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

Plasma neurohormones were sequentially analysed in 98 patientswith acute myocardial infarction randomized to treatment withenalapril or placebo for 4–6 months. Plasma angiotensinconverting enzyme activity was rapidly suppressed by enalapril,but unaffected by placebo (P = 0.0001). No significant differenceswere found in the plasma levels of angiotensin II, aldosterone,atrial natriuretic peptide, noradrenaline, adrenaline or dopaminebetween the two treatment groups. Among patients with infarctsize above median, plasma angiotensin II increased during head-uptilt at one month in the placebo group, but not in the enalaprilgroup. Left ventricular end-diastolic volume (LVEDV) and leftventricular endsystolic volume (LVESV) were evaluated by echocardiographyin 28 patients (placebo 15, enalapril 13) and changes in leftventricular volumes between baseline and 4–6 months werecalculated. Only in the placebo group was a positive correlationfound between plasma levels of noradrenaline at day 5–7and the subsequent increase in LVEDV (r = 0.78, P = 0.005) andLVESV (r = 0.75, P = 0.008). The same trend was found for angiotensinII, adrenaline and dopamine levels at days 5–7 and thesubsequent increase in left ventricular volumes. In the placebogroup a negative correlation was found between plasma aldosteroneat days 5–7 and the subsequent increase in left ventricularejection fraction (r = –0.77, P = 0.006) during the studyperiod. Although circulating neurohormones were not significantlyinfluenced by enalapril treatment, it is concluded that enalaprilmay influence the relationship found between sustained neurohormonalactivation and left ventricular remodelling after acute myocardialinfarction.