Abstract

We performed a histologic analysis of coronary lesions obtained by directional atherectomy from 100 patients with stable, unstable and evolving angina pectoris. Histologic analysis was performed by two pathologists unaware of the clinical history or angiographic findings. This included notation of the presence or absence of various matrix components and quantitative scoring (0-3+) of cellular lesion components. Forty-seven patients (47%) had native coronary lesions. Twenty-five patients (25%) had restenosis after previous balloon angioplasty and twenty-eight (28%) were treated for primary saphenous vein graft disease. There were no differences in the average histologic appearance of atherosclerotic lesions resulting in stable, unstable and evolving angina pectoris. Saphenous vein graft lesions were typically rich in dense connective tissue and extracellular lipid and mononuclear infiltrate. Restenosis lesions were rich in acid mucopolysaccharide and vascular smooth muscle cells and revealed no histologic differences according to the clinical syndrome. Native coronary artery lesions, from patients with unstable angina, more often contained organizing thrombi (30% vs 0%, P < 0.05), cholesterol crystals (20% vs 0%, P < 0.05) and harbored a more intense vascular smooth muscle cell infiltrate (2.1 vs 1.4, P < 0.05) when compared to lesions from patients with stable angina pectoris. There was no difference in the intensity of inflammatory or foam cell infiltration. Vascular smooth muscle cells, appearing as intimal hyperplasia, are more prominent in lesions resulting in unstable angina. There is, however, no difference in the intensity of inflammatory or foam cell infiltrate. The histologic appearance of coronary lesions producing the syndrome of unstable angina pectoris is quite heterogenous. In order to establish the role of inflammation in the development of non-fatal acute coronary syndromes, improved sampling methods or a larger sample size will be required.

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