral artery.61

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 62Figure 4: VERTEBRAL STEAL SYNDROME: OCCLUSION OF THE BRACHIOCEPHALIC TRUNKTwo angiographic images(belonging to the samepatient), depictingocclusion of thebrachiocephalic trunk andsteal syndrome throughthe right vertebral artery.The latter, shows acompletely inverteddirection of blood flow,eventually filling the rightsubclavian artery and theright common carotidartery. The left paneldemonstrates an anteroposteriorview, while theright panel, an obliqueview of the same case.Note that the twovertebral arteries have thesame diameter, thusfacilitating the vertebralsteal.Figure 5: VERTEBRAL STEAL SYNDROME: OCCLUSION/SEVERE STENOSIS OF THE SUBCLAVIAN ARTERYThe angiographic imagedemonstrates a typical case of apatient with pre-occlusive stenosisof the left subclavian artery. In suchcases with a high-degree stenosis,the ipsilateral vertebral artery isseldom visible, being filled mostly ina retrograde manner, from thecontralateral vertebral artery,through the posterior cerebralcirculatory system. Note also theextensive lesions on the subclavianartery (comprising its first, secondand even third part: stenting of theorigin of the subclavian artery willtreat only partially theatherosclerotic lesions, while thestent itself might also cover theorigin of the left vertebral artery.62

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 63ascending cervical artery.Figure 6: VERTEBRAL STEAL SYNDROME:OCCLUSION OF THE SUBCLAVIAN ARTERY +VERTEBRAL ARTERY (V1-V2): STEAL THROUGHCOLLATERALSTwo of the patients in this series,had this very angiographic aspect, ofvertebral steal syndrome, but withoccluded origin and first tract of thevertebral artery (V1 and partially, V2). Inspite of the occluded large portions ofvertebral artery, the steal occurred throughenlarged collaterals and anastomoticpathways between the suboccipital andupper intraosseous vertebral artery and thesubclavian artery. The subclavian arterywas filled, as demonstrated in theangiographic image; the patients hadpalpable distal pulse in the left upper limb,although experiencing limb ischemia withexercise. The intraosseous portion of thevertebral artery (V2) remained onlypartially patent, the patients requiring asuboccipital approach of the vertebralartery and revascularization at this verylevel (V3). The enlarged collateral vesselsare the deep cervical artery and theFigure 7: VERTEBRAL ARTERY STENOSIS +BILATERAL INTERNAL CAROTID STENOSISFive patients of this series presented with bilateral carotid stenosis and stenosis of the dominant(or unique) vertebral artery, requiring a complex revascularization, consisting of: simultaneous bilateralcarotid endarterectomy + re-implantation of the vertebral artery into the common carotid artery. Thearterial lesions and the surgical solutions are illustrated in figure 7, as follows:Figure 7a, demonstrates a severe stenosis of the right carotid artery at the level of its bifurcationand a pre-occlusive stenosis of the origin of the right internal carotid artery. There is a faint fillingof the distal cervical and intracranial portion of the right internal carotid artery63

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 64Figure 7b, demonstrates the angiographic aspect of the left carotid artery, with a tight stenosis atthe very origin of the left internal carotid arteryFigure 7c, illustrates the severe stenosis at the origin of the left vertebral artery64

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 65Figure 7d: completion angiogram. Contrast medium injected into the left common carotid artery(the right side not shown) in an oblique (left panel) and lateral view (right panel). The reimplantedleft vertebral artery is filled concomitantly with the remainder carotid system; there isno stenosis or kinking of the re-implanted vertebral artery. The left carotid bifurcation is enlarged(best visible in the right panel, lateral view)Figure 7e: completion angiogram in a patient with similar lesions, but with a re-implanted rightvertebral artery. Note the enlarged carotid bifurcations, and the absence of the left vertebralartery65

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 66Figure 8: VERTEBRAL ARTERY STENOSIS + IPSILATERAL CAROTID STENOSIS. Angiographic andintraoperative aspect in the case of a patient with left vertebral artery stenosis, ipsilateral (left) carotidartery stenosis and contralateral (right) internal carotid artery occlusion. The stenosis of the left carotidartery was moderate, but with an ulcerated plaque. The left internal carotid artery represented however,the sole vascular supply for the anterior part of the cerebral circulation. The left vertebral artery was alsostenosed, as well as the left subclavian artery. The surgical solution comprised: the re-implantation of theleft vertebral artery into the left common carotid artery + endarterectomy of the left carotid bifurcation(eversion technique). The intraoperative aspect and the excised carotid plaque – are all depicted in theright panels. The operation was performed under loco-regional anesthesia.Figure 9: VERTEBRAL ARTERY STENOSIS +CONTRALATERAL CAROTID ARTERYSTENOSIS. The case illustrated hereby,had a left vertebral artery stenosis, leftcarotid artery occlusion andcontralateral (i.e. right) carotid arterystenosis.Figure 9a: angiographic aspect of thearterial lesions. The right carotid artery ismoderately stenosed but with ulceratedplaque. The right internal carotid arteryrepresents the sole arterial sourcevascularising the anterior cerebralsystem (note the bilateral filling of theanterior and middle cerebral arteries inthe left panel). The left internal carotidartery is occluded. The left vertebralartery is severely stenosed; the leftsubclavian artery depicts numerousstenoses in its initial portion.66

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 67Figure 9b: intraoperative aspect. The surgical solution consisted in endarterectomy of the rightcarotid bifurcation (left panel) and re-implantation of the left vertebral artery into the leftcommon carotid artery (right panel) – under loco-regional anesthesia. The aspect of the excisedplaque is also demonstrated.Figure 10: MULTIPLE NECK VESSEL ARTERIAL DISEASE + LOWER LIMBA case with multiple and complex arterial lesions in the neck vessels + lower limbs, is presented.Figure 10a: angiographicaspect of the neck vessels,demonstrating stenosis of theright subclavian and of theright common carotid artery,stenosis of the right carotidbifurcation, stenosis of the leftcarotid bifurcation, stenosis ofthe left vertebral artery at itsorigin and absent rightvertebral artery.67

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 68Figure 10b: angiographicaspect of the inferior aorticsystem. The patient hadstenoses of the infrarenalaorta, multiple stenoses ofthe right iliac artery andocclusion of the left iliacarteryFigure 10c: completionangiogram. The commontrunk of a trifurcated prosthesiswas inserted on the ascendingaorta (median sternotomyand pericardiotomy). Thebranches were anastomosedas follows: one branch to theright subclavian artery, thesecond branch to the rightcarotid bifurcation, the thirdbranch, was tunnelledtransdiaphragmatically,extraperitoneally and wasanastomosed to the left deepfemoral artery (and is shown infigure 10d). The left carotidbifurcation was treated byendarterectomy and patchenlargement, while the leftvertebral artery was reimplantedinto the leftcommon carotid artery.68

