Neurohormonal effects of early treatment with enalapril after acute myocardial infarction and the impact on left ventricular remodelling

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Abstract
Plasma neurohormones were sequentially analysed in 98 patients with acute myocardial infarction randomized to treatment with enalapril or placebo for 4–6 months. Plasma angiotensin converting enzyme activity was rapidly suppressed by enalapril, but unaffected by placebo (P = 0.0001). No significant differences were found in the plasma levels of angiotensin II, aldosterone, atrial natriuretic peptide, noradrenaline, adrenaline or dopamine between the two treatment groups. Among patients with infarct size above median, plasma angiotensin II increased during head-up tilt at one month in the placebo group, but not in the enalapril group. Left ventricular end-diastolic volume (LVEDV) and left ventricular endsystolic volume (LVESV) were evaluated by echocardiography in 28 patients (placebo 15, enalapril 13) and changes in left ventricular volumes between baseline and 4–6 months were calculated. Only in the placebo group was a positive correlation found between plasma levels of noradrenaline at day 5–7 and the subsequent increase in LVEDV (r = 0.78, P = 0.005) and LVESV (r = 0.75, P = 0.008). The same trend was found for angiotensin II, adrenaline and dopamine levels at days 5–7 and the subsequent increase in left ventricular volumes. In the placebo group a negative correlation was found between plasma aldosterone at days 5–7 and the subsequent increase in left ventricular ejection fraction (r = −0.77, P = 0.006) during the study period. Although circulating neurohormones were not significantly influenced by enalapril treatment, it is concluded that enalapril may influence the relationship found between sustained neurohormonal activation and left ventricular remodelling after acute myocardial infarction.

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