To evaluate the relative thrombolytic efficacy and complications of intracoronary vs high-dose, short-term intravenous streptokinase infusion in patients with acute myocardial infarction, we performed baseline coronary arteriography and then randomly allocated 51 patients with acute myocardial infarction to receive either intracoronary (n = 25) or intravenous (n = 26) streptokinase. Patients getting the drug by the intracoronary route received 240,000 IU of streptokinase into the infarct-related artery over 1 hr, whereas those getting the drug by the intravenous route received either 500,000 IU of streptokinase over 15 min (n = 10) or I million IU of streptokinase over 45 min (n = 16). Angiographically observed thrombolysis occurred in 76% (19/25) of the patients receiving intracoronary streptokinase, in 10% (1/10) of the patients receiving 500,000 IU of streptokinase intravenously, and in 44% (7/16) of the patients receiving 1 million IU of streptokinase intravenously. Among patients in whom thrombolysis was observed, mean elapsed time from onset of streptokinase infusion until lysis was 31 ± 18 min in patients receiving intracoronary streptokinase and 38 + 20 min in those receiving intravenous streptokinase (p = NS). Among patients in whom intravenous streptokinase "failed," intracoronary streptokinase in combination with intracoronary guidewire manipulation recanalized only 7% (1/15). Fibrinogen levels within 6 hr after streptokinase were significantly lower in the patients receiving intravenous streptokinase (39 ± 17 mg/dl) than the levels in those receiving intracoronary streptokinase (88 + 70 mg/dl) (p < .05) but were similar 24 hr after streptokinase in the two groups. Bleeding requiring transfusion occurred in one patient in each group. Thus, in this prospective randomized trial of intracoronary vs intravenous streptokinase, hemorrhagic complications were few, although both regimens produced a systemic lytic state. Although the thrombolytic efficacy of intracoronary streptokinase was superior to that of high-dose, short-term intravenous streptokinase, the higher-dose intravenous regimen (1 million IU over 45 min) achieved thrombolysis in a significant minority (44%) of patients and might be useful therapy for patients not having access to emergency catheterization.Circulation 68, No. 5, 1051No. 5, -1061No. 5, , 1983 RECENTLY, intracoronary streptokinase has achieved considerable popularity as a means for recanalizing acutely thrombosed coronary arteries in patients with evolving acute myocardial infarction. 1 Unfortunately, emergency coronary arteriography and intracoronary streptokinase infusion require sophisticated equipment and a specially trained operator and

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Accumulated creatine kinase MB isoenzyme release (sigma CK-MB) during acute myocardial infarction was correlated with biplane left ventricular (LV) angiographic estimates of percent abnormally contracting segment (%ACS) and ejection fraction (EF) in 35 patients who underwent diagnostic angiography at a mean of 33 +/- 4 days post myocardial infarction (MI). Of the 35 patients, 18 had no evidence of prior MI and their sigma CK-MB showed good correlation with %ACS (r = 0.84) and with EF (r = - 0.78). An additional two patients with first (inferior) infarct secondary to stenosis of the right coronary artery proximal to the origin of the right ventricular arterial blood supply had disproportionately large sigma CK-MB, suggesting a combination of LV and RV necrosis. In the 15 patients with prior infarct, there was no significant correlation between sigma CK-MB and %ACS or EF. However, in the subgroup of patients with anterior MI, %ACS correlated with sigma CK-MB, both in patients with no prior MI (r = 0.88, N = 12) and in patients with prior MI (r = 0.69, N = 9). These independent angiographic and enzymatic data suggest that enzymatic infarct size estimates utilizing accumulated CK-MB release may be a valid and reliable clinical measure for assessing the extent of LV necrosis in the setting of acute anterior myocardial infarction. However, limitations may exists in certain cases of inferior MI, probably because of concomitant right and left ventricle necrosis.