Nifedipine in acute myocardial infarction: an assessment of left ventricular function, infarct size, and infarct expansion. A double blind, randomised, placebo controlled trial.

Abstract

SUMMARY The influence of nifedipine on left ventricular ejection fraction, infarct size, and infarct expansion was studied in a prospective, double blind, randomised, placebo controlled trial in 132 patients with low risk acute myocardial infarction of < 12 hours duration, defined by an initial left ventricular ejection fraction >35% and clinical Killip class of <II. Sixty four patients were assigned to nifedipine 120 mg/day and 68 to placebo. Treatment was started on average (SEM) 8-0 (0 2) hours after onset of pain and continued for six weeks. Gated blood pool scans, thallium scans, and cross sectional echocardiograms were performed before treatment and at 10 days. There were no significant differences between the two groups in age, sex, cardiac risk factors, or use of other medications. Mean (SEM) global left ventricular ejection fraction was not different before treatment (nifedipine group 53 (2%), placebo group 55 (2%) and did not differ at 10 days (nifedipine group 54 (2%), placebo group 52(2%). There were also no differences in regional wall motion or regional ejection fractions. Thallium defects quantified by computer analysis were similar in both groups before treatment (nifedipine 7-8 (0-7), placebo 7 9 (0-7)) and at 10 days (nifedipine 5-3 (0-7) placebo 5-3 (0-7)). In the subgroup of patients with transmural infarction who had good quality echocardiograms and serial studies (n = 30), there was no difference in mean (SEM) baseline infarct segment lengths between the two groups (nifedipine 70(4) mm, placebo 65 (4) mm); however, the nifedipine group demonstrated no significant change in infarct segment length between the initial and 10 day studies (+ 0-6 (3) mm) while there was a significant increase in the infarct segment length in the placebo group (+ 7-8 (4) mm). The infarct segment length increased by > 1 cm in seven (47%) placebo patients but in only one (7%) nifedipine patient. The nifedipine group had a significant initial 10% decrease in mean arterial pressure whereas there was no change in the placebo group; this blood pressure difference persisted for 10 days.Thus although the early administration of nifedipine has no detectable effect on clinical outcome and infarction size, it may reduce early infarct expansion via an afterload reduction mechanism in patients with transmural infarction. These initial results must be interpreted with caution and need to be confirmed in a larger trial.

Prevention of ventricular remodeling after myocardial infarction and in congestive heart failure

“…Future research might permit the development of adjunctive agents that protect the collagen matrix and allow postinfarction mortality to be lowered to less than 5%. Beta-adrenergic blockers [125] and calcium channel blockers [125,175] can also have beneficial effects on postinfarct remodeling via a decrease in heart rate and contractility, and they have both been shown to decrease infarct expansion and to limit ventricular dilation [125,175]. A recent North American registry [143] indicated that patients treated with thrombolytic therapy also received adjunctive intravenous nitroglycerin (76%), oral beta-blockers (30%), intravenous beta-blockers (17%), and calcium channel blockers (30%), as well as intravenous heparin (97%) and aspirin (84%).…”

Thrombolytic Therapy in Acute Myocardial Infarction

“…There are no indications that calcium entry blockers have any beneficial effect in patients with myocardial infarction, either in the acute phase or during follow-up (37,38). One study reported a reduction of reinfarction in the first two weeks after a "non-Q-wave" infarction (39).…”

Myocardial infarction in rats: effects of metabolic and pharmacologic interventions

“…It reduced LVSP in sham-operated rats and induced a reduction in heart rate and a further decline in LVSP and in LV dP/dt .... in animals with myocardial infarction (Table 1). A decrease in mean arterial pressure was also observed in patients with acute myocardial infarction when the calcium antagonist nifedipine was given (7). Treatment with calcium antagonists may be beneficial due to reduction in afterload mediated by peripheral vasodilation and an increase in coronary flow via coronary artery dilation and antispasmic effects.…”