Preliminary clinical and laboratory observations suggest that nifedipine might prevent progression of threatened myocardial infarction by reversing coronary spasm or 57 [75% for nifedipine-treated patients). Furthermore, infarct size index was similar among placebo-and nifedipine-treated patients (16.9 + 1.5 MB-CK-geq/m ,n 65, and 17.0 ± 1l.5 MB-CK-geq/m', n = 68, respectively) with threatened myocardial infarction who exhibited infarction and for those with acute myocardial infarction. Among the 171 eligible patients randomly assigned to drug or placebo, 6 month mortality did not differ significantly (8.5% for placebo vs 10. 1 % for nifedipine, NS), but mortality in the 2 weeks after randomization was significantly higher for nifedipine-treated patients (0% for placebo compared with 7.9% for nifedipine, p = .0 18). There were no significant differences in 2 week and 6 month mortalities in the group of all participating patients, which included 10 patients randomly assigned therapy but retrospectively determined to be ineligible. Two week mortality for this group (n = 181) was 2.3% for placebo-and 7.5% for nifedipine-treated patients and 6 month mortality was 11.4% for placebo-and 10.8% for nifedipine-treated patients. Thus, nifedipine therapy did not prevent progression of threatened myocardial infarction to the acute event or limit infarct size in patients who experienced infarction. There was a statistically significant increase in 2 week mortality with nifedipine in the group of eligible patients randomly assigned to a regimen, but mortality was balanced when results were analyzed for all patients taking part in the randomization protocol.

The Synchrotron Medical Research Facility (SMERF) at the National Synchrotron Light Source has been completed and is operational for human coronary angiography experiments. The imaging system and hardware have been brought to SMERF from the Stanford Synchrotron Radiation Laboratory where prior studies were carried out. SMERF consists of a suite of rooms at the end of the high-field superconducting wiggler X17 beam line and is classified as an Ambulatory Health Care Facility. Since October of 1990 the coronary arteries of five patients have been imaged. Continuously improving image quality has shown that a large part of both the right coronary artery and the left anterior descending coronary artery can be imaged following a venous injection of contrast agent.

Intracoronary thrombolysis during acute myocardial infarction in human beings is associated with rapid release of creatine kinase and improvement of the cardiac ejection fraction. To examine the phenomenon of spontaneous coronary-artery recanalization, we studied the release of creatine kinase MB and sequential radionuclide ventriculograms in 52 patients with transmural myocardial infarction. Patients were divided into two groups according to whether the release of creatine kinase MB (time from base-line to peak serum level) was rapid (n = 24) or slow (n = 28). Patients with slow release had no significant change in global or regional ejection fraction from the time of admission to discharge. However, global ejection fraction in patients with rapid release improved from 0.38 +/- 0.09 (mean +/- S.D.) to 0.48 +/- 0.08 (P less than 0.001). The regional ejection fraction of Q-wave regions also improved, from 0.33 +/- 0.11 to 0.43 +/- 0.13 (P less than 0.001). A negative correlation (r = -0.52, P less than 0.001) existed between time to peak enzyme level and degree of improvement in ejection fraction. With increasing left ventricular damage, patients with rapid release had greater increments in creatine kinase MB than comparable patients with slow release (P = 0.03), suggesting enzyme washout. These data are consistent with the idea that spontaneous reperfusion, leading to altered enzyme release and improvement in ventricular function, is not uncommon after acute myocardial infarction.

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