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 6910 d) 10 e)Figure 10d and e: angiographic images of the third branch of the prosthesis, as it travels across thediaphragm and through the extraperitoneal space, to be eventually anastomosed with the left deepfemoral artery.Figure 11: VERTEBRAL ARTERY RE-IMPLANTATIONAngiographic image of re-implanted vertebral arteries into the common carotid arteries. Leftpanel: latero-terminal anastomoses; right panel, latero-lateral anastomoses between the commoncarotid and the vertebral artery, respectively. CCA = common carotid artery. ICA = internal carotidartery. ECA = external carotid artery. VA = vertebral artery.69

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 70Figure 12: COMMON CAROTID-TO-VERTEBRAL ARTERY BYPASSAngiographic image demonstrating anoccluded left subclavian artery (SC) andthe bypass between the common carotidartery (CCA) and the former. In our caseseries, a 6 mm. PTFE graft was used,whenever a re-implantation of thesubclavian artery was rendered difficulteither by the quality of the vessels or inpatients with a short neck.Figure 13: ENDARTERECTOMY OF CAROTIDBIFURCATION AND CAROTID-TO-SUBCLAVIANARTERY BYPASSIntraoperative aspect uponcompletion of the surgical procedureconsisting of left carotid endarterectomy andbypass between the endarterectomisedbifurcation and the subclavian artery, using a8 mm. Armed PTFE graft. The graft is tunnelledunderneath the sternocleidomastoid muscle.The common carotid artery (CCA), thecarotid bifurcation (ECA and ICA) and thesubclavian artery (SC) were approachedthrough a longitudinal cervical incision,slightly curved inferiorly at supraclavicularlevel. The distal portion of the graft functionsas an angioplasty patch over the carotidbifurcation. Note also that the subclavianartery was approached in its second/thirdsegment, without the need of cutting theanterior scalene muscle. The anastomoses ofthe PTFE graft was performed first on thesubclavian artery.70

Horia Muresian ■ 2009, vol. 8, no. 1-2, pp. 71Figure 14: ENDARTERECTOMY OF CAROTID BIFURCATION + CAROTID-TO-SUBCLAVIAN ARTERYBYPASS + CAROTID-TO-SUBOCCIPITAL VERTEBRAL ARTERY BYPASSCompletion angiogram in the case of a patient with multiple arterial lesions on the left side,consisting of: subclavian artery occlusion, stenosis of the carotid bifurcation and occlusion of thevertebral artery. The vertebral artery remained patent at the level of the suboccipital portion (V3segment). The surgical solution included: 1. Common carotid-to-subclavian artery bypass, using a 8 mm.PTFE graft; 2. Carotid endarterectomy and patch angioplasty (PTFE patch); 3. Revascularization of thevertebral artery through a saphenous vein bypass between the surgically enlarged carotid bifurcationand the suboccipital vertebral artery (V3).14a14bFigure 14a depicts the general view of the operationFigure 14b shows in detail the area of the former carotid bifurcation that actually became a“neo-carotid trifurcation”.The carotid bifurcation and the suboccipital vertebral artery were approached through a single uppercervical incision, while the common carotid and the subclavian artery, through a single supraclavicularincision.REFERENCES1. Carney AA. Diagnosis and treatment of brain ischemia. In: Carney AA, Anderson EM eds. Advances in Neurology.New York, Raven Press 1981:pp 249-2822. Humphries AW, Young JR, Beven EG, Lefevre FA, Dewolfe VG. Relief of vertebrobasilar symptoms by carotidendarterectomy. Surgery 1965; 57:48-523. Vorster W, Plooy PT, Meiring JH. Abnormal origin of internal thoracic and vertebral arteries. Clin Anat 1998;11:33-374. Berguer R. Vertebral artery reconstruction for vertebrobasilar insufficiency. In Ernst CB, Stanley JC (Eds): CurrentTherapy in Vascular Surgery. Toronato BC Decker, 1987:62-655. Rohkamm R. Color Atlas of Neurology. Thieme Stuttgart, New York, 2004:10-146. Lee JH, Choi CG, Kim DK, Kim GE et al. Relationship between circle of Willis morphology on 3D time-of-flight MRangiograms and transient ischemia during vascular clamping of the internal carotid artery during carotidendarterectomy. AMNR Am J Neuroradiol 2004; 25:558-5647. Pasco A, Papon X, Bracard S et al. Persistent carotid-vertebrobasilar anastomoses. How and why differentiatingthem. J. Neuroradiol, 2004; 31:391-39671

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 728. Yilmaz E, Ilgit E, Taner D. Primitive persistent carotid-basilar and carotid vertebral anastomoses: a report of sevencases and a review of the literature. Clin Anat 1995; 8:36-469. Sunada I, Yamamoto S, Matsuoka Y, Nishimura S. Endarterectomy for persistent primitive hypoglossal artery – casereport. Neurol Med Chir (Tokyo), 1991; 31:104-10810. Woodcock RJ, Cloft HJ, Dion JE. Bilateral Type 1 proatlantal arteries with absence of vertebral arteries. AJNR Am JNeuroradiol 2001; 22:418-42011. Hutchinson NA, Miller JDR. Persistent proatlantal artery. J Neurosurg Psychiat, 1970; 33:524-52712. Jain R, Gandhi D, Gujar S, Mukehrji SK. Case 67: Persistent stapedial artery. Radiology 2004; 230:413-41613. Yilmaz T, Bilgen C, Savas R, Alper H. Persistent stapedial artery: MR angiographic and CT findings. AJNR Am JNeuroradiol 2003; 24:1133-113514. Roll JD, Urban MA, Larson TC III, Gailloud P et al. Bilateral aberrant internal carotid arteries with bilateral persistentstapedial arteries and bilateral duplicated internal carotid arteries. AJNR Am J Neuroradiol 2003; 24:762-76515. Yamada Y, Kondo A, Tanabe H. Trigeminal neuralgia associated with an anomalous artery originating from thepersistent primitive trigeminal artery. Case report. Neurol Med Chir (Tokyo) 2006; 46:194-19616. Schmahmann JD. Vascular syndromes of the thalamus. Stroke 2003; 34:2264-227817. Gao P, Chen Z, Jiao L, Ling F. The correlation of carotid plaque pathophysiologic features and neurologicalsymptoms: a meta-analysis of observational studies. Neurology India 2008; 55(2):122-12918. Clark K, Perry MO. Carotid-vertebral anastomoses. An alternative technique for repair of the subclavian stealsyndrome. Ann surg 1996; 163:414-41619. Imparato AM. Vertebral artery reconstruction: a nineteen-year experience. J Vasc Surg 1985:2:626-634 / EdwardsWH, Mulherin JL. The surgical approach to significant stenosis of vertebral and subclavian arteries. Surgery 1980;87:20-2820. Lang J, Kessler B. About the suboccipital part of the vertebral artery and the neighboring bone-joint and nerverelationships. Skull Base 1991; 1(1):64-7121. Wassermann BA, Wityk RJ, Trout HH III, Virmani R. Low-grade carotid stenosis. Looking beyong the lumen with MRI.Stroke 2005; 36:2504-251322. Takaya N, Yuan C, Chu B et al. Association between carotid plaque characteristics and subsequent ischemiccerebrovascular events: a prospective assessment with MRI – initial results. Stroke 2006; 37:818-82323. Gao P, Chen Z, Ling F. The correlation of carotid plaque pathophysiologic features and neurological symptoms: ameta-analysis of observational studies. Neurology India 2007; 55(2):122-12924. Fisher M, Paganini-Hill A, Martin A, et al. Carotid plaque pathology. Thrombosis, ulceration and strokepathogenesis. Stroke 2005; 36:253-257LIST OF TABLES TABLE 1: Patient demographics TABLE 2: Clinical presentation TABLE 3: Comorbidities TABLE 4: Arterial lesions in the case series TABLE 5: Types of anesthesia used TABLE 6: Surgical procedures72

