Key result
Targeted cascade screening yields elevated Lp(a) in ~30% of first-degree relatives of CAD patients.
Why the study?
Elevated lipoprotein(a) contributes to coronary artery disease, but the effectiveness of cascade screening for elevated Lp(a) in relatives of CAD patients was unclear.
Does cascade screening initiated from CAD patients with elevated Lp(a) improve the identification of relatives with elevated Lp(a) compared to screening from patients with low Lp(a)?
Observational (n=1,499)
Does cascade screening initiated from CAD patients with elevated Lp(a) improve the identification of relatives with elevated Lp(a) compared to screening from patients with low Lp(a)?
Answers are grounded in this paper and cite their sources.
Cascade screening for elevated Lp(a) is highly effective when initiated from CAD patients with elevated Lp(a), requiring only 3.3 first-degree relatives to be screened to identify one affected individual.
BACKGROUND AND AIM: Elevated lipoprotein(a) [Lp(a)] contributes to coronary artery disease (CAD). This study aimed to determine the effectiveness of cascade screening for elevated Lp(a) in patients with CAD. METHODS: Lp(a)-based cascade screening in first-degree relatives (FDR) and second-degree relatives (SDR) of index patients with CAD was performed. Index patients were recruited into pre-defined Lp(a) strata: low (<70 nmol/L), moderately elevated (70-169 nmol/L), and elevated (≥170 nmol/L). Proportions of elevated Lp(a) in relatives were determined within each index stratum, and participation rate was evaluated. RESULTS: 735 index patients (mean age 66.5 years, 76.9% male) participated, with 333, 149, and 253 in the low, moderately elevated, and elevated Lp(a) strata, respectively. Of 1120 invited relatives, 764 relatives (68.2%) were screened. Lp(a) was elevated in 30.2% of FDR and 19.4% of SDR of index patients with elevated Lp(a) compared with 6.2% in FDR (p < 0.001) and 5.6% in SDR (p = 0.007) of index patients with low Lp(a). The number (95%CI) of FDR needed to be screened to identify one individual with elevated Lp(a) was 3.3 (2.7-4.2) when the index patient had elevated Lp(a), compared with 16.1 (10.0-30.8) for low Lp(a) (p < 0.001). Corresponding numbers for SDR were 5.1 (3.4-8.8) and 17.8 (9.3-45.2) (p = 0.006). CONCLUSIONS: Cascade screening for elevated Lp(a) in relatives of patients with CAD is feasible in a real-world setting. Screening was up to five times more effective when initiated from patients with elevated Lp(a) than with low.
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Littmann et al. (2026) conducted an observational in Coronary artery disease (n=1,499). Cascade screening from index patients with elevated Lp(a) (≥170 nmol/L) vs. Cascade screening from index patients with low Lp(a) (<70 nmol/L) was evaluated on Elevated Lp(a) in first-degree relatives (NNT 3.3, 95% CI 2.7-4.2, p=<0.001). Cascade screening initiated from CAD patients with elevated Lp(a) identified elevated Lp(a) in 30.2% of first-degree relatives, compared to 6.2% when initiated from patients with low Lp(a) (P<0.001).
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