Despite low-density lipoprotein cholesterol lowering with statins, patients with high lipoprotein(a) levels may face an elevated risk of atherosclerotic cardiovascular disease, according to a recent meta-analysis.

In the study, published in Circulation, investigators examined the independent contribution of lipoprotein(a) [Lp(a)] and low-density lipoprotein cholesterol (LDL-C) to atherosclerotic cardiovascular disease (ASCVD) risk across 27,658 participants in six statin trials. The study aimed to determine whether LDL-C reduction alone could sufficiently offset ASCVD risk associated with elevated Lp(a) levels.

The investigators found that Lp(a) and LDL-C independently contributed to ASCVD risk, with an elevated Lp(a) level (> 50 mg/dL) significantly increasing risk regardless of LDL-C levels achieved via statin therapy. Among the participants receiving statins, those in the lowest LDL-C quartile (< 77.34 mg/dL) but with high Lp(a) had a 38% higher risk of ASCVD compared with those with lower Lp(a) levels (hazard ratio [HR] = 1.38, 95% confidence interval [CI] = 1.06–1.79). The greatest ASCVD risk was observed among the participants with both high Lp(a) and LDL-C levels, with an HR of 1.90 (95% CI = 1.46–2.48).

The findings indicated that both LDL-C and Lp(a) are independent risk factors for ASCVD. Current LDL-C–lowering strategies may not fully address Lp(a)-mediated risk, as Lp(a) levels remain largely unaffected by statins. Recognizing elevated Lp(a) levels may contribute to more comprehensive cardiovascular risk assessment and management.

Full disclosures can be found in the published study.