ISSN 1583-3534, Claudia Gherman et al ■ 2009, vol. 8, no. 1-2, pp. 73-77Atherosclerosis – a multifactorial entityPlaying a role in the occurence of vascular diseasesClaudia Gherman, Laura Palcău, Ş. Rădulescu, H. Silaghi, A. MironiucSurgical Clinic No.II,"Iuliu Haţieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania,Correspondence address: Dr. Claudia Gherman, "Iuliu Haţieganu" University of Medicine and Pharmacy, Surgical ClinicNo.II, Str. Clinicilor Nr. 4-6, 400006, Cluj-Napoca, Romania, Tel/fax: 0040.264.597523, e-mail: ghermanclaudia@yahoo.comAbstractAtherosclerosis is the main pathological process that affects the arteries, being adegenerative disease characterized by the accumulation of cells and lipids in a conjunctive matrix atthe level of the arterial intima.The result of this process is the formation of arterial stenoses, whose evolution in time will leadto obstructions, embolies or thromboses of the arteries.Atherosclerotic lesions develop progressively through a succession of events which lead to theformation of atheromatous plaques with stability or instability. Atherosclerosis has proved to be theresult of a chronic inflammatory process, which, in turn, is the response to advanced endotheliallesions.Key words: atherosclerosis, chronic vascular inflammation, vascular disease1. Atherosclerosis – a multifactorial entityAtherosclerosis describes the sum of the alterations of the arterial walls, and it is characterized byendothelial dysfunction, vascular inflammation, and deposits of lipids, cholesterol, and cell degradationproducts in the intima of the arterial wall. Atherosclerosis has proved to be the result of a chronicinflammatory process, which, in turn, is the response to advanced endothelial lesions (1).Atherosclerotic lesions develop progressively through a succession of events which lead to theformation of mature lesions – i.e atheromatous plaques. The uncomplicated atheromatous plaquesexhibit four large cell types in their structure, involved in the physiopathologic process of atheromaformation: endothelial cells, smooth muscle cells, macrophages, and T lymphocytes (2).Endothelial cells produce and release numerous mediators involved in the local control andregulation of the vascular tonus, blood flow, vascular permeability, and the activity of the smoothmuscle cells, and are thus involved in the immune response (Table 1) (2). By means of cell adhesionmolecules, the endothelial cells control the cellular passage at the level of the arterial wall (3,4).Endothelial cells are also involved in coagulation, and they play a role in plaque aggregation;thus, in the case of a local thrombotic event, the endothelial cells secrete vasodilatory substances suchas prostacyline (PGI2), E2 prostaglandin (PGE2), nitric oxide (NO) and endothelium-dependent relaxingfactor (EDRF) (5).Sustaining the vascular tonus depends on the endothelial cells which secrete in equal measurevasoconstrictory and vasodilatory substances. The balance between the secretion of endothelin(vasoconstrictory factor) and NO (vasodilatory factor) is, certainly, most important. In hyperlipidemia, thealteration of vascular tonus regulation occurs together with arterial structure modification (6).Secondary to the aggression, whether mechanical or chemical, the endothelium will react by: an increase in leukocyte adhesion via intercellular adhesion molecules – i.e. ICAM-1, andvascular adhesion molecules – i.e. VCAM-1, and via an increase in E-selectins; permeability alteration; procoagulant activity; an increase in the secretion of constrictive substances, growth factors, and cytokines (7).73

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 74Table 1. Products released by endothelial cells (2)FunctionProduction of matrix componentsVascular tonus controlCell proliferation controlCoagulation controlInflammatory processes controlSecreted productsFibronectin, laminin, collagen (type I, II, III, IV), proteoglycansNO, PGI2, PGE2, the conversion enzyme of angiotensin (ECA),thromboxane (TXA2), leukotrienes, endothelin-1platelet-derived growth factor (PDGF), endothelium-derivedgrowth factor (EDGF), fibroblast growth factor (FGF), insulin-likegrowth factor 1 (IGF-1), granulocyte-monocyte colonystimulating factor (GM-CSF)Von Willebrand factor (vWF), thromboplastin, the plateletactivatingfactor (PAF), plasminogen activator inhibitor 1 and 2(PAI-1, PAI-2), high-molecular-weight kininogen (HMWK),thrombo-moduline, antithrombin III, heparan sulphate, adenosinediphosphate, tissue plasminogen activator, protein CInterleukin 1, 6, 8; leukotrienes B4, C4, D4, E4, cell adhesionmolecules (CAM), the major histocompatibility complex II (MHCII)The atherosclerotic process is a chronic, insidious one. Many theories have tried to explain theinception of the process. One of the theories is that of endothelial dysfunction.Endothelial cell dysfunction is the result of an increase in vascular permeability, increasedleukocyte adherence, and the functional imbalance of pro- and antithrombotic factors, growthmodulators and vasoactive substances. Endothelial cell dysfunction also favors the progression of theatherosclerotic process.(5,8)The leukocytes accumulated at the place of the injury release growth factors which induce themigration of vascular smooth muscle cells at an intimal level. This theory of the response to injurypostulates the fact that thrombocytes present in the damaged endothelial zone intensely secretemitogenic factors, in this way stimulating the proliferation of smooth muscle cells (9, 10, 11).This hypothesis incorporates three important processes involved in atherogenesis:1. focal intimal migration, proliferation, and accumulation of various cells, such asmacrophages and smooth muscle cells2. increased production of the extracellular matrix3. lipid aggregationThese processes are triggered at the moment when the vascular endothelium is exposed toinjury. Continuous exposure of the vascular endothelium to injury triggers a chronic focal inflammatoryresponse (8, 12) that plays a role in the progression of atherosclerotic lesions. (8, 13)Intimal hyperplasia is an element of the parietal response to any type of aggressions, andespecially secondary to local haemodynamic modifications. In the case of a venous graft model inarterial position with hypercholesterolemic animals, hyperplasia plays a permissive role in thedevelopment of atherosclerotic lesions (13).In the course of atherogenesis, the covering of the lipid and necrotic deposits with a “mantle” ofsmooth muscle cells accredits the idea according to which intimal hyperplasia may be an answer tobiochemical stimuli, to accomplish an “encystantion” of the thrombogen residue (13).The concept of plaque stability/instability suggests the fact that the development of the smoothmuscle cells in the intimal area concurs to the stabilization of the plaque and, in this manner, to adecrease in clinical events. Beside these rapports with atherogenesis, the hypertrophic growth of theintima participates in the reduction of the arterial lumen surface area, and thus in the formation ofstenoses (11, 14, 15).2. The role of atherosclerosis in the occurence of vascular diseasesAround the world, the pathology connected with atherosclerosis represents, after infectiousdiseases, the second cause for morbi-mortality. In the developed countries, it occupies first place by far,before oncological pathology and traumatic pathology. Moreover, chronic obliterative arteriopathy ofthe lower limbs, which affects 12% of the general population and 20% of the individuals over 70 years ofage, has proved to be an independent risk factor for general mortality and especially for cardiovascularmortality.The average life span of patients with aortoiliac occlusive disease is visibly diminished because ofthe evolution of the disease itself, and especially because of the complications that occured against an74

