PMID- 8682064
OWN - NLM
STAT- MEDLINE
DCOM- 19960821
LR  - 20190512
IS  - 0195-668X (Print)
IS  - 0195-668X (Linking)
VI  - 16 Suppl N
DP  - 1995 Dec
TI  - Neurohormonal activation and congestive heart failure: today's experience with 
      ACE inhibitors and rationale for their use.
PG  - 65-72
AB  - 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.
FAU - Sigurdsson, A
AU  - Sigurdsson A
AD  - Department of Medicine, Ostra University Hospital, Goteborg, Sweden.
FAU - Swedberg, K
AU  - Swedberg K
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Eur Heart J
JT  - European heart journal
JID - 8006263
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Neurotransmitter Agents)
SB  - IM
MH  - Angiotensin-Converting Enzyme Inhibitors/adverse effects/*therapeutic use
MH  - Cardiac Volume/drug effects/physiology
MH  - Dose-Response Relationship, Drug
MH  - Drug Administration Schedule
MH  - Female
MH  - Heart Failure/*drug therapy/mortality/physiopathology
MH  - Hemodynamics/drug effects/physiology
MH  - Humans
MH  - Hypertrophy, Left Ventricular/drug therapy/mortality/physiopathology
MH  - Male
MH  - Neurotransmitter Agents/*blood
MH  - Randomized Controlled Trials as Topic
MH  - Survival Rate
MH  - Treatment Outcome
MH  - Ventricular Dysfunction, Left/drug therapy/mortality/physiopathology
RF  - 53
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
AID - 10.1093/eurheartj/16.suppl_n.65 [doi]
PST - ppublish
SO  - Eur Heart J. 1995 Dec;16 Suppl N:65-72. doi: 10.1093/eurheartj/16.suppl_n.65.