Intermittent Coronary Occlusion in Acute Myocardial Infarction

We performed continuous electrocardiographic ST-segment monitoring and serial coronary adenography in 45 consecutive patients presenting in the early stages of acute myocardial infarction. During cardiac catheterization, 28 episodes of arteriographically confirmed coronary reopening and subsequent reocclusion were observed in 16 patients before (3 episodes) and during (25 episodes) continuous intracoronary infusion of streptokinase. In addition, ST-segment monitoring demonstrated 12 episodes of spontaneous transient return of the ST segment to the base line in eight patients between the time of admission and the performance of coronary arteriography. During arteriographically documented reocclusion, intracoronary isosorbide dinitrate (2 mg) reestablished the patency of the coronary artery within one to two minutes in 14 of 28 episodes that occurred in 11 of 16 patients. After streptokinase infusion, intracoronary administration of isosorbide dinitrate was followed by dilatation of the infarct-related stenosis from a mean value (±SD) of 1.12±0.3 mm (58.1±12.1 percent) to 1.33±0.4 mm (51.6± 12.9 percent; P = 0.004). Spontaneous intermittent coronary recanalization and reocclusion resulting from a variable combination of thrombosis and vasoconstriction are frequent during the early phase of acute myocardial infarction. We propose that the combination of intracoronary streptokinase and isosorbide dinitrate may increase the rate of stable coronary recanalization. (N Engl J Med 1987; 317:1055–9.) IN patients with acute myocardial infarction, the onset of continuous chest pain is the usual clinical marker of coronary occlusion. However, the interval between the onset of chest pain and the development of electrocardiographic signs of myocardial infarction in patients appears to be much more variable than the same interval after sudden coronary occlusion is induced in animals. 1 In some patients Q waves may appear on the electrocardiogram within less than one hour, but in others they appear only several hours after the onset of symptoms. This variability is usually attributed to differences in the development of collateral vessels or . . .