Claudia Gherman et al ■ 2009, vol. 8, no. 1-2, pp. 75atherosclerotic background with other localizations. Of these patients it is estimated that 50-55% will diedue to coronary vascular complications, and another 10-12% as a result of cerebral vascularcomplications. As a matter of fact, the survival rate 5 years after the completion of reconstructiveoperations varies between 75-87%, and between 40-64% 10 years after these operations, respectively.(Table 2)(16).Table 2. The risk of the occurence of atherosclerosis according to arterial topographyFrequentlyExceptionallyThe descending thoracic aorta (ulcerated plaque)The subrenal abdominal aorta (aneurysm)CoronaryThe vessels of the aortic treeThe carotid bifurcationThe basilar trunkRenal arteriesLower limb: iliac, superficial femoral, and popliteal arteriesDigestive arteries – less oftenUpper limbsPulmonary arteriesAtherosclerosis is the main pathological process that affects the arteries, being a degenerativedisease characterized by the accumulation of cells and lipids in a conjunctive matrix at the level of thearterial intima. The result of this process is the formation of arterial stenoses, whose evolution in time willlead to obstructions, embolies or thromboses of the arteries.Coronary localizationThe direct consequence of coronary atherothrombosis is the acute coronary syndrome. Inunstable angor, the thrombus formed in contact with the ruptured plaque may be responsible fortransitory occlusive episodes, and it explains the manifestations of rest angor.Vasomotricity anomalies frequently coexist and are favored by the release of vasoconstrictingsubstances at the level of the blood platelets.Embolic phenomena are possible during unstable angor and sometimes result in the moderateincrease of cardiac (troponin) enzymes. The occurence of a complete, permanent occlusion triggersthe occurrence of a myocardic infarction, if it is not a territory “protected” by preexistent collateralcirculation (16).Atherosclerotic touch to cerebral vesselsAtherosclerotic touch to cerebral arteries is associated with acute manifestations. The cerebralterritory is characterized by the existence of collateral networks.The erosion, rupture, and thrombosis mechanisms play an important role in the production ofacute accidents.Even if the total occlusion at the point of rupture is possible, the embolization of thromboticfragments is more frequently incriminated in the physiopathology of transitory or constituted ischemiccerebral accidents (17).The carotid atherosclerotic diseaseThe carotid atherosclerotic disease localized at the origin of the internal carotid or in the terminalportion of the common carotid is an important cause of cerebral vascular accidents. Itsacknowledgment as a cause for the neurological symptoms is very important bearing in mind that it canbe resolved by carotid thrombendarterectomy.The atheromatous plaques form especially at the level of the bifurcation of the common carotidand especially in the carotid sinus.(18)The atheromatous lesion which interests the internal carotid is, more often than not, limited to theorigin of the vessel and the carotid sinus, the common carotid proximal to the sinus and the distal internalcarotid being usually unaffected. The predilection for this area is certainly due to the flow turbulencecaused by the bifurcation and the increased diameter of the sinus (18, 19, 20).Localization at the level of the abdominal aorta and lower limb arteriesThe abdominal aorta aneurysms are in 80% of the cases secondary to the atheroscleroticprocess. The majority are asymptomatic. The symptomatology occurs at the same time as the increasein size of the aneurysm through compression on the adjacent structures.75

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 76The infrarenal aorta and the iliac arteries are the preferred localizations for the chronic occlusiveatherosclerotic disease in the case of symptomatic patients with chronic obliterative arteriopathy of thelower limbs.Critical lower limb ischemia. The main cause of critical ischemia is atherosclerosis. When theocclusion reaches the critical stenosis which can no longer be compensated for by post-stenoticvasodilation and collateral circulation (20, 21, 22).Touch to the visceral arteriesThe chronic obstructive disease of the digestive arteries is rarely diffuse. The lesions are, moreoften than not, localized in the initial section of the large vessels.The proximal localization and the slow development of the lesions allow the development of arich collateral circulation. Even the complete occlusion of the inferior mesenteric artery or celiac trunkmay not be very significant because of the development of this collateral circulation.The acute occlusion of these vessels does not benefit from compensatory mechanisms.Chronic ischemia and entero-mesenteric infarction are often the result of thrombosis on anatheromatous plaque but they may also be encountered in the case of mesenteric embolism (23).Conclusions1. Atherosclerosis still continues to be the subject of complex studies, and it has been attempted toestablish numerous interactions between the predisposing and determining factors which, actingon different histological structures of the arterial wall, interact in this fashion with each other.2. If the theory of inflammation is finally rehabilitated, the multifactorial origin of the atheroscleroticarterial affection still remains a reality and the subject of numerous studies and much researchwork.3. Atherosclerosis is the main pathological process which affects the arteries, being a degenerativedisease characterized by the accumulation of cells and lipids in a conjunctive matrix at the levelof the arterial intima, which will lead to stenoses, obstructions, embolies, or thromboses of thearteries.References1. Defraigne JO, Development of Atherosclerosis for the Vascular Surgeon In Liapis C.D, Balzer K,Benedetti-Valentini F, et al (eds); European Manual Of Medicine,Vascular Surgery; ed Springer-Verlag Berlin Heidelberg, 2007;1.2:23-342. Stary HC, Chandler AB, Glagov S. A definition of initial fatty streak and intermediate lesions ofatherosclerosis: a raport from the Committee on Vascular Lesions of the Council onAtherosclerosis, American Heart Association. Arterio Thromb 1994;14:8403. Herman AG. New insights into the etiopathogenesis of atherosclerosis and atherothrombosis. BullMem Acad R Med Belg. 2006;161(3-4):213-254. Kreienberg PB, Darling RC III, Fowkes FGR. The epidemiology and etiology of atherosclerosis InDavies AH, Brophy CM (eds) Vascular Surgery, Springer-Verlag London Limited 2006;1;11-185. Rauch U, Osende JI, et al. Thrombus formation on atherosclerotic plaques: pathogenesis andclinical consequence. Ann Intern Med 2001; 134:224-2386. Toussait J.F., Jacob M.P., Lafrost L. (eds) L’atherosclerose. Physiopathologie, diagnostics,therapeutiques. Paris,Ed. Masson,2005, pg.44-497. Tedgui A, Mallat Z. Cytokines in atherosclerosis: pathogenic and regulatory pathways. Physiol Rev,2006;86:515-5818. Allaire E. Remodelage parietal dans l’atherosclerose. In: Toussait J.F., Jacob M.P., Lafrost L. (eds)L’atherosclerose. Physiopathologie, diagnostics, therapeutiques. Paris,Ed. Masson,20059. Shimzu K., Suguyama S., Aikawa M. et al. Host bone-marrow cells are a source of donor intimalsmooth-muscle-like cells in murine aortic transplant arteriopathy. Nat Med, 2001;7:738-74110. Mizerska M, Goch JH. [Etiopathogenesis of atherosclerosis - a clinical problem that is still relevant].Pol Merkur Lekarski. 2006 Feb;20(116):133-876

