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Vol. 2, Issue 2 (2013)

Blood Levels Dynamics of Aldosterone, Marker of Heart Failure NT-proBNP, a Proinflammatory Cytokine TNFα, and Apoptosis Inducer FAS-ligand Under the Influence of Enalapril With Candesartan in Patients With Decompensated Chronic Pulmonary Heart Disease

Author(s):
Vitaliy Seredyuk
Abstract:
The aim of our research was to investigate the effects of prolonged use of angiotensin converting enzyme (ACE) inhibitor enalapril and an angiotensin II receptor blocker (ARB) candesartan on the blood levels of aldosterone, N-terminal fragment of brain natriuretic peptide (NT-proBNP), tumor necrotic factor-α (TNF-α) and apoptosis inducer Fas-Ligand (FasL) in patients with decompensated chronic pulmonary heart disease (CPHD). 74 patients (11 women and 63 men) with decompensated CPHD with heart failure (HF) NYHA Class III were examined. Their average age was (62,8 ± 3,7) years. The patients were randomized into two clinical groups: the first (main) group consisted of 39 patients which additionally received the ARB candesartan (candesartan, "Ranbaxy", India-USA-Canada) and the second (control) group consisted of 35 patients which received only a basic therapy and ACE inhibitor enalapril. An increase in blood levels of aldosterone, marker of HF NT-proBNP, a proinflammatory cytokine TNF-α, and apoptosis inducer  Fas-Ligand is marked in patients with decompensated CPHD with HF NYHA Class III, in comparison with healthy individuals. The combined use of ACE inhibitor enalapril and the angiotensin II receptor blocker candesartan within 6 months promotes blood levels reduction of aldosterone, NT-proBNP, TNF-α, and FasL, that leads to the delay of HF progression in patients with decompensated CPHD.
Pages: 78-85  |  1085 Views  6 Downloads
How to cite this article:
Vitaliy Seredyuk. Blood Levels Dynamics of Aldosterone, Marker of Heart Failure NT-proBNP, a Proinflammatory Cytokine TNFα, and Apoptosis Inducer FAS-ligand Under the Influence of Enalapril With Candesartan in Patients With Decompensated Chronic Pulmonary Heart Disease. Pharma Innovation 2013;2(2):78-85.
The Pharma Innovation Journal