Abstract

Synopsis: Early detection of arterial wall thickening, the subclinical phase of atherosclerosis, may be useful for identifying individuals at risk for future cardiovascular events. Carotid intima media thickness (CIMT)-assessed rate of atherosclerosis progression is a risk factor for clinical cardiovascular events, but the relationships between various coronary heart disease (CHD) risk factors and CIMT progression are unclear. Purpose: The aim of this study was to investigate associations between CHD risk markers and CIMT progression in individuals at moderate CHD risk. Methods: Participants included men (45–75 years) and women (55–74 years) in the control arm of a clinical trial. All had at least one major CHD risk factor and baseline posterior CIMT 0.7–2.0 mm, without significant stenosis. Posterior wall (n = 134) and anterior wall with contrast (n = 72) CIMT were assessed by the use of high-resolution B-mode ultrasound at baseline, 12 months and ∼18 months. Fasting lipoprotein lipid, apolipoprotein (apo), inflammatory, and oxidative stress markers were evaluated. Results: Anterior wall CIMT was significantly greater at baseline than posterior wall CIMT (0.86 vs 0.77 mm, P < .001). On average, posterior wall CIMT progressed and anterior wall CIMT regressed (0.0091 vs −0.0164 mm/yr, respectively, P = .014). Baseline CIMT was inversely associated (P < .001) with CIMT progression in both walls. After adjustment for baseline CIMT, significant predictors of anterior wall CIMT progression in linear regression analyses included triglycerides (TG, P = .006), high-density lipoprotein cholesterol (HDL-C, inverse, P = .006), and ratios, including total cholesterol (TC)/HDL-C (p=0.013), TG/HDL-C (P = .005), and Apo B/HDL-C (P = .021). Significant baseline CIMT-adjusted predictors of posterior CIMT progression included TC (P = .028), low-density lipoprotein cholesterol (LDL-C, P =.035), non-HDL-C (P =.004), TG (P =.016), apoB (P =.005), and ratios of TC/HDL-C (P < .001), TG/HDL-C (P =.015), apoB/apoA1 (P =.012), and apoB/HDL-C (P =.004). Oxidative stress and inflammatory markers were generally unrelated to CIMT progression. Conclusions: The strongest predictors for CIMT progression in anterior and posterior walls were lower baseline CIMT, increased TG, and elevated lipid ratios, including TC/HDL-C, TG/HDL-C, and apoB/HDL-C. Non-HDL-C was a stronger predictor than LDL-C. These results support the hypothesis that TG-rich lipoproteins are associated with CIMT progression, either directly, or as an indicator of a greater number of circulating atherogenic particles.

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