Objective. Carotid distensibility (CD) is a measure of carotid artery elasticity that has been introduced as a risk factor for cardiovascular disease. Information regarding reproducibility of sonographic CD measures is limited. The objective of this study was to evaluate the inter-reader reliability of sonographic measurements of common carotid artery (CCA) diameters and derived metrics of CD. Methods. Two independent readers (R1 and R2) measured the systolic diameter (SD) and diastolic diameter (DD) for the right CCA from the B/M-mode sonographic registrations among 118 subjects. The derived CD metrics (strain, elastic modulus [E], stiffness [β], and CD) were calculated. The inter-reader type 3 intraclass correlation coefficients (ICC3,1) for carotid diameters were calculated. Results. The mean SDs ± standard deviation were 7.15 ± 1.43 mm for R1 and 7.24 ± 1.43 mm for R2. The mean DDs were 6.71 ± 1.36 mm for R1 and 6.68 ± 1.41 mm for R2. The mean differences of SD and DD between R1 and R2 were 0.08 ± 0.40 mm (paired t test, P = .04) and 0.03 ± 0.43 mm (paired t test, P = .46), respectively. Inter-reader type 3 intraclass correlation coefficients were 0.96 for SD and 0.95 for DD. We observed a significant association of demographics with carotid diameters but not with derived CD metrics or risk factors. Conclusions. Our results suggest good reproducibility of CCA diameters measured with B/Mmode sonography. However, very small changes in linear measurements of carotid diameters can have big effects on estimates of arterial mechanical properties such as strain and Young's modulus. The standard boundary identification methods may not be precise and reproducible enough for use in a clinical setting.

Background Subclinical atherosclerotic plaque is an important marker of increased vascular risk. Identifying factors underlying the variability in burden of atherosclerotic carotid plaque unexplained by traditional vascular risk factors may help target novel preventive strategies. Methods As a part of the carotid substudy of the Northern Manhattan Study (NOMAS), 1,790 stroke-free individuals (mean age 69±9; 60% women; 61% Hispanic, 19% black, 18% white) were assessed for total plaque area (TPA) burden using 2D carotid ultrasound imaging. Multiple linear regression models were constructed. Model 1 used pre-specified traditional risk factors: age, sex, LDL-cholesterol, diabetes mellitus, pack-years of smoking, blood pressure (BP), and treatment for BP; and Model 2, an addition of socioeconomic and less traditional risk factors. The contributions of the components of the Framingham heart risk score (FRS) and the NOMAS global vascular risk score (GVRS) to the TPA were explored. Results Prevalence of carotid plaque was 58%. Mean TPA was 13±19mm2. Model 1 explained 19.5% of the variance in TPA burden (R2=0.195). Model 2 explained 21.9% of TPA burden. Similarly, FRS explained 18.8% and NOMAS GVRS 21.5% of the TPA variance. Conclusions The variation in preclinical carotid plaque burden is largely unexplained by traditional and less traditional vascular risk factors, suggesting that other unaccounted environmental and genetic factors play an important role in the determination of atherosclerotic plaque. Identification of these factors may lead to new approaches to prevent stroke and cardiovascular disease.

BACKGROUND AND PURPOSE The genetic influence on carotid atherosclerotic plaque is mostly unknown. This study examines the association between carotid plaque and single nucleotide polymorphisms (SNPs) in selected genes implicated in inflammation and endothelial function. METHODS A total of 43 genes (197 SNPs) involved in inflammation and endothelial function were interrogated in 287 Dominicans from the Northern Manhattan Study (mean age 64±7 years, 58% women) who had undergone high-resolution B-mode ultrasound for examination of carotid plaque. Using an additive genetic model, multiple logistic regression analyses were conducted, a within gene haplotype analysis was performed and interactions between genes were examined. Results were validated in an independent set of 301 Dominicans. RESULTS Carotid plaque was present in 143(47%) participants. Nine genes had at least one SNP associated (p≤0.01) with carotid plaque phenotypes: TNF, NOS2A, IL6R, TNFSF4, PPARA, IL1A, TLR4, ITGA2, HABP2. SNPs in TNFSF4, PPARA, TLR4, ITGA2, and HABP2 were also implicated with the same carotid phenotype in the validation analysis. Haplotype analysis revealed an additional gene of interest, VCAM1. CONCLUSIONS We report novel associations between variations in ten genes involved in inflammation and endothelial function and carotid plaque phenotypes in a Dominican sample, with replication for five genes in an independent Dominican sample.