Claudia Gherman et al ■ 2009, vol. 8, no. 1-2, pp. 7711. Travis J.A., Hughes M.G., Wong J.M. et al. Hyaluronan enhances contraction of collagen bysmooth muscle cells and adventitial fibroblasts: Role of CD44 and implications for constrictiveremodeling. Circ Res, 2001; 88:77-8312. Davies M.G., Owens E.L., Mason D.P. et al. Effect of platelet-derived growth factor receptor-alphaand –beta blockade on flow-induced neointimal formation in endothelialized baloon vasculargrafts. Circ Res, 2000; 86:779078613. Feldman L.J., Aguirre L., Ziol M et al. Interleukin-10 inhibits intimal hyperplasia after angioplasty orstent implantation in hypercolesterolemic rabbits. Circulation, 2000;101:908-91614. Ward M.R., Pasterkamp G., Yeung A.C., Borst C. Arterial remodeling. Mechanisms and clinicalimplications. Circulation, 2000; 102:1186-119115. Durand E., Addad F., Boulanger C. et al. Facteurs predictifs mecaniques et fonctionnels de larestenose et du remodelage arteriel apres angioplastie experimentale. Arch Mal Coeur Vaiss,2001; 94:605-61116. Thammat O. Atherosclerose, hypertension, thrombose. Module 9. Med-Line Editions, 200317. Cândea V., Vasilescu A. Ischemia vertebro-bazilară. In: Cândea V. Chirurgie Vasculară. Bolilearterelor. Ed. Tehnică, Bucureşti, 200118. Băila S., Moldovan H., Vasile R., Rădulescu B. Boala carotidiană aterosclerotică. In: Cândea V.Chirurgie Vasculară. Bolile arterelor. Ed. Tehnică, Bucureşti, 200119. Furtado AD, Adraktas DD, Brasic N, Cheng SC, Ordovas K, Smith WS, Lewin MR, Chun K, Chien JD,Schaeffer S, Wintermark M. The Triple Rule-Out for Acute Ischemic Stroke: Imaging the Brain,Carotid Arteries, Aorta, and Heart. AJNR Am J Neuroradiol. 2010 Apr 1.20. Bugnicourt JM, Chillon JM, Tribouilloy C, Canaple S, Lamy C, Massy ZA, Godefroy O. Relationbetween intracranial artery calcifications and aortic atherosclerosis in ischemic stroke patients. JNeurol. 2010 Mar 31.21. Bărzoi D.F., Diaconescu I. Ischemia acută a membrelor. In: Cândea V. Chirurgie Vasculară. Bolilearterelor. Ed. Tehnică, Bucureşti, 200122. Ferreira AC, Macedo FY. A review of simple, non-invasive means of assessing peripheral arterialdisease and implications for medical management. Ann Med. 2010 Mar; 42(2):139-5023. Cândea V., Băila S. Patologia arterelor digestive abdominale. In: Cândea V. Chirurgie Vasculară.Bolile arterelor. Ed. Tehnică, Bucureşti, 200177

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ISSN 1583-3534, Ionel Droc et al ■ 2009, vol. 8, no. 1-2, pp. 79-82Ruptured popliteal artery aneurysm. Case reportIonel Droc, Murgu V., Francisca Blanca Calinescu,Stefan Diaconu, Popescu Carmen, Chiriac LiviuArmy’s Center For Cardiovascular Diseases, Bucharest RomaniaWe present a case of a popliteal artery aneurysm in a 55 years old male, who presented withright thigh and popliteal region pain, and a pulsatile mass in the popliteal fossa. Angiography andangio CT revealed a popliteal artery aneurysm, which was subsequently resected and bypassed. Thepopliteal vein was found thrombosed and the long saphenous vein was therefore sparedPopliteal aneurysms are the most frequent aneurysms found in the lower limbs. They are found inabout 1% of the adult population and are infrequent in females. They are associated with the presenceof contralateral aneurysm in 30-50% of cases and with abdominal aortic aneurysms in 30-60%. Their maincomplication is arterial ischemia secondary to the thrombosis of the aneurysm, although it can also bepresented in the form of compression symptoms or distal embolization. Spontaneous rupture is anuncommon complication and it is associated with arterial diameters of > 4 cm. The amputation rateassociated with ruptured popliteal aneurysms is 25% [1].Case reportA 55-years old male patient presented to our department complaining of pain and swelling inthe right popliteal fossa. The medical history revealed a prior left femoro- tibial by-pass using theipsilateral long saphenous vein (LSV), intervention made for multiple aneurysms along the superficialfemoral and popliteal artery, which caused ischemic symptoms due to distal embolization. He alsounderwent PTA for a right external iliac critical stenosis in february 2010.The physical examination showed inflammation in the popliteal fossa with a pulsatile masscausing considerable increase in its diameter. All peripheral pulses were palpable.Fig. 1: Ruptured popliteal aneurysm clinical presentationUrgent duplex scanning was performed, showing a giant 8,5/12,5 cm, partially thrombosedaneurysm of the right popliteal artery.We performed an angiography that confirmed the diagnosis of true popliteal artery aneurysm,revealing also an infra-renal abdominal aortic aneurysm with a diameter of 4,3 cm and several othersmaller aneurysms along the hypogastric arteries.79

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 80Fig. 2a) arteriography of the aneurysm before rupture b) hypogastric artery aneurysmThree days after his admission the patient reported sudden pain in the popliteal fossa with anincrease of the limb diameter. An emergency CT-angiography was performed, which confirmed therupture of the popliteal aneurysm.Fig. 3: CT-angiography image of the rupturedpopliteal aneurysm, and abdominal aorta aneurysmUrgent surgical intervention consisting offemoro-popliteal by-pass and aneurysm excision wasdecided upon.At the time of the operation, dissectionposterior to the aneurysm revealed an adherent,thrombosed popliteal vein. As it was likely that longsaphenous vein (LSV) was now a significant channelfor venous return, it was not used for bypass. Instead abelow-knee femoro-popliteal bypass was performedusing a polytetrafluoroethylene (PTFE) prosthesis.Because of its massive size and the initial dissectionneeded for distal control, we resected the aneurysmcompletely.Fig. 4: Intraoperatory aspect of the aneurysm before excision80

