Key result
Elevated Lp(a) >50 mg/dL is linked to ~24% higher ASCVD risk across all CAC strata.
Why the study?
The utility of coronary artery calcium scoring in individuals with elevated lipoprotein(a) for ASCVD risk assessment is unclear due to Lp(a)'s propensity toward noncalcified plaque.
Does elevated Lp(a) increase the risk of incident ASCVD across different strata of coronary artery calcium scores in individuals without known ASCVD?
Cohort (n=11,319)
Yes
Does elevated Lp(a) increase the risk of incident ASCVD across different strata of coronary artery calcium scores in individuals without known ASCVD?
Elevated Lp(a) is associated with a higher relative risk for ASCVD across all CAC strata, including CAC=0, though absolute event rates remain low when CAC=0.
Answers are grounded in this paper and cite their sources.
Caution warranted interpreting CAC=0 as low risk in elevated Lp(a); leaves open optimal integration of both markers for ASCVD stratification.
BACKGROUND: The utility of coronary artery calcium (CAC) scoring in individuals with elevated lipoprotein(a) [Lp(a)] for atherosclerotic cardiovascular disease (ASCVD) risk assessment is currently unclear given the propensity of Lp(a) toward noncalcified plaque. OBJECTIVES: The authors aimed to evaluate the interaction between elevated Lp(a) (>50 mg/dL) and CAC score, and the association of Lp(a) with ASCVD risk across strata of CAC. METHODS: A pooled cohort of participants without known ASCVD from 4 U.S.-based prospective cohort studies with baseline Lp(a) and CAC measurements was used. The association between elevated Lp(a) across CAC strata and incident ASCVD (myocardial infarction, stroke, coronary revascularization) was evaluated in multivariable Cox regression models. RESULTS: The study included 11,319 participants (mean age 56 years, 54% women) with 1,569 incident ASCVD events over 14.8 year mean follow-up. Lp(a) >50 mg/dL (HR: 1.24; 95% CI: 1.09-1.41) and CAC >0 (HR: 2.44; 95% CI: 2.14-2.77) were independently associated with ASCVD risk (P interaction = 0.80). Among individuals with CAC = 0, ASCVD incidence rates were low overall, but higher with Lp(a) >50 mg/dL vs ≤50 mg/dL (4.9 vs 3.8/1,000 person-years, HR: 1.28; 95% CI: 1.01-1.60). Among those with CAC >0, increased risk was again noted with elevated Lp(a) (21.2 vs 18.2/1,000 person-years, HR: 3.03; 95% CI: 2.52-3.64). Similar results were observed when examining further CAC strata with the greatest risk noted with both CAC ≥300 and Lp(a) >50 mg/dL (HR: 6.12; 95% CI: 4.80-7.81). Consistent results were noted by age and sex with greater absolute risk in general among individuals >50 years of age and men. CONCLUSIONS: Elevated Lp(a) is associated with higher relative risk across CAC strata, including CAC of 0. Among individuals with CAC of 0, absolute event rates remain low even when Lp(a) is elevated. CAC scoring remains a powerful tool for risk assessment among individuals with elevated Lp(a).
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Bhatia et al. (2026) conducted a cohort in without known ASCVD (n=11,319). Elevated Lipoprotein(a) (>50 mg/dL) vs. Lipoprotein(a) ≤50 mg/dL was evaluated on incident ASCVD (myocardial infarction, stroke, coronary revascularization) (HR 1.24, 95% CI 1.09-1.41). Elevated Lipoprotein(a) >50 mg/dL was independently associated with increased risk of incident ASCVD (HR 1.24; 95% CI 1.09-1.41), with consistent relative risk increases across all CAC strata.
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