Evaluation of Carotid Plaque Neovascularization in Patients With Coronary Heart Disease on Contrast‐Enhanced Ultrasonography

OBJECTIVES: To examine the repeatability of quantitative time-intensity curve analysis of neovascularization within carotid plaques with contrast-enhanced ultrasonography (US) and to investigate carotid plaque neovascularization in patients with coronary heart disease using contrast-enhanced US and the correlation between risk factors and acute coronary syndrome (ACS). METHODS: Sixty patients with ACS and 60 with stable coronary artery disease (CAD) underwent conventional carotid and contrast-enhanced US, and plaque enhancement was observed and analyzed quantitatively. Carotid contrast-enhanced US was performed within 1 month of ACS occurrence. Interobserver and intraobserver variability of the measurements was assessed. The peak signal intensity was the maximum number of contrast microbubbles that local tissues could accumulate, reflecting the local microvascular density and representing the capillary volume. RESULTS: The ACS group had higher low-density lipoprotein cholesterol (mean ± SD, 3.21 ± 0.75 versus 2.53 ± 0.71 mmol/L; P < .01) and high-sensitivity C-reactive protein (CRP; 3.76 ± 0.19 versus 2. 93 ± 0.15 mg/L; P < .01) levels than the stable CAD group. The proportion of soft plaques in the ACS group (81%) was higher than in the stable CAD group (53%). The proportion of plaque enhancement, peak signal intensity, and plaque-to-carotid lumen enhancement intensity ratio were higher in the ACS group than the stable CAD group. The peak signal intensity was correlated with the high-sensitivity CRP value. Logistic regression analyses indicated that age (65-74 years), high-sensitivity CRP, and enhancement intensity were correlated with the occurrence of ACS. The sensitivity and specificity of the peak signal intensity in carotid plaques were 80.0% and 88.3%, respectively (cutoff value, 9.97 dB; area under the receiver operating characteristic curve, 0.865). The time-intensity curve measurements had good repeatability. CONCLUSIONS: Carotid plaque enhancement is a potential independent risk factor for ACS occurrence. These results illustrate the correlation of carotid plaque vulnerability with the coronary artery symptomatic state according to the common pathogenetic mechanism of atherosclerosis.