Mechanisms Involved in Cardiac Enlargement and Congestive Heart Failure Development after Acute Myocardial Infarction

Abstract

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 (VO₂max 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.

Influence of Aerobic Exercise Training on Brain Natriuretic Peptide Secretion in Patients in the Chronic Phase of Myocardial Infarction

“…19 In fact, the degree of left ventricular remodeling is regarded as an important factor in determining the prognosis of MI. [20][21][22] Seals et al reported that left ventricular dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter because it has usually more extensive myocardial damage compared with inferior AMI. 23 Moreover, considerable attention has been directed to determining whether exercise therapy in the chronic phase of AMI could affect the process of left ventricular remodeling.…”

Captopril

“…A number of other controlled trials also demonstrated that early treatment with captopril after myocardial infarction inhibited left ventricular remodelling, as demonstrated by statistically significant attenuation of left ventricular systolic and diastolic volume expansion [35][36][37][38] and changes in expansion index, thinning ratio, [37] anterior segment length [39] and ejection fraction.l3 4 ] © Adis International Limited. Similar results were noted in a double-blind study of 77 patients receiving 3 months of treatment with captopril 100 mg/day or placebo starting 24 to 48 hours after Q-wave myocardial infarction.l 34 ] While left ventricular volume indices increased markedly among placebo recipients, they were decreased or only modestly increased with captopril, and the difference between treatment groups was statistically significant.…”