Early Contributors to Healthy Arterial Aging Versus Premature Atherosclerosis in Young Adults: The Bogalusa Heart Study

Abstract

Background Early identification of healthy arterial aging versus premature atherosclerosis is important for optimal atherosclerotic cardiovascular disease risk stratification and prevention. We sought to identify predictors for the long‐term absence of carotid plaque among young adults. Methods and Results We included 508 participants from the Bogalusa Heart Study without clinical atherosclerotic cardiovascular disease who were free of carotid plaque at baseline (2001–2002) and underwent ultrasound imaging at follow‐up (2013–2016). Modified Poisson regression estimated the persistent absence of plaque over 12.8 years. Participants were on average age 36.2 years at baseline, 64% were women, and 29% were Black. Although nearly all participants (97%) had a 10‐year atherosclerotic cardiovascular disease risk <7.5%, there were 162 people (32%) who developed premature atherosclerosis. Aside from younger age (risk ratio [RR], 1.21; 95% CI, 1.07–1.36, per 10 years) and a total cholesterol/high‐density lipoprotein cholesterol ratio <3.5 (RR, 1.15; 95% CI, 1.01–1.30), normal values of traditional risk factors did not predict long‐term absence of plaque. Independent from traditional markers including glomerular filtration rate, serum calcium‐phosphate product (RR, 1.07; 95% CI, 1.01–1.14, per 1‐SD lower), phosphate (RR, 1.15; 95% CI, 1.03–1.29, per 1 mg/dL lower), and dietary sodium <2300 mg/day (RR, 1.20; 95% CI, 1.02–1.41) were significantly associated with the non‐development of plaque. Conclusions Nearly one third of young adults with a low burden of traditional risk factors developed premature atherosclerosis. Beyond younger age and an ideal lipoprotein profile, lower calcium‐phosphate homeostasis and low sodium intake were associated with long‐term absence of carotid plaque. These results suggest that dietary and intrinsic minerals are early contributors to the development of arterial aging phenotypes.