Ionel Droc et al ■ 2009, vol. 8, no. 1-2, pp. 81Fig. 5: Aspect of the evacuated thrombusFig. 6: Intraoperatory aspect of the opened andevacuated aneurysmFig. 7: Distal anasthomosis of the PTFE graftThe patient had an uneventful postoperativecourse, apart from a mild oedema, and regainedambulatory function of the extremity. The controlduplex scanning reported good patency of thegraft. The patient was discharged from the hospitalwith antithrombotic and antibiotic treatment(ciprofloxacin) for 2 weeks. He was also included ina follow-up program to assess the development ofthe 4.3 cm abdominal aoric aneurysm, and themultiple, bilateral, small hypogastric arteryaneurysms. The follow-up of the revascularizationtechnique (1 month, 6 months and then annually) through duplex scanning is important, not only for theearly detection of potential graft problems, but also to verify the complete exclusion of the aneurysmand to avoid potential problems related to leakages [1].DiscussionAfter the aortoiliac system, the popliteal artery is the most common site of aneurysm formation.The ratio of popliteal to aortic aneurysms is estimated to be 1:10 to 1:20, and 5% to 10% of those withaortic aneurysms have popliteal aneurysms. Associated aneurysms are common.Approximately 50% ofpatients have bilateral popliteal aneurysms, one third have aotic aneurysms, and one fourth havefemoral aneurysms. The incidence of extrapopliteal aneurysms is highest among those with bilateralpopliteal aneurysms; up to 78% os such patients have aortic aneurysms. These patients continue todevelop other, remote aneurysms, and new aneurysms have been documented in 6% of treatedpatients at 1 year and 49% at 10 years, illustrating the need for lifelong surveillance.Popliteal aneurysms classically manifest in several ways. In about one half of affected patients,they manifest with limb ischemia from thrombosis (around 32%) or embolization (around 20%).Approximately 37% of the aneurysms are asymptomatic and are detected by palpation orultrasonographic examination. Popliteal aneurysms can also manifest with symptoms from compressionof adjacent structures (around 10%), notably nerve (causing paresthesias or other deficits) or vein(leading to deep venous thrombosis). By contrast rupture is rare, with an overall incidence of 2.1%.Unfortunately, no reports describing rupture documents the size of the aneurysm. It may be thatthe relatively tigh bony and musculofascial relations of the popliteal artery offer some degree ofprotection [2].81

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 82ConclusionsPopliteal artery aneurysms are limb threatening because of their potential to cause embolism,thrombosis, and, uncommonly, rupture. Their timely diagnosis before complications is a relevent clinicalissue. For instance, elective repair of a popliteal aneurysm results in substantially better outcomes thanrevascularization for acute aneurysmal thrombosis or delayed revascularization for chronic limb ischemiaresulting from repeated subclinical embolism.Ultrasonography or CT angiography are the radiological investigations of choice. A CTangiography is still the gold standard test for diagnosing ruptured popliteal aneurysms. It isrecommended to perform a preoperative arteriogram to assess the run-off and rule out distalembolization [1].When contemplating exclusion bypass for such operations, it would be useful to have anultrasound scan of the venous system to allow appropriate preoperative planning in term of conduitformation [3].The 14% incidence of popliteal artery aneurysm among men with aortic aneurysm suggests thatroutine Doppler ultrasound scanning should be considered as a screening test in male patient with AAA.The etiology of femoral and popliteal aneurysms probably involves the interaction of a geneticalteration that predisposes to the loss of the arterial wall integrity following local forces such as repeatedflexion of the arteries at the hip and knee.The familial as well as genetic basis of these lesions remain unresolved at the present time [2].Definition of the genetic basis for aneurysms, aortic or peripheral, will hopefully be aided by thecomplete mapping of the human genome, which will form the basis for determining if gene functionsexists that interact to produce these diseases.Unfortunately, the clinical relevance ot these lower extremity aneurysms discovered inassociation with AAAs is ill defined at present, and there remains a need for a prospective natural hystorystudy to establish their actual significance [4].References1. A. Ysa, M.R. Bustabad, A Arruabarrena, E. Perez. Rupture of an infected popliteal aneurysm. Casereport and review of the literature EJVES 2007; 14:39-442. Karl A. Illig, Matthew J. Eagleton, Cynthia K. Shortell, Kenneth Ouriel. Ruptured popliteal arteryaneurysm J Vasc Surg1998; 27-4:783-7863. A Chaudhuri, M.P. Armon Occult deep vein thrombosis due to a superficial femoral artery aneurysm: Acase report EJVES 2006; 11; 40-414. Aparna Diwan, Rajabrata Sakar, James C. Stanley Incidence of femoral and popliteal arteryaneurysms in patients with abdominal aortic aneurysms. J Vasc. Surg. 2002; 31-5:863-86982

ISSN 1583-3534, I. Cordos et al ■ 2009, vol. 8, no. 1-2, pp. 83-88Right pneumonectomy with superior vena cava resection andreconstruction with PTFE vascular prosthesis – case reportI. Cordos, R. Matache, M. Codresi, A. Istrate"Cornel Carpinişanu" Thoracic Surgery Clinic, “Marius Nasta” National Pneumology Institute BucharestAbstractPurpose: Superior vena cava (SVC) system invasion by lung and mediastinal malignancies haslong been considered a contraindication for surgical resection. We present two case report of a 49 yrsold patient and a 45 yrs old patient, both with non-small cell lung cancer, invading vena cava superior(T4). On CT scan was identified a neoplastic thrombus in vena cava, right before flowing into theatrium.Materials and methods: We performed a right pneumonectomy and a superior bilobectomywith vena cava resection in the invaded area, followed by reconstruction with PTFE vascularprosthesis. Limfadenectomy was also performed.Results: First case died in hospital 4 th day after the operation, with neurological complication,mechanical ventilation more than 48 hours and multisystem failure. The procedure went withoutincident in second case, in the end, the thrombus was removed inside the resected part of the venacava, with right lung. Postoperative, the patient went well, without developing any complications, andhe was discharged in the 7 th day after surgery.Conclusions: In particular cases, the resection and reconstruction with prosthesis of the greatvessels invaded by cancer can and must be performed and may achieve permanent cure in patientswho would have been defined as inoperable until now.Key words: PTFE prosthesis, cava, lung resectionIntroductionBronchogenic carcinoma can involve the superior vena cava by direct extension of the primarytumor or by nodal metastasis. The stage T4 is defined as a tumour with any of invasion of themediastinum, heart, great vessels, trachea, oesophagus, vertebra, or carina or separate tumour nodulesin the same lobe, or malignant pleural effusion. There are two possible techniques for resecting thesuperior vena cava. It may be performed en bloc with the pulmonary resection. For minimalinvolvement, a side-biting clamp can be applied and the vena cava simply oversewn or patched if thelumen is compromised. Patches can include Gore-Tex or pericardium. For full reconstruction, thepreferable method is a ringed Gore-Tex sleeve patch as outlined by Dartevelle and colleagues. In 1987,Dartevelle and colleagues first reported a technique of caval reconstruction using Gore-Tex grafts [1].Superior vena cava (SVC) system invasion by lung and mediastinal malignancies has long beenconsidered a contraindication for surgical resection [2]. The oncologic value of superior vena cava(SVC) resection for lung and mediastinal malignancies remains controversial. Concerning lung cancer, amulticentric international study reports a risk of developing postoperative complications and mortality of30% and 12%, respectively, with a 5-year probability of survival of 21%. The same study, analyzing theresults between 1996-2006, demonstrated an improvement of the outcome with a 6% of postoperativemortality, with a 5-year probability of survival of 28% [3].In the case of lung tumors, infiltration of SVC can achieve satisfactory long-term results afterneoadjuvant chemotherapy, only when pathologic N2 disease is excluded by preoperativemediastinoscopy. A study from 1998 to 2004 on 70 consecutive patients (52 with lung cancer and 18 withmediastinal tumors) underwent SVC system resection. In a study, there were 25 replacements (36%) of83

