Abstract

To detect the optimal predictors of vulnerable atherosclerotic plaques. Forty New Zealand white rabbits underwent balloon-induced abdominal aortic wall injury and were fed a high cholesterol and saturated fat diet containing 1% cholesterol for 8 weeks. Rabbits were then randomly divided into two groups: group A (n = 20, the aortic segments rich in plaques were incubated transluminally with recombinant adenovirus carrying p53) and group B [n = 20, incubated transluminally with β galactosidase (LacZ) genes]. Two weeks later, rabbits underwent pharmacological triggering with injection of Chinese Russell's viper venom (CRVV) and histamine. Before pharmacologically triggering, concentrations of hs-CRP, sVCAM-1 and sICAM-1 were measured by means of Enzyme-linked-immunosorbent assay (ELISA). Fibrinogen was analyzed by nephelometer. Ultrasound imaging, accuracy densitometry (AD) examination and intravascular ultrasound (IVUS) were performed to analyze the in vivo features of vulnerable plaques. Logistic regression was used to detect the predictors for vulnerable plaques. The ratio of plaque rupture after pharmacological triggering was significantly higher in group A (89.5%, 17/19) than in group B (22.2%, 4/18). Serum hs-CRP level was significantly higher in plaque rupture group than in non-rupture group before pharmacological triggering (P < 0.05). In the meantime, parameters derived from ultrasound imaging [intima-media thickness (IMT) and peak velocity (VP), values of accuracy densitometry], measurements of IVUS [external elastic membrance area (EEMA), plaque area (PA), plaque burden (PB), eccentric index (EI) and remodeling index (RI)] were significantly larger in plaque rupture group than in non-rupture group. Logistic regression showed that EI (OR = 26.917), PA (OR = 19.301), sVCAM-1 (OR = 1.339) and AII-c% (OR = 0.458) were independent predictors for plaque rupture (all P < 0.05). The major predictors of vulnerable plaques were eccentric index (EI) and plaque area (PA), sVCAM-1 and AII-c% in this model.

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