Complete occlusion of the infarct-related coronary artery is a frequent finding soon after Q-wave (transmural) myocardial infarction. We performed coronary arteriography to study the frequency of total coronary occlusion and of angiographically visible collateral vessels in 341 patients within one week of non-Q-wave myocardial infarction. In this cross-sectional study, 192, 94, and 55 patients underwent coronary arteriography within 24 hours of peak symptoms, between 24 and 72 hours after peak symptoms, and between 72 hours and seven days after peak symptoms, respectively. In the three groups, total occlusion of the infarct-related vessel was found in 26 percent (49 of 192), 37 percent (35 of 94), and 42 percent (23 of 55) of the patients, respectively (P less than 0.05). The presence of visible collateral vessels increased in parallel: 27 percent (52 of 192), 34 percent (32 of 94), and 42 percent (23 of 55), respectively (P less than 0.05). The frequency of subtotal occlusion (i.e., greater than or equal to 90 percent stenosis) decreased inversely: 34 percent (65 of 192), 25.5 percent (24 of 94), and 18 percent (10 of 55), respectively (P less than 0.05). Thus, in contrast to Q-wave infarction, total coronary occlusion of the infarct-related vessel is infrequently observed in the early hours of non-Q-wave infarction, but it increases moderately in frequency over the next several days. These cross-sectional data suggest that non-Q-wave infarction may be related to a preserved but marginal blood supply, which sufficiently disrupts the relation between the supply of and the demand for myocardial oxygen to cause tissue necrosis.

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To define the outcome of patients given medical or surgical therapy for Q wave myocardial infarction, 387 patients were followed up for 10 to 13 years (mean 11.4). On study entry the groups had similar distributions for variables such as mean age, gender, previous myocardial infarction, abnormal creatine kinase activity, area of infarction, number of vessels diseased and clinical classification. The hospital mortality rate of the medical versus surgical group was 11.5% (23 of 200) versus 5.8% (11 of 187) (p = 0.07). Early reperfusion (that is, less than or equal to 6 h) resulted in a lower mortality rate than did medical therapy--2% (2 of 100) versus 11.5% (23 of 200) (p less than 0.05)--whereas the hospital mortality rate with late reperfusion was 10.3% (9 of 87). The long-term mortality rate of the medical and surgical groups was 41% (82 of 200) versus 27% (51 of 187) (p = 0.0007) with use of an adjusted Cox proportional hazards model. In the survivors, the differences between medical and surgical groups in recurrent myocardial infarction, mortality associated with reinfarction and sudden death were prospectively followed and evaluated by the life table method. Recurrent myocardial infarction was not prevented by surgical reperfusion or medical therapy (23% in both groups), however, the mortality rate in patients with recurrent infarction was higher in the medical therapy group--36.6% (15 of 41) versus 17.5% (7 of 40) (p = 0.04). The mortality difference did not depend on early or late surgical reperfusion. In the in-hospital survivors, the incidence of sudden death was 17.5% in the medical (31 of 177) versus 7.4% (13 of 176) in the surgical group (p = 0.01). This difference was much more pronounced in the early reperfusion group. Functional class was significantly lower than that for medical therapy in the early reperfusion but not the late reperfusion group. Thus, in comparable groups given medical and surgical therapy for acute myocardial infarction and followed up for greater than or equal to 10 years, surgical reperfusion appears to offer improved longevity in selected cases (when implemented early) but does not prevent recurrent myocardial infarction. The associated mortality with recurrent myocardial infarction is less as is the incidence of sudden death. Finally, lower functional class occurs most often in patients given early reperfusion.