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European Heart Journal 1996 17(10):1488-1494;
Copyright © 1996 by the European Society of Cardiology.
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© 1996 The European Society of Cardiology

Coronary stenosis progression differs in patients with stable angina pectoris with and without a previous history of unstable angina

J. C. Kaski, L. Chen, R. Crook, I. Cox, D. Tousoulis and M. R. Chester

Coronary Artery Disease Research Group, Department of Cardiological Sciences, St. George's Hospital Medical School London, U.K.

accepted 4 January 1996.

Juan Carlos Kaski, MD, Head, Coronary Artery Disease Research Group, Department of Cardiological Sciences, Disease Research Group, Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, U.K.

Abstract

OBJECTIVES: To compare the evolution of stenoses respon sible for acute coronary events with those not associated with acute coronary syndromes.

METHODS AND RESULTS: We prospectively studied angiographic stenosis progression in 190 stable angina patients, with single vessel disease, who were awaiting non-urgent coronary angioplasty. Sixty four patients had a previous history of unstable angina (Group I) and 126 patients had no history of unstable angina (Group 2). Culprit stenoses were classified as ‘complex’ or ‘smooth’. At restudy, 8 ± 4 months after the first angiogram, 12 of 63 culprit stenoses in Group 1 had progressed and seven of 125 in Group 2 (19% vs 6%, P=0·004) Thirteen of 68 complex culprit stenoses had progressed, compared with only 6 of 120 smooth culprit stenoses (l9% vs 5%, P=0·003). Coronary events occurred in 12 Group I patients and nine Group 2 patients (P=0·02).

CONCLUSIONS: In patients with stable angina, stenoses associated with previous episodes of unstable angina are more likely to progress than stenoses not associated with previous unstable angina. Unstable coronary atherosclerotic plaques, even those that have been clinically stable for more than 3 months, may retain the potential for rapid progression to total occlusion.

(Eur Heart J 1996; 17: 1488–1494)

Key Words: Rapid disease progression • complex stenoses • unstable angina


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