Key result
Lp(a) independently compounds ASCVD risk, which LDL-C lowering fails to fully offset.
Why the study?
The relationship between lipoprotein(a) level, low-density lipoprotein cholesterol level, and atherosclerotic cardiovascular disease risk at different thresholds is not well defined.
Do elevated Lp(a) levels increase ASCVD risk independently of achieved LDL-C levels in statin-treated patients?
Population
27,658 participants enrolled in 6 placebo-controlled statin trials
Comparison
Baseline Lp(a) level and statin-achieved LDL-C level associations with ASCVD risk
Design
Participant-level meta-analysis of placebo-controlled statin trials
Authors
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Lp(a) and LDL-C levels are independent and additive predictors of ASCVD risk, demonstrating that LDL-C lowering with statins does not fully offset Lp(a)-mediated risk.
Meta-Analysis (n=27,658)
Yes
Do elevated Lp(a) levels increase ASCVD risk independently of achieved LDL-C levels in statin-treated patients?
Hazard Ratio: 1.38 (95% CI 1.06–1.79)
Lp(a) and LDL-C levels are independent and additive predictors of ASCVD risk, demonstrating that LDL-C lowering with statins does not fully offset Lp(a)-mediated risk.
Bhatia et al. (2024) conducted a meta-analysis in Atherosclerotic cardiovascular disease (ASCