Mechanisms involved in cardiac enlargement and congestive heart failure development after acute myocardial infarction.
For 3 months, we followed up 40 patients with acute myocardial infarction, 20 were randomly assigned to treatment with captopril and 20 to placebo, to elucidate mechanisms inducing left ventricular volume enlargement and development of congestive heart failure. Echocardiographic follow-up could be obtained in 28 patients, 11 of whom showed more than a 10% increase in left ventricular systolic and/or diastolic volumes (captopril n = 3/15, placebo n = 8/13, p = 0.05). Volume increase was significantly associated with an impairment in exercise capacity (VO2 max in patients with vs. without volume enlargement 24.7 +/- 1.7 vs. 29.5 +/- 1.9 ml O2/kg/min; p < 0.05). Plasma renin activity, angiotensin II and catecholamines were normal in the acute and chronic postinfarction phase in patients on placebo as well as in patients 12-24 h after captopril intake. Plasma atrial natriuretic peptide concentration (ANP) was increased immediately after myocardial infarction, but ANP levels almost normalized in patients with captopril treatment, while they continued to be elevated in patients on placebo. The only technical parameter able to predict left ventricular volume increases was the sphericity index (28.7 vs. 35.7; p = 0.07). We concluded that morphologic deformation and filling pressures as estimated from elevated ANP levels are major factors promoting remodelling following myocardial infarction. ACE inhibitors might exert their favorable effect predominantly by reducing filling pressure.
Kleber
F X
FX
Munich-Schwabing Hospital, Academic Teaching Hospital, Ludwig Maximilians University, FRG.
Nussberger
J
J
Niemöller
L
L
Doering
W
W
D009320:Atrial Natriuretic Factor / Q000097:blood; D002216:Captopril / Q000627:therapeutic use*; D006328:Cardiac Catheterization; D002306:Cardiac Volume / Q000187:drug effects / Q000502:physiology; D004311:Double-Blind Method; D004837:Epinephrine / Q000097:blood; D005080:Exercise Test / Q000187:drug effects; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D011446:Prospective Studies; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
D009320:Atrial Natriuretic Factor; D002216:Captopril; D009638:Norepinephrine; D004837:Epinephrine