Effects of amlodipine versus enalapril on left ventricular remodelling after reperfused anterior myocardial canine infarction.
B. I. Jugdutt
Abstract
B. I. Jugdutt
Abstract
OBJECTIVE: To compare the effects of the calcium channel blocker amlodipine with those of the angiotensin-converting enzyme (ACE) inhibitor enalapril on left ventricular (LV) remodelling and dysfunction during healing after reperfused anterior myocardial infarction (MI). ACE inhibitors and reperfusion are known to limit LV remodelling after MI. However, the effects of ACE inhibitors and calcium channel blockers on LV remodelling after reperfused MI have not been compared. METHODS: Changes in LV topography and function (quantitative echocardiograms) and hemodynamics were measured over six weeks in dogs that were randomized 24 h after reperfusion, done after 2 h of anterior MI, to oral amlodipine (5 mg bid; n = 7), enalapril (5 mg bid; n = 6) or no drug (controls; n = 6) for six weeks. Postmortem LV topography was measured at six weeks. RESULTS: Scar sizes after six weeks were similar in the three groups. Both enalapril and amlodipine reduced the rate pressure product, but decreases in mean arterial and left atrial pressures were more sustained over six weeks with enalapril. Compared with controls over six weeks, both enalapril and amlodipine preserved LV volumes, global ejection fraction, regional function and infarct segment length, but enalapril blocked the increase in non-infarct wall thickness, attenuated the infarct wall thickness, preserved shape and decreased global LV mass more than amlodipine. Sham-operated dogs (n = 3) showed no significant structural changes. CONCLUSIONS: Both enalapril and amlodipine preserve LV volumes and function during healing after reperfused MI, but enalapril more effectively limits hypertrophy, attenuates infarct wall thickness and preserves shape.
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OBJECTIVE: To compare the effects of the calcium channel blocker amlodipine with those of the angiotensin-converting enzyme (ACE) inhibitor enalapril on left ventricular (LV) remodelling and dysfunction during healing after reperfused anterior myocardial infarction (MI). ACE inhibitors and reperfusion are known to limit LV remodelling after MI. However, the effects of ACE inhibitors and calcium channel blockers on LV remodelling after reperfused MI have not been compared. METHODS: Changes in LV topography and function (quantitative echocardiograms) and hemodynamics were measured over six weeks in dogs that were randomized 24 h after reperfusion, done after 2 h of anterior MI, to oral amlodipine (5 mg bid; n = 7), enalapril (5 mg bid; n = 6) or no drug (controls; n = 6) for six weeks. Postmortem LV topography was measured at six weeks. RESULTS: Scar sizes after six weeks were similar in the three groups. Both enalapril and amlodipine reduced the rate pressure product, but decreases in mean arterial and left atrial pressures were more sustained over six weeks with enalapril. Compared with controls over six weeks, both enalapril and amlodipine preserved LV volumes, global ejection fraction, regional function and infarct segment length, but enalapril blocked the increase in non-infarct wall thickness, attenuated the infarct wall thickness, preserved shape and decreased global LV mass more than amlodipine. Sham-operated dogs (n = 3) showed no significant structural changes. CONCLUSIONS: Both enalapril and amlodipine preserve LV volumes and function during healing after reperfused MI, but enalapril more effectively limits hypertrophy, attenuates infarct wall thickness and preserves shape.
Key concepts: Enalapril, Amlodipine, Medicine, Cardiology, Internal medicine, Myocardial infarction, ACE inhibitor, Ejection fraction