Increased intimal apoptosis in coronary atherosclerotic vessel segments lacking compensatory enlargement

Objectives In a histopathologic study, we. assessed the balance of cell pro liferation and apoptosis by counting the number of apoptotic and proliferat ing cell nuclear antigen-positive cells in freshly harvested atherectomy sp ecimens from 34 patients. Background Remodeling of human coronary, arteries is an adaptive process th at alters vascular lumen size. Methods Intravascular ultrasound was performed prior to atherectomy. Total vessel area (area within the external elastic lamina [EEL]), lumen area and plaque area were measured at the region of interest (ROI), and at a proxim al and distal reference segment, utilizing the formula Delta(%) = 100 x (RO I-reference segment)/reference segment. Positive arterial remodeling (R+) r esulting in luminal expansion was defined as Delta EEL >10%. Absence of rem odeling (0 < <Delta>EEL <10%) and constrictive arterial remodeling (<Delta> EEL <0) were considered as neutral remodeling (R0) and negative remodeling (R-), respectively. Results In R- lesions, apoptotic indices (APO) were significantly elevated (17.17<plus/minus>2.19%) compared with R+ lesions (4.89 +/-1.7%; p=0.0007). In a rabbit iliac percutaneous transluminal coronary angioplasty model int imal. apoptosis was increased four weeks after balloon angioplasty injury ( APO 8.8 +/-0.03%) compared with contralateral untreated segments (APO 3.0 /-0.04%, n=6). Lesions with an EEL/intimal area <3.0 showed significantly m ore intimal apoptosis than untreated lesions (p=0.02). Conclusions The data indicate that constrictive remodeling of atherosclerot ic coronary lesions is associated with increased apoptosis of intimal cells . We speculate that increased apoptosis is due to extensive plaque healing after episodes of symptomatic or asymptomatic plaque rupture, (J Am Coll Ca rdiol 2001;38:1333-9) (C) 2001 by the American College of Cardiology.