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The association of myocardial infarction with normal coronary arteries was analyzed prospectively. A series of 259 consecutive men aged 60 years or less underwent selective coronary angiography 30 days after a definite infarct. Coronary arterial lesions were documented in 251 patients, normal coronary arteries in the remaining 8. The latter patients had a significantly lower (p less than 0.001) mean age than the former; no patient older than 50 years had patent coronary arteries, whereas 5 of the 11 patients under age 35 had normal arteries. The prevalence of risk factors was similar in both groups of patients. Although there were no group differences in infarct size or location, patients with normal coronary arteries had a higher ejection fraction (p less than 0.01) and a lower left ventricular end-diastolic pressure (p less than 0.05). A previous history of angina or infarction and the occurrence of new coronary events were confined to patients with coronary arterial lesions. The clinical course of patients presenting with normal angiograms was uneventful. Transient coronary occlusion, the most likely mechanism of infarction in this group of patients, could not be ascribed to either spasm or platelet hyperactivity.

Prevalence, prognosis, and coronary anatomy associated with nontransmural myocardial infarction (MI) were prospectively assessed in 458 consecutive men admitted to our coronary care unit with a first MI. Cardiac catheterization was performed in 402 of the 436 survivors within 1 month of the acute event. Mean follow-up was 33 months (range 5 to 72). Nontransmural MI was diagnosed in 28 patients (6%). These patients were younger (46 +/- 10 versus 51 +/- 7 years, p less than 0.001) and had lower peak creatine kinase values (601 +/- 319 versus 1,141 +/- 923 U, p less than 0.01) and better ejection fraction (63 +/- 8 versus 46 +/- 14, p less than 0.001) than did their counterparts. Survivors of nontransmural MI also had fewer affected arteries (p less than 0.001) and a lower prevalence of total or subtotal occlusion (greater than 90%) in the involved artery (p less than 0.01). Mortality in the acute phase and long-term survival at 4 years (Kaplan-Meier) in patients with nontransmural MI (94%) were similar to those in patients with transmural MI (90%). The occurrence of new nonfatal coronary events was also similar in both groups of MI survivors. Thus, in the absence of symptoms, more aggressive management to improve survival does not seem warranted after nontransmural MI.

Coronary anatomy as it relates to left ventricular function was assessed prospectively in patients who survived acute myocardial infarction. The study population included 259 consecutive male patients age 60 years or younger who underwent catheterization 30 days after the acute event. Coronary artery obstructive lesions (greater than 50% reduction in luminal diameter) were found in 241 patients (93%), 118 (45%) of whom had total and 76 (29%) subtotal (greater than 90%) stenosis) occlusion of at least one coronary artery. Normal coronary vessels were seen in eight patients (3%) and nonobstructive lesions in 10 (4%). One-, two- and three-vessel disease were present in 89, 86 and 66 patients, respectively. Patients with normal coronary arteries or nonobstructive lesions had higher ejection fractions than those with obstructive lesions in one, two or three vessels (p less than 0.05). Ejection fraction was lower (p less than .001) and the percentage of akinetic segments higher (p less than 0.001) in patients with total or subtotal lesions and no collaterals. Adequate collaterals, seen in 29 patients (11%), significantly improved regional wall motion (p less than 0.05) and decreased the percentage of akinetic segments (p less than 0.001). Thus, in a substantial number of patients (32% in our series), the infarcted area is spontaneously reperfused by collaterals or through the involved artery. Both mechanisms ameliorate wall motion in corresponding areas.