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(Circulation. 1995;92:2033-2035.)
© 1995 American Heart Association, Inc.

Articles

Angina Pectoris and Disease Progression

Erling Falk, MD, PhD; Valentin Fuster, MD, PhD

From Mount Sinai Medical Center, New York, NY.

Correspondence to Valentin Fuster, MD, PhD, Director, Cardiovascular Institute, Mount Sinai Medical Center, One Gustave L. Levy Pl, Box 1030, New York, NY 10029-6574.

Key Words: Editorials • angina • angiography • plaque • prognosis

	Introduction

 
A seemingly paradoxical finding for years puzzled cardiologists who were engaged in evaluating coronary angiograms: the number and severity of coronary stenoses were similar in patients with stable and unstable angina, despite the worse short-term prognosis of the latter.^{1 2} In 1985, Ambrose et al³ offered an explanation that since has been confirmed by many others: the difference between these two ischemic syndromes relates to the morphology of the culprit lesion rather than the number and severity of coronary stenoses. The distinct angiographic morphology characteristically seen in unstable angina was originally classified as a type II eccentric lesion and described as "an asymmetric stenosis usually in the form of a convex intraluminal obstruction with a narrow base or neck, due to one or more overhanging edges or borders that were very irregular or scalloped."³ Culprit stenoses in unstable angina, however, are not necessarily eccentric, and the term "complex" lesions is now generally preferred. Postmortem studies and coronary angioscopy in living patients have revealed that plaque disruption, often with superimposed nonocclusive thrombosis, is usually responsible for the "complex" morphology seen by angiography.^{4 5 6}

In patients with angina pectoris, previous studies on short-term prognosis have focused primarily on unstable angina-producing stenoses, ie, culprit lesions. Patients with stable or unstable angina pectoris, however, have many nonculprit plaques in their coronary arteries that could also influence the prognosis. Nonetheless, not much attention has been paid to nonculprit plaques in such patients. Therefore, the approach taken by Kaski, Chen, and colleagues,^{7 8} assessing the entire coronary tree rather . . . [Full Text of this Article]

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