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Circulation, Vol 78, 1335-1344, Copyright © 1988 by American Heart Association

ARTICLES

Angiographic features in the infarct-related artery after intracoronary urokinase followed by prolonged anticoagulation. Role of ruptured atheromatous plaque and adherent thrombus in acute myocardial infarction in vivo

S Nakagawa, Y Hanada, Y Koiwaya and K Tanaka
First Department of Internal Medicine, Miyazaki Medical College, Japan.

To unravel sequential morphological features in infarct-related coronary arteries (IRCA), we performed coronary angiography (CAG) before, during, and immediately after intracoronary urokinase infusion in 43 consecutive patients. After 1 month of rigorous anticoagulation by intravenous heparin and subsequent oral warfarin or after the same period of treatment by antiplatelet agents, we repeated CAG in all patients except for one, who died 6 days after thrombolytic therapy. Thirty-two IRCAs were totally occluded, and 11 were severely occluded at baseline. With recanalization and/or reduction in luminal narrowing at the site of the occlusion by progressive removal of the overlying thrombus and plaque content, we recognized the development of extraluminal contrast pooling in an ellipsoid shape (type A), single or paired linear radiolucency(ies) with or without outpouching (type B), and definite outpouching (type C). The development of type A, B, and C lesions occurred in 4, 6, and 0 IRCAs immediately after thrombolytic therapy and in 0, 18, and 3 IRCAs 1 month later, respectively. Throughout the study, at least one of type A-C lesions developed in 23 of 43 (53.5%) IRCAs. Lesion development proceeded from total or severe occlusion to type A, then to type B or C, both accompanied by progressive reduction in luminal narrowing and frequent enlargement of outpouching. A postmortem study in one patient whose CAG immediately after thrombolytic therapy was interpreted as a type B lesion demonstrated a ruptured plaque with paired ridges. Serial observations in vivo indicate that many IRCAs are associated with a complex underlying spatial structure, probably composed of some part of ruptured atheromatous plaque with or without adherent thrombus. Recognition and identification of such complex structures beneath the accumulated thrombus are of great importance in both CAG interpretation and elucidation of the pathophysiological sequence of acute myocardial infarction in vivo and may enable prevention or more effective therapy of acute coronary events.

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