Frequency of low-grade residual coronary stenosis after thrombolysis during acute myocardial infarction

Abstract

The clinical, angiographic and demographic characteristics of 42 patients with low-grade (<50%) residual stenosis at the infarct lesion after thrombolysis for acute myocardial infarction (MI) were assessed. The study group (group I) represented 21% of 198 consecutive patients receiving thrombolytic therapy over a 59-month period. Data on the 156 remaining patients were pooled for comparison (group II). Group I patients were predominantly men (86%) who were cigarette smokers (81%). Group II patients were predominantly men (75%, p > 0.10) but were significantly older (52 ± 12 vs 56 ± 10 years, p = 0.02). Prior acute MI or angina was unusual in group I. Sixty percent had no significant (>50%) residual coronary artery disease while 25% had residual single artery disease. Average significant (>50% diameter stenosis) residual vessel disease was 0.6 ± 1.0 for group I and 1.9 ± 0.9 for group II (p < 0.001). In group I, average residual infarct lesion diameter stenosis was 36 ± 7% in the right anterior oblique and 34 ± 8% in the left anterior oblique views. Thirty-nine group I patients were discharged with medical therapy and 100% follow-up was obtained over a mean interval of 18 ± 17 months. Fifteen patients experienced chest pain after acute MI accounting for 17 discrete events. Fifty-nine percent of group I had a benign course on follow-up. Eight events were classified as unstable angina, 4 as acute MI and 5 as atypical angina. Documented coronary vasospasm occurred in 3. The infarct narrowing accounted for 58% of documented ischemia and 41% of symptomatic events. Antiplatelet agents, warfarin and residual lesion morphology did not clearly influence frequency of events, whereas data regarding cigarette smoking were suggestive (p = 0.06). Events clearly associated with the infarct narrowing occurred earlier (4 ± 4 months) than events not related to (23 ± 15 months, p < 0.01). Ischemic events unrelated to the infarct lesion were often related to progressive stenosis or occlusion at the site of previously nonsignificant disease.