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 84the SVC system by prosthesis, whereas the remaining underwent partial resection. Major postoperativemorbidity and mortality rates in lung cancer patients were 23% and 7.7%, respectively (50% and 5.6% inmediastinal tumors). In the lung cancer group, 5-year survival probability was 31%, and it was affectedby mediastinal nodal status (5-year survival in N0–N1 patients 52%, 21% in N2 patients, 0 in N3 patients)[4]. The caval reconstruction requires great technical expertise and, although it likely adds significantprocedural time, the long-term survival and patency of SVC prosthetic reconstruction appears toexceed the related morbidity and operative mortality. This has recently been pointed out by Yildizelyand Dartevelle [5] in their report of 39 patients with non-small-cell lung carcinoma invading the SVC:median survival time was 19 months, and the actuarial 5- and 10-year survivals were 29.4% and 22.1%,respectively, with a 7.7% early mortality (related to right pneumonectomy) [6]. Surgery for T4 NSCLC maybe effective in those patients without mediastinal (N2) lymph node involvement.The poor prognosis of locally advanced lung cancer treated by radiotherapy (5-year survival 5%),or chemo radiotherapy (5-year survival 5% to 17%), the improvement of both technical devices andsurgical experience have renewed the interest in the use of SVC resection. In the last two decades,several series of SVC resections have been published, confirming feasibility and reporting long-termsurvival data [4]. In a study from 1988 to 2002, Politi L. et al. performed 37 SVC resections: 21replacements with polytetrafluoroethylene (PTFE) prostheses and 16 tangential exereses. The mainindication for a prosthetic replacement was infiltration of more than 30% of the circumference of theSVC. There were 4 thromboembolic complications (19%), with one intraoperative death (4.8%).Tangential resection of the SVC for infiltration

I. Cordos et al ■ 2009, vol. 8, no. 1-2, pp. 85Postoperatively, in patients with PTFE prosthesis, anticoagulation therapy was continued usinglow-molecular-weight heparin and maintained afterward with oral anticoagulants. Some studies testedthe hypothesis that PTFE replacement may interfere with perioperative outcomeCase No 1First case was M.N., male, 45 years old, with no significant cardiopulmonary references, heavysmoker (50 AP), that in the past 3 months developed moderate dyspnea, dry cough, weight loss (at least7 kg/1 month, BMI = 17.11), nocturnal sweating, recurrent headache, and about 2 weeks he becamedysphonic. At admission in our Clinic he was balanced hemodynamic and respiratory, with no particularaspects at the clinical examination. Biologic: non-specific inflammatory syndrome, mild anemicsyndrome. EKG: right atrium overload, sinusal tachycardia (over 110/min). Spirometry shows ventilatordysfunction of both components (restrictive and obstructive) FEV1 = 2 L (62%), FVC = 2.76 L (66.7%), FEV1/FVC = 63.2%. Chest X-ray shows: macro nodular opacity, round, 6/5 cm, with irregular borders, in theright hillumFigure 2: Frontal chest radiography showing in the right hillum a round-shaped opacity (the tumor)Figure 3: The same patient, but in sagital view, a chest x-ray indicating the pulmonary tumor in the rightupper lobe85

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 86Bronchoscopy: small tumor on right vocal chord; no tumoral invasion in the explored area. Onthe right side is identified an anatomical variation: two orifices of the right upper bronchia. Extrinsiccompression on ventral segmental bronchia.Computer tomography: Right upper lobe pulmonary tumor in the anterior segment, invadingsuperior vena cava and superior pulmonary vein, about 6/5 cm, at 2,4 cm from carinaFigure 4: Computed tomography: Right upper lobe pulmonary tumor invading superior vena cava,superior pulmonary veinFigure 5: Intraoperative aspect of the tumorinvading superior vena cavaIn this case the only surgicaloption remains upper bilobectomy withresection of the superior vena cava.The risks and the benefits of thisoperation are accurately explained tothe patient, and his decision is to chosethe surgical path.Intraoperative, the diagnosis isconfirmed: right upper lobe pulmonarytumor invading superior vena cava andsuperior pulmonary vein. First step wasto perform bilobectomy (anatomicalvariation: two right upper lobar bronchi)and leave on SVC a small tumor. Thenwe performed superior vena cavaresection in this area (from the junctionbetween the two brachiocephalictrunks, to the flowing of the SVC into theright atrium).After that, the reconstruction with PTFE prosthesis is feasible. Limfadenectomy is also performed(right laterotracheal superior and inferior, infracarinar, hillar).Postoperative evolution was complicated by the installation of a large left parieto-occipitalstroke (possible tumoral embolectomy). In the second day after the surgery, appears acute ischemia ofthe left limb, that requires immediate desobstruction with Fogarty catheter of the femoral artery, andfasciotomy for reperfusion edema. The evolution of the stroke is still unfavorable, despite maximalanticoagulant and antibiotic treatment, or mechanical ventilation. In the 2nd and 3rd day after thesurgery, the patient suffers few episodes of ventricular arrhythmia, that disappear spontaneous. Theevolution is complicated with multiple systemic organ failure, and death in the 3rd day after theoperation.86

I. Cordos et al ■ 2009, vol. 8, no. 1-2, pp. 87Figure 6: After the removal of the tumor with the invaded region of the superior vena cava, PTFEprosthesis is placed. The pulmonary right lower lobe is preserved.Case No 2The second case is M.D., male, 48 years old, smoker(aprox. 30 AP), known with an operation for a herniatedlombar disc, which presents for two months moderatedyspnea, productive cough, fever and fatigue. Recently, hereports minor haemoptysis. At hospitalization, clinicalexamination distinguishes diminished vesicular murmur, roughrales in the right side of the thorax, well-balancedhaemodynamic and respiratory, no other pathologicobservations.Biologic: leukocytosis (16200/mms) and high values ofthe inflammatory markers.Spirometry: moderate restrictive ventilator dysfunction [FVC =2.48 L (57,4%), FEV1=2.01 L (59,1%)].Bronhoscopy: right main bronchus formed by 3cartilages, with normal aspect. Ventral segmentary bronchiblocked by tumoral process. Bronchial biopsy: epidermoidcarcinoma.Figure 7: Chest X-ray: The right upper lobe pulmonary tumor is excavated (tumor necrosis)Computer tomography: Right upperlobe pulmonary tumor invading the interlobarfissure, 6/5.5 cm, with necrotic aspect.Mediastinal adenopathies. Minimal rightpleuresia.Figure 8: Normal aspect in postoperativeperiod after right pneumonectomy87

