Prediction of atherosclerotic plaque ruptures with high-frequency ultrasound imaging and serum inflammatory markers

Prediction of atherosclerotic plaque ruptures with high-frequency ultrasound imaging and serum inflammatory markers. Am J Physiol Heart Circ Physiol 293: H2836-H2844, 2007. First published August 17, 2007; doi:10.1152/ajpheart.00472.2007.-Atherosclerotic plaque rupture and thrombosis are the main causes of acute coronary syndrome. In the present study, we investigated whether ultrasound imaging and inflammatory parameters are predictive of plaque rupture in a newly established animal model. We developed a rabbit model for plaque rupture by locally delivering recombinant p53 adenovirus to plaques in rabbits fed a high-cholesterol diet for 10 wk, and plaque rupture was triggered using Chinese Russell's viper venom and histamine. We found that 81.1% of rabbits transfected with p53 (n = 37) had the ruptured plaques, which was significantly higher than results in rabbits transfected with the control vector (26.3%,n = 38; P < 0.001). Among measured biomarkers, high-sensitive C-reactive protein, soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1 were significantly different between rabbits with and without ruptured plaques. Using high-frequency duplex and intravascular ultrasound imaging techniques, we obtained a list of parameters. With the multivariate logistic regression model, we identified that plaque eccentric index, plaque area, high-sensitive C-reactive protein, and corrected integrated backscatter intensity were significant predictors of plaque rupture, with odds ratios of 7.056 [95% confidence interval (CI): 1.958, similar to 25.430], 1.942 ( 95% CI: 1.058, similar to 3.564), 1.025 ( 95% CI: 1.007, similar to 1.043), and 0.856 ( 95% CI: 0.775, similar to 0.946), respectively. Localized p53 overexpression technique induces plaque rupture, and the combined measurement of ultrasound and biochemical markers is a valuable tool in predicting plaque rupture.