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(Circulation. 1995;91:2295-2298.)
© 1995 American Heart Association, Inc.

Articles

Angiographic and Clinical Progression in Unstable Angina

From Clinical Observations to Clinical Trials

Pierre Théroux, MD

From the Department of Medicine, Montreal Heart Institute, Montreal, Quebec, Canada.

Correspondence to Pierre Théroux, MD, Montreal Heart Institute, 5000 Belanger Street, Montreal, Quebec, HIT 1C8, Canada.

Key Words: Editorials • angiography • angina • clinical trials

	Introduction

 
Chen et al¹ took advantage of a long waiting list for coronary angioplasty at their institution to describe the angiographic and clinical evolution of coronary lesions causing unstable angina. The study involved a small number of patients, with no controls. Patients enrolled were highly selected and treated unconventionally, at least by North American standards. The authors assessed lesion severity by quantitative coronary angiography and lesion morphology by conventional descriptors.

The data confirmed the many previous observations of complex lesions in unstable angina^{2 3} and emphasized their rapid progression.^{4 5} More importantly, they provided an opportunity to discuss new challenging concepts in unstable angina.

	Angiographic Anatomy of Culprit Coronary Lesions

 
Although coronary angioscopic and endovascular ultrasound studies have stressed its limitations, angiography is the only widely used diagnostic test in clinical practice. Angiographic morphology has clear clinical implications to evaluate pathophysiology^{2 3} and prognosis^{6 7} and to orient treatment, including coronary angioplasty.⁸ Particularly relevant findings in addition to the conventional description of the severity and number of lesions are ulcerations, filling defects, eccentricity, and irregularities.^{2 7}

	Progression Versus Occlusion

 
Progression and progression to complete occlusion are usually considered at the same level of significance in angiographic studies of lesion evolution. The two findings, however, may correspond to different pathophysiological mechanisms.⁹ In the study by Chen et al,¹ 72% of patients with a coronary event showed progression. Of the 29 lesions that progressed, 69% progressed to complete occlusion. This progression was independent of conventional risk factors and of the extent of coronary disease. Progression was also the hallmark of culprit lesions, occurring in 25% of the . . . [Full Text of this Article]

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