Document Detail


Neurohormonal activation and congestive heart failure: today's experience with ACE inhibitors and rationale for their use.
MedLine Citation:
PMID:  8682064     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Treatment with angiotensin converting enzyme (ACE) inhibitors delays deterioration and improves survival in chronic congestive heart failure and left ventricular dysfunction. In two large placebo-controlled trials with survivors of acute myocardial infarction, but with left ventricular dysfunction, mortality was significantly lower in the ACE inhibitor arms, with risk reductions of 19% (with captopril) and 27% (with ramipril). A study of left ventricular dysfunction in more than 4000 patients resulted in significantly fewer myocardial infarctions among patients given enalapril than in those receiving placebo; the risk reduction was 24%. Knowledge of the degree of neurohormonal activation in patients with congestive heart failure (New York Heart Association [NYHA] Functional Class II-III) appears to be of major importance in determining the efficacy of ACE inhibition. Patients with plasma concentrations above normal show the greatest increase in survival when treated with ACE inhibitors compared to similarly treated patients with low or normal neurohormonal plasma levels as well as those treated with placebo or direct-acting vasodilators. In a study of 239 patients with NYHA Class IV heart failure, randomized to receive enalapril or placebo, mortality was significantly reduced in patients receiving enalapril who had plasma noradrenaline, adrenaline, angiotensin II, aldosterone, or atrial natriuretic peptide levels above median values. No significant differences in survival between groups were found in patients with hormone levels below the median. A study in 804 men with congestive heart failure who received either enalapril or hydralazine plus isosorbide dinitrate showed the greatest reduction in mortality after 2 years in enalapril treated patients with plasma noradrenaline levels > 900 pg.ml-1 or plasma renin levels > 16 ng.ml-1.h-1. These results indicate that the main rationale for ACE inhibition in chronic congestive heart failure, in left ventricular dysfunction, and after myocardial infarction is the modulation of prolonged neurohormonal activation. Knowledge of this effect may provide the means to forestall disease progression and thus offer long-term treatment benefits.
Authors:
A Sigurdsson; K Swedberg
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  European heart journal     Volume:  16 Suppl N     ISSN:  0195-668X     ISO Abbreviation:  Eur. Heart J.     Publication Date:  1995 Dec 
Date Detail:
Created Date:  1996-08-21     Completed Date:  1996-08-21     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8006263     Medline TA:  Eur Heart J     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  65-72     Citation Subset:  IM    
Affiliation:
Department of Medicine, Ostra University Hospital, Göteborg, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin-Converting Enzyme Inhibitors / adverse effects,  therapeutic use*
Cardiac Volume / drug effects,  physiology
Dose-Response Relationship, Drug
Drug Administration Schedule
Female
Heart Failure / drug therapy*,  mortality,  physiopathology
Hemodynamics / drug effects,  physiology
Humans
Hypertrophy, Left Ventricular / drug therapy,  mortality,  physiopathology
Male
Neurotransmitter Agents / blood*
Randomized Controlled Trials as Topic
Survival Rate
Treatment Outcome
Ventricular Dysfunction, Left / drug therapy,  mortality,  physiopathology
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Neurotransmitter Agents

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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