Coronary thrombolysis by intravenous streptokinase in acute myocardial infarction: acute and follow-up studies.

Coronary arteriography was performed before, immediately after, and 9 to 14 days after administering i.v. streptokinase (850,000 to 1,500,000 IU) to 43 patients within 6 hours of myocardial infarction. Ventricular function was determined by contrast ventriculography before and 9 to 14 days later and by radionuclide studies at clinical follow-up 8 months later. Early reperfusion occurred in 49% of patients, but in only 35% was it sustained. In patients with sustained reperfusion, early ventricular dysfunction was significantly reduced 9 to 14 days and 10 months later, and frequency of infarction, sudden death, and angina pectoris was not increased at follow-up. No serious bleeding occurred.

High-dose, brief intravenous streptokinase early in acute myocardial infarction.

An acute thrombus at the proximal border of a high-grade atherosclerotic obstruction is the usual cause of myocardial infarction. Although intracoronary thrombolysis is potentially an exciting new therapy for reducing the extent of myocardial infarction by lysing coronary clot, a number of major difficulties limit its widespread application. It is a complex procedure requiring intracoronary visualization and infusion within a few hours of onset of symptoms. Since intravenous streptokinase could be widely applied if effective, we and others have wondered whether high-dose, brief-duration intravenous streptokinase infusion given early in myocardial infarction would lyse coronary clots without bleeding. To date we have treated 13 patients within 6 hours of onset of symptoms and with ECG and angiographic evidence of typical myocardial infarction caused by coronary clot. Clot lysis and angiographically proved coronary reperfusion were achieved in 6 patients within 1 hour of starting a systemic intravenous infusion of 850,000 IU of streptokinase. Schroeder et al., in Berlin, West Germany, achieved angiographically proved coronary reperfusion in 11 of 21 patients with acute myocardial infarction following a 30-minute intravenous streptokinase infusion of 500,000 IU. Neuhaus et al., in Göttinen, West Germany, achieved angiographically proved coronary reperfusion in 24 of 39 similar patients within 48 minutes by intravenous infusion of 1,700,000 IU of streptokinase. In these three studies, no serious bleeding occured; left ventricular function was improved in patients who achieved coronary reperfusion. We conclude that rapid intracoronary clot lysis and coronary reperfusion can be achieved early in myocardial infarction by brief-duration systemic intravenous infusion of high-dose streptokinase without a high incidence of serious bleeding.

Congenital absence of the left circumflex coronary artery in the systolic click syndrome.

The anatomy of the coronary artery circulation was examined by means of selective coronary arteriography in 19 patients, evaluated because of disabling chest pain and ECG abnormalities, with typical clinical findings of the systolic click syndrome (SCS). In 17 (89.5%), the elft circumflex coronary artery (LCCA) was absent; a single marginal branch arose from the left main vessel, but no vessel was present in or near the atrioventricular (A-V) groove. In contrast, the LCCA was identified in 74 of 78 control patients (94.9%) considered to have representative normal distribution of coronary artery branches, All but two patients with SCS exhibited reduced contraction of the segment of left ventricular (LV) myocardium surrounding the mitral valve ring (extent of systolic diameter decrease 1.4 +/- 3.1% vs normal 31.8 +/- 3.4%, P lwss than 0.001), as well as of the LV inflow tract (diameter decreasce 16.2 +/- 2.5% vs normal 38.6 +/- 1.8% P less than 0.001); both of these regions of the left ventricle derive their vascular supply from the LCCA, An identical segmental LV contraction disorder was observed in seven patients with functionally single vessel occlusive coronary artery disease involving the LCCA, An identical finding in this study was a relatively high incidence of absent LCCA (42%) in 19 patients with atypical angina and normal coronary arteriograms. It is concluded that a congenital anomaly of the coronary circulation, with absent LCCA, may be responsible for segmental myocardial dysfunction in some patients with SCS. In turn, this segmental contraction disorder may determine functional abnormality of the mitral valve apparatus.