REMODELING OF THE CORONARY-ARTERIES AFTER THROMBOLYSIS

The occurrence of coronary thrombosis leading to myocardial infarction is more closely related to disruption of an atheromatous plaque than to the severity of the stenosis caused by the plaque. The plaque disruption appears to be a spontaneous event and its mechanism remains unknown. Plaques of complex morphology are more frequently found in patients with unstable angina and myocardial infarction than in patients with stable angina. Complex plaque morphology is therefore related to coronary thrombosis, although the exact nature of this relationship is unclear. The development of coronary thrombosis may cause intermittent coronary occlusion leading to eventual or immediate persistent occlusion. Spontaneous lysis of thrombus can occur, although this is often too late to prevent myocardial infarction. The administration of fibrinolytic drugs promotes early lysis and patency, often revealing an underlying lesion of complex morphology. Remodelling occurs over the next week so that some complex lesions become smooth. Persistent complex morphology is associated with an increased incidence of subsequent unstable angina and myocardial reinfarction.