Abstract 15703: Coronary Plaque Instability is Associated With Carotid Arterial Inflammation Activity as Assessed by FDG PET-CT
Background: Plaque vulnerability is widespread throughout the entire coronary tree beyond the culprit vessels. In this study, we investigated whether coronary plaque instability is linked to inflammation activity of remote carotid arterial wall.
Methods: Among subjects with ACS or stable angina (SA) from July 2007 to October 2009, 75 patients (pts) [39 ACS pts (17 STEMI, 9 NSTEMI, 13 UA) vs. 36 SA pts] underwent 18F-FDG PET/CT within 1 week after diagnosis were prospectively enrolled. Carotid PET signals were quantified at the 8 slices, every 4 mm interval, extending superiorly and inferiorly from the site showing the most intense arterial FDG signals. Standardized uptake value (max, meanSUV) and mean target-to-background ratio (meanTBR; averaged arterial wall SUV/venous blood pool SUV) were measured.
Results: Baseline characteristics including statin therapy were similar except serum cholesterol (ACS vs SA; 185.4 ± 41.0 vs 162.6 ± 50.5, p=0.037). Carotid meanTBR, maxSUV, and meanSUV were significantly higher in ACS pts (ACS vs. SA; meanTBR: 1.767 ± 0.03 vs. 1.448 ± 0.03, p<0.001 (Figure); maxSUV: 2.042 ± 0.05 vs. 1.783 ± 0.04, p=0.001; meanSUV: 1.680 ± 0.036 vs. 1.520 ± 0.03, p=0.001, respectively). During 3.4 years of median follow-up period, 3 cerebrovascular events occurred in ACS group whereas none in SA (p=0.057, by log-rank test). hsCRP was significantly increased in ACS patients compared to SA pts (ACS vs. SA; 11.93 ± 24.75 vs. 2.24 ± 2.11, p=0.019).
Conclusions: This study provided in vivo evidence that the patients presenting with ACS have increased inflammation activity in the vascular wall of remote carotid arterial districts. Our findings suggest that widespread activation of inflammation could contribute to instability at remote vascular plaques in patients with coronary plaque instability.
- © 2013 by American Heart Association, Inc.