The biologic behavior of balloon hyperinflation-induced arterial lesions in hypercholesterolemic pigs depends on the presence of foam cells.

Lack of a large-animal model of accelerated atherosclerosis has limited study of the biologic behavior of atherosclerotic lesions. We hypothesized that mechanical vascular trauma combined with diet-induced hypercholesterolemia would result in rapid development of complex atherosclerosis-like lesions. Accordingly, we induced deep injury to a carotid artery by repetitive balloon hyperinflations in minipigs that were fed either an atherogenic diet (n = 30) or a standard diet (controls, n = 4) and examined the resultant lesions 1 month later. The neointimal lesions that evolved in 23 patent vessels from cholesterol-fed animals were complex, exhibiting infiltration of smooth muscle and foam cells and evidence of organized thrombus, recent thrombus, hemorrhage, and calcification. Lesions were separable histologically into two groups: foam-cell rich (n = 12), with 33 +/- 10 foam cells per high-power field, and foam-cell poor (n = 11), with 4 +/- 1 foam cells per high-power field. Minipigs with foam cell-rich lesions had higher serum cholesterol levels than those with foam cell-poor lesions (712 +/- 178 vs 468 +/- 240 mg/dL, P < .02). The incidence of intralesional thrombus was also significantly greater in foam cell-rich than in foam cell-poor lesions (50% vs 9%, P < .04). In addition, the degree of luminal stenosis was greater in the presence of lesions containing thrombus compared with those without thrombus (60 +/- 38% vs 30 +/- 29%, P = .05). Lesions in the control animals were fibrocellular and lacked foam cells and thrombus. Thus, hypercholesterolemia appeared to affect lesion composition and behavior.(ABSTRACT TRUNCATED AT 250 WORDS)