August 19, 2020
JACC: Journal of the American College of Cardiology
TAKE-HOME MESSAGE
- This study used data from 12,149 ARIC study participants to evaluate the relationship between two variables, elevated plasma Lp(a) and a family history (FHx) of coronary heart disease (CHD), and risk of atherosclerotic disease (ASCVD) and CHD over 21 years of follow-up. Eligible participants were initially free of prevalent heart disease. There were independent associations between both variables, Lp(a) and FHx of CHD, and ASCVID (HR, 1.17 and 1.24, respectively). ASCVD risk was higher for individuals with elevated Lp(a) or FHx versus individuals without either risk factor. People with both elevated Lp(a) and FHx were at higher risk than those with neither risk factor or just one risk factor.
- When elevated Lp(a) and FHx were added to a model, risk reclassification and discrimination indices were improved. FHx and Lp(a) are cardiovascular risk factors and may be useful in making decisions regarding primary prevention, although further research is needed to determine the best way to incorporate them into clinical decision-making.
Abstract
This abstract is available on the publisher’s site.
BACKGROUND
Elevated lipoprotein(a) (Lp[a]) and family history (FHx) of coronary heart disease (CHD) are individually associated with cardiovascular risk, and Lp(a) is commonly measured in those with FHx.
OBJECTIVES
The aim of this study was to determine independent and joint associations of Lp(a) and FHx with atherosclerotic cardiovascular disease (ASCVD) and CHD among asymptomatic subjects.
METHODS
Plasma Lp(a) was measured and FHx was ascertained in 2 cohorts. Elevated Lp(a) was defined as the highest race-specific quintile. Independent and joint associations of Lp(a) and FHx with cardiovascular risk were determined using Cox regression models adjusted for cardiovascular risk factors.
RESULTS
Among 12,149 ARIC (Atherosclerosis Risk In Communities) participants (54 years, 56% women, 23% black, 44% with FHx), 3,114 ASCVD events were observed during 21 years of follow-up. FHx and elevated Lp(a) were independently associated with ASCVD (hazard ratio [HR]: 1.17; 95% confidence interval [CI]: 1.09 to 1.26, and HR: 1.25; 95% CI: 1.12 to 1.40, respectively), and no Lp(a)-by-FHx interaction was noted (p = 0.75). Compared with subjects without FHx and nonelevated Lp(a), those with either elevated Lp(a) or FHx were at a higher ASCVD risk, while those with both had the highest risk (HR: 1.43; 95% CI: 1.27 to 1.62). Similar findings were observed for CHD risk in ARIC, in analyses stratified by premature FHx, and in an independent cohort, the DHS (Dallas Heart Study). Presence of both elevated Lp(a) and FHx resulted in greater improvement in ASCVD and CHD risk reclassification and discrimination indexes than either marker alone.
CONCLUSIONS
Elevated plasma Lp(a) and FHx have independent and additive joint associations with cardiovascular risk and may be useful concurrently for guiding primary prevention therapy decisions.