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Pokaż cały numer - FPN - Farmaceutyczny Przegląd Naukowy

Pokaż cały numer - FPN - Farmaceutyczny Przegląd Naukowy

Pokaż cały numer - FPN - Farmaceutyczny Przegląd Naukowy

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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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