Romanian Journal of Cardiovascular Surgery ■ 2009, vol. 8, no. 1-2, pp. 88Following investigations, we decided surgical treatment. Intraoperative, the lung tumor isconfirmed in the right upper lobe, crossing into inferior lobe, and invading superior vena cava. Weperformed right pneumonectomy with resection of the superior vena cava and reconstruction with PTFEprosthesis. This time, the lung was removed in block with the invaded portion of the SVC.Limfadenectomy was also performed, from the laterotracheal inferior and superior, infracarinar,periesophageal, triangular ligament and hillar nodes.Postoperative evolution was favorable, after the establishment of anticoagulant therapy, andthe early suppression of the drainage. The patient followed at home the anticoagulant therapyaccording the recommendations.ConclusionsInfiltration of the superior vena cava (SVC) due to advanced non small cell lung cancer (NSCLC)can be treated by prosthetic replacement or tangential resection. The absence of suitable prostheticmaterial for SVC replacement, the technical incertitude concerning the effect of SVC clamping, the fearof graft thrombosis and infection after pulmonary resection, and finally, the oncologic prognosis afterinitial SVC resection experiences have limited its diffusion as a surgical treatment. Our limited experienceoffers no statistical data until this moment. This procedure still remains a challenge for many of theRomanian Thoracic Surgery Units. These two cases offer us the possibility to change the approachregarding the surgical treatment of a lung non-small cancer invading the superior vena cava. SVCtangential resection involves fewer surgical problems. SVC replacement associated with pulmonaryresection can be performed in selected cases. It should not be considered as palliative treatmentbecause of the important perioperative risks.Bibliography[1] Al. Patterson, F. G. Pearson, J.D. Cooper - Pearson's Thoracic & Esophageal Surgery – chapter 132[2] F. Venuta, E.A. Rendina and G. Furio Coloni - Lung resections combined with vena cava replacement- MMCTS (May 12, 2006). doi:10.1510/mmcts.2004.000 141[3] L. Spaggiari, F. Petrella, F. Leo - Superior vena cava resection for lung and mediastinal malignancies -MMCTS (October 9, 2006). doi:10.1510/mmcts.2005.001511[4] L. Spaggiari, F. Leo, G. Veronesi - Superior Vena Cava Resection for Lung and MediastinalMalignancies: A Single-Center Experience with 70 Cases - Ann Thorac Surg 2007; 83:223-230.[5] B. Yildizeli, et al. - Results of primary surgery with T4 non-small cell lung cancer over a 25 year period ina single center: the benefit is worth the risk - Ann Thorac Surg. 2008; 86:1065–1075[6] Th. W. Shields, J. LoCicero III, C. E. Reed, R. H. Feins - The Use of Prosthetic Grafts to Replace theSuperior Vena Cava (Ch. 179) – General Thoracic Surgery 7th edition 978-0-7817-7982-1[7] L. Politi, C. Crisci, F. Montinaro - Prosthetic replacement and tangential resection of the superior venacava in chest tumors - J Cardiovasc Surg (Torino). 2007 Jun; 48(3):363-8.[8] N. Halkic, L. Henchoz, D. Gintzburger - Superior vena cava syndrome caused by invasive epidermoidcarcinoma - The Journal of Cardiovascular Surgery 2000 June; 41(3):499-501[9] C. Lequaglie, B. Conti, P.P. Brega-Massone - The difficult approach to neoplastic superior vena cavasyndrome: surgical option - The Journal of Cardiovascular Surgery 2003 October; 44(5):667-71[10] S. Yamamoto, T. Shirakusa, K. Kawahara - Resection and prosthetic reconstruction of superior venacava for non-small cell advanced lung cancer patients - Chirurgia 2008 February; 21(1):1-4[11] M. Lucchi, A. Viti, F. Melfi - IIIB-T4 non-small cell lung cancer: indications and results of surgicaltreatment - The Journal of Cardiovascular Surgery 2007 June; 48(3):369-7488

The 5-th Romanian National Congress of Cardiovascular Surgerywith international participationSIBIU, ROMANIA, 30 Septembrie – 2 Octombrie, 2010Dear Colleagues,The Romanian Cardiovascular Surgery Society (RSCVS) has the honor and pleasure toinvite you to the 5th National Congress of Cardiovascular Surgery. The event will take placebetween September 30 to October 2, 2010, at Hotel Hilton Palace in Sibiu. As usual, we will have asguests a number of distinguished colleagues from abroad, who will present lectures on varioustopics, which we hope will be both useful and pleasant. Along with them, dear guest, we kindlyhope, that you will also share your personal experience during this conference.The main topic of the conference is:Progress in cardio-thoracic and vascular surgeryTogether with the Organizing Committee we hope that you will honour us with yourpresence and we assure you of our consideration.For further details about abstracts policy,deadlines, fees and accommodation, please visit us on: www.event-consulting.ro89Looking forward to meeting youMircea Birsan MD, PhDRSCVS’s President

R.S.C.V.S EXECUTIVE COMMITTEE President Prof. Mircea BârsanElected president Prof. Vlad IliescuFormer President Prof. Radu DeacVice President Prof. Marian GasparProf. Grigore TinicaTreausurer Dr. Horatiu SuciuGeneral Secretary Dr. Ionel DrocDr. Adrian MolnarLocal Organizing CommitteeCol dr. Ioan Barb - Military Hospital SibiuProf. Dr. Ioan Manitiu - Sibiu Clinical Hospital,Department of Cardiology“Lucian Blaga” University – “Victor Papilian”Medical SchoolConference Secretary: +004. 0264-591531Dr. Ioan MureşanDr. Irina NicaDr. Cosmin OlariuDr. Sigismund PappDr. Diana SacuiScientific CommitteeProf. Dr. Mircea BârsanProf. Dr. Aurel AndercouProf. Dr. Radu DeacProf. Dr. Marian GaşparProf. Dr. Vlad IliescuProf. Dr. Ioan SocoteanuProf. Dr. Grigore TinicăDr. Traian ScridonDr. Horaţiu MoldovanDr. Mircea PătruţDr. Adrian MolnarDr. Horaţiu SuciuDr. Ionel DrocDr. Viorel GoleanuDr. Marina PacescuHotel Hilton Palace, Sibiu, RomaniaOrganizing AgencyEVENT CONSULTINGB-dul 21 Decembrie 1989, Nr.108,cod 400124 Cluj-Napoca,Telefon: + 264-55-11-75Fax: + 264-55-11-85E-mail: office@event-consulting.ro90