Farm Przegl Nauk, 2010,7, 10-14Risk factors of adverse cardiac eventsin patients with chronic systolic heart failureCzynniki ryzyka niekorzystnych zdarzeń sercowychu chorych z przewlekłą skurczową niewydolnością sercaAleksander Owczarek 1 , Bożena Szyguła-Jurkiewicz 2 , Krzysztof Helewski 3 ,Karolina Klimaszewska 4 , Romuald Wojnicz 31Division of Statistics in Sosnowiec, Medical University of Silesia, Katowice, Poland2III Department of Cardiology in Zabrze, Medical University of Silesia, Katowice, Poland3Department of Histology & Cardiology in Zabrze, Medical University of Silesia, Katowice, Poland4Student Scientific Society, III Department of Cardiology in Zabrze, Medical University of Silesia, Katowice, PolandAbstractChronic heart failure (HF) is an arising important medicalproblem. Apart from neuroendocrine system activation,it is also characterized by an inflammatory component.Pro-inflammatory cytokines exacerbate haemodynamicabnormalities, exert direct toxic effects on the heart andcontribute to cachexia. A prospective study has been accomplishedin the group of 164 patients with stable systolicheart failure in order to investigate the association betweenhypercoagulability, inflammation, NT-pro BNP and theclinical outcome. Major adverse cardiac event (MACE)experienced 43.3% of patients. Independent inflammatoryrelatedrisk factors of MACE in patients with HF are plasmalevels of: high sensitivity C-reactive protein, fibrinogen,D-dimers and NT-pro BNP.Key words: high sensitivity C-reactive protein, heart failure,risk factors, MACEStreszczeniePrzewlekła niewydolność serca (HF) stanowi istotny problemmedyczny. Oprócz aktywacji układu współczulnego,niewydolność serca charakteryzuje się również zwiększonąaktywnością układu odpornościowego. Krążące wekrwi cytokiny prozapalne nasilają zaburzenia hemodynamiczne,wywierają bezpośredni toksyczny wpływ na sercei wtórnie przyczyniają się do wyniszczenia organizmupacjenta. W celu oceny związku między czynnikami odzwierciedlającymiaktywność układu immunologicznego,krzepnięcia oraz NT-pro BNP a rokowaniem odległym,przeprowadzono badanie prospektywne w grupie 164pacjentów ze stabilną skurczową niewydolnością serca.U 43.3% pacjentów wystąpiło niekorzystne zdarzeniesercowe (MACE). Niezależnymi czynnikami związanymize zwiększonym ryzykiem wystąpienia MACEu tych chorych okazały się stężenia w surowicy: białkaC-reaktywnego wysokiej czułości, fibrynogenu,D-dimerów i NT-pro BNP.Słowa kluczowe: białko C-reaktywne wysokiej czułości,niewydolność serca, czynniki ryzyka, niekorzystne zdarzeniesercowo-naczyniowe (MACE)IntroductionCardiovascular diseases are the leading cause of morbidity,disability and premature mortality in developedcountries. Chronic heart failure (HF) is an arising importantmedical problem. It accounts for at least 5% of admissionsto general medical and geriatric wards and for almost 2% ofthe total healthcare expenditure (dependent on the country)[1]. It has been estimated that only in Europe HF affects 10million people [2]. Most common causes of HF are: coronaryartery disease leading to myocardial infarction (systolicdysfunction), hypertension and valvular heart disease, infections,‘idiopathic’ dilated and alcoholic cardiomyopathy[3].Heart failure is a clinical syndrome resulting from astructural and functional cardiac disorder. It impairs the abilityof the ventricle to fill with or eject blood according tothe needs of the body, or precludes it from doing so in theabsence of increased filling pressures. It is a multisystemdisorder which is characterized by abnormalities of cardiac,skeletal muscles as well as renal function, stimulation ofthe sympathetic nervous system and a complex pattern ofneurohormonal changes [4]. Figure 1 presents the overviewof main pathophysiology pathways in HF. As heart failureadvances there is a relative decline in the counter regulatoryeffects of endogenous vasodilators such as: nitric oxide,prostaglandin, bradykinin, atrial and brain natriureticpeptides (ANP, BNP). Other factors that play a role in thepathogenesis of HF include: the endothelin and adenosinereceptor systems, vasopressin, pro-inflammatory cytokines10
copyright © 2010 Grupa dr. A. R. Kwiecińskiego ISSN 1425-5073(mainly: tumour necrosis factor alpha TNF-α, C-reactiveprotein CRP, interleukin IL-1 and IL-6) [3, 5].Apart from neuroendocrine system activation, heart failureis characterized by an inflammatory component. Themechanisms of inflammation play an important role in theprocess of left ventricular remodelling including structuraland functional changes of the myocardium which are notonly in part responsible for the development of symptomsbut also for the disease progression. Pro-inflammatory cytokinesexacerbate haemodynamic abnormalities, exert directtoxic effects on the heart and contribute to cachexia [6].Also, it has been reported that inflammation is strictly correlatedwith clotting activation which has clinical relevanceto HF [7].The aim of this study was to investigate the associationbetween hypercoagulability, inflammation, NT-pro BNPand the clinical outcome – MACE (rehospitalisation, death,heart transplantation), in patients with chronic systolic heartfailure.Materials and methodsA prospective study has been accomplished in the groupof 164 patients (mostly man – 83.54%) with stable systolicheart failure, selected according to criteria of inclusionand exclusion. According to the European Guidelines forheart failure management, all patients – at least during threemonths before hospital admission, were treated with angiotensineconverting enzyme inhibitor (Captopril) or angiotensinereceptor antagonist (ARA), β‐blocker (metoprololCR or carvedilol) in maximal tolerated doses and with patientfitted doses of digoxine, spironolactone and furosemide[8]. The study protocol was accepted by the Bioethical Committeeof Silesian Medical University in Katowice: NN-043-10/95 and NN-6501-158/I/06/07; the patients gave theirconscious consent to participate in the study.Inclusion criteria:stable systolic heart failure – increased left ventricularend–diastolic diameter LVEDd>57mm and reduced leftventricular ejection fraction LVEF
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