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(Circulation. 1998;97:10-11.)
© 1998 American Heart Association, Inc.

Editorials

Pathophysiological Insight Into the Possible Optimal Therapies for Acute Myocardial Infarction and Unstable Angina

Richard W. Smalling, MD, PhD; ; H. Vernon Anderson, MD

From the Division of Cardiology, Department of Medicine, The University of Texas Medical School at Houston and The Hermann Heart Center, Hermann Hospital, Houston, Tex.

Correspondence to Richard W. Smalling, MD, PhD, UT-Houston Medical School, 6431 Fannin, Room 1.246, Houston, TX 77030.

Key Words: myocardial infarction • thrombolysis

The optimal treatment of unstable ischemic coronary syndromes has not been settled, and little in vivo pathological information in humans has been available to help guide the care of patients with these complicated problems. Dr Van Belle and colleagues¹ have given us new insight into the underlying pathophysiological substrate in patients sustaining acute myocardial infarction who then underwent coronary angioscopy before coronary interventions up to 1 month after their index event. Of these patients, 98% were treated with aspirin, 66% had thrombolytic therapy, and 100% had been treated with heparin for at least 72 hours after admission. Despite this intense antithrombotic regimen, the residual lesions were angiographically severe in 76%, and complete occlusions were found in 14% of the patients. By angioscopy, the majority of the infarct-related lesions were yellow (79%), and many were ulcerated (36%) or had visible residual thrombus (77%). Eighteen percent of the patients had large clumps of platelets adherent to the plaque, even late in the course after infarction. The fact that these plaques remained "active" for up to 30 days is quite interesting and unsettling. There was an equal prevalence of yellow ulcerated plaques with thrombus, whether they were studied between 0 and 10 days or 10 and 30 days after admission. Furthermore, the use of thrombolytics seemed to promote an increased incidence of ulcerated plaques, and adherent thrombus, although smaller, was still present. Other investigators have suggested that mechanical restoration of infarct artery patency reduces both the incidence of "active" plaques and the presence . . . [Full Text of this Article]

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