Preponderance of acute proximal left anterior descending coronary arterial lesions in fatal myocardial infarction: A clinicopathologic study

To determine whether an acute lesion in a specific segment of the cororiary tree is more likely than other obstructions to cause fatal myocardial infarction, 77 autopsy patients Who died of acute myocardial infarction were studied. Multiple coronary stenoses were present in 92 percent of these patients, arid the proximal left anterior descending coronary artery before the first septal perforator accounted for only 23 percent of the critical narrowings (greater than 70 percent of luminal diameter). In contrast, acute thrombotic coronary events associated with fatal myocardial infarction occurred most often in the proximal left anterior descending artery, accounting for 61 percent of acute lesions; this rate compared with 8 percent of acute lesions occurring in the mid or distal left anterior descending artery, 18 percent of those in the right, 6 percent of those in the left circumflex and 7 percent of those in the left main coronary artery. Of the autopsy patients, 32 (40 percent) had 77 prior nonfatal myocardial infarcts of which only 17 (22 percent) were anteroseptal infarcts related to occlusion of the proximal left anterior descending coronary artery. The amount of infarcted myocardium in the hearts with acute proximal left anterior descending coronary arterial lesions was somewhat more extensive but not significantly different from that of hearts with other acute coronary lesions. Fifty survivors of myocardial infarction who underwent cardiac catheterization were studied for comparison. In those patients, proximal left anterior descending coronary disease accounted for 17 percent of critical narrowings and only 22 percent of nonfatal infarcts. These findings suggest that an acute proximal left anterior descending coronary arterial lesion is more likely to result in fatal myocardial infarction than are critical obstructions elsewhere in the coronary arterial tree. Because the quantity of the infarct does not appear to be sufficient to explain these differences, qualitative differences in anteroseptal myocardium are suggested.