Myocardial Infarction

Abstract

The rationale for the use of nifedipine in patients with acute myocardial infarction (MI) is based on the various cardiovascular actions of the compound: reduction of myocardial oxygen consumption by attenuation of cardiac and vascular smooth muscle tension; augmentation of oxygen and substrate supply after increased coronary blood flow with dilatation of epicardial coronary arteries (particularly in coronary obstructions) and dilatation of coronary resistance and collateral vessels; myocardial 'protection', i.e. reduction of myocardial damage via a complex intracellular mechanism, the primary outcome of which is the maintenance of an energy level sufficient to preserve the ionic homeostasis of the myocyte. The effect of nifedipine on reinfarction and mortality rates was evaluated in 6 well designed studies involving 8670 patients with evolving or established acute MI. Compared with placebo, short term therapy (for up to 6 months) with nifedipine 30 to 120 mg/day initiated, in some patients, as early as 3 hours after the onset of symptoms did not reduce either reinfarction rate or mortality. In one study (SPRINT I) [Israeli Sprint Study Group 1988], where a regimen of nifedipine 30 mg/day was only started 7 to 21 days after infarction, the exceptionally low mortality rate (5.7%) over 10 months in the placebo group precluded the demonstration of a beneficial effect of nifedipine. These results collectively suggest that nifedipine does not prevent the 'secondary' coronary events of plaque rupture and thrombus formation associated with MI and sudden cardiac death. However, the suppression of early lesions by nifedipine (as demonstrated in the INTACT study [Lichtlen et al. 1990]) might reduce 'primary' progression and improve the long term survival after MI.