Effects of early intracoronary streptokinase on infarct size estimated from cumulative enzyme release and on enzyme release rate: A randomized trial of 533 patients with acute myocardial infarction

Abstract

The effects of early intracoronary streptokinase (SK) on enzymatic infarct size and rate of enzyme release were studied in a randomized multicenter trial. A total of 533 patients with acute myocardial infarction (AMI) were allocated to either the SK treatment group (n = 269) or the conventional (control) treatment group (n = 264). Enzymatic infarct size was represented by the cumulative quantity of α-hydroxybutyrate dehydrogenase (HBDH) released by the heart per liter of plasma in the first 72 hours. Rate of enzyme release was represented by the ratio of HBDH quantities released in 24 hours and 72 hours. On an “intention to treat” basis, the SK group had a smaller (by 30%; p = 0.0001) median enzymatic infarct size and a higher (by 35%; p = 0.0001) median rate of enzyme release than the control group. Limitation of infarct size was less apparent in patients treated with intracoronary SK only (25%) than in patients treated with intravenous plus intracoronary SK (34%). Compared to the control group, the enzyme release rate in patients treated with intracoronary SK only was slightly less (34%) than that in patients treated with intravenous plus intracoronary SK (38%). Patients with a patent infarct-related coronary artery at acute angiography had a median infarct size which was 55% ( p = 0.0001) smaller than the median infarct size of the control group, and the median rate of enzyme release was 38% ( p = 0.001) higher than the median release rate of the control group. Patients with successful recanalization during intracoronary SK infusion had a median infarct size which was 31% ( p = 0.002) smaller than the median infarct size of the control group and a median rate of enzyme release which was 42% ( p = 0.0001) higher than the median release rate of the control group. Patients with persistent coronary occlusion in spite of thrombolytic therapy had a median infarct size which was 11% (NS) higher than the median infarct size of the control group, although the median rate of enzyme release was still 23% ( p = 0.02) higher than the median release rate of the control group. It is concluded that thrombolysis in the early phase of AMI limits infarct size and that intracoronary SK treatment ltself accelerates the process of enzyme release from infarcted myocardium, independent of the angiographic result.