Abstract P175: Predicting Healthy Arterial Aging Versus Premature Atherosclerosis In Young Adults: The Bogalusa Heart Study

Abstract

Introduction: Early differentiation of healthy arterial aging versus premature atherosclerosis is important for optimal atherosclerotic cardiovascular disease (ASCVD) risk stratification and prevention. We sought to identify predictors for the long-term absence of carotid plaque in young adults. Hypothesis: Calcium and phosphate are found in excess in atherosclerotic lesions, therefore we hypothesized that mineral markers may help to explain residual heterogeneity in arterial aging phenotypes beyond traditional ASCVD risk factors. Methods: We included 508 participants from the Bogalusa Heart Study without clinical ASCVD who were free of carotid plaque at baseline (2001-02) and underwent ultrasound at follow-up (2013-16). Modified Poisson regression estimated the persistent absence of carotid plaque over 12.8 years. Results: Participants were on average 36.2 years old at baseline, 64% were women, and 29% were African American. Although a majority (97%) of participants had a 10-year ASCVD risk <7.5%, only 68% remained free of plaque ( Figure ). Beyond younger age (RR=1.20, 95% CI: 1.07-1.36, per 10 years) and a total cholesterol-HDL-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=1.08, 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: 1.03-1.41) significantly associated with non-development of plaque. Conclusions: Lower calcium-phosphate homeostasis and low sodium intake independently associated with long-term absence of carotid plaque. However, nearly one-third of young adults with a relatively low burden of traditional risk factors developed premature atherosclerosis. These results suggest that dietary and intrinsic minerals are early contributors to the development of arterial aging phenotypes.