Abstract

Introduction: Racial differences in Lp(a) distributions are well known, with higher levels in Black adults compared to White adults. It is unclear whether the risk implications of higher Lp(a) levels are the same in Black and White adults. Furthermore, the contribution of racial differences in Lp(a) to disparities in ASCVD in the US has not been well characterized in long-term cohort studies. Objective: We evaluated the relative risk associations for higher Lp(a) and estimated the related population-attributable fraction (PAF) for ASCVD in Black and White adults. Methods: We performed a prospective analysis of 9,519 Black and White participants at ARIC Visit 4 (1996-1999) without baseline ASCVD. Plasma Lp(a) was measured from stored Visit 4 plasma samples using an apo(a) isoform-insensitive assay (Denka Seiken). Lp(a) was categorized as <30, ≥30 to <50, 50≥ to <100 and ≥100 mg/dL. We assessed the association of higher Lp(a) categories with incident coronary heart disease (CHD) and ASCVD (CHD and ischemic stroke) overall and stratified by race, with tests for interaction. We calculated the PAF for ASCVD and CHD associated with Lp(a) ≥30 mg/dL, overall, and for Black and White adults. Results: The mean age was 63±6 years, with 59% women and 23% Black adults. There was a higher prevalence of Lp(a) > 30 mg/dL among Black than White adults (54 vs 24%). During a follow-up of 24 years, there were 2,235 ASCVD and 1,715 CHD events. Higher Lp(a) categories were associated with progressively higher risk, with Lp(a) ≥100 mg/dL associated with hazard ratios of 1.71 (95% CI 1.38-2.12) for ASCVD and 1.67 (1.30-2.13) for CHD, with no significant differences by race (Table). The PAF associated with elevated Lp(a) was two times higher in Black than White adults for ASCVD (10.7 vs 4.7%) and CHD (10.5 vs 4.3%). Conclusion: Differences in Lp(a) distributions likely contribute to racial disparities in ASCVD. Evolving therapies targeting Lp(a) lowering could assist in addressing disparities in ASCVD.

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