Compensatory enlargement and stenosis develop in ApoE(-/-) and ApoE*3-Leiden transgenic mice

Atherosclerotic mouse models develop little ischemic organ damage and no in farctions, despite the presence of large atherosclerotic lesions. Therefore , we hypothesize that luminal changes do not follow atherosclerotic lesion development. Because a phenomenon that may explain the discrepancy between luminal changes and lesion size is vascular remodeling, we measured paramet ers of vascular remodeling in the carotid arteries (CAs), thoracic aorta (T A), and abdominal aorta (AA) of apolipoprotein E (apoE)-deficient (apoE(-/- )) and apoE*3-Leiden mice, 2 well-known mouse models of atherosclerosis. At herosclerotic lesions were classified (American Heart Association [AHA] typ es II through V), and plaque thickness, compensatory enlargement versus con strictive remodeling, lumen diameter, stenosis, and media thickness were me asured relative to the nondiseased arterial wall. In CAs, plaque thickness increased during atherogenesis. CAs showed compensatory enlargement (apoE(- /-) 55%, apoE*3-Leiden 38%). Regression analysis revealed a positive correl ation between plaque and lumen area (for apoE(-/-), R=0.95; for apoE*3-Leid en, R=0.90). Medial thinning and elastolysis were also observed. During ath erogenesis, lumen diameter decreased (apoE(-/-) -69%, apoE*3-Leiden -40%), and stenosis > 70% developed. TA and AA showed similar features, but neithe r developed a progressive decrease in lumen diameter or stenosis > 70%. In CAs, TA, and AA of apoE(-/-) and apoE*3-Leiden mice, atherogenesis is assoc iated with compensatory enlargement, medial thinning, and elastolysis. A pr ogressive decrease in lumen diameter and stenoses > 70% occur only in CAs. Vascular remodeling is more prominent in apoE(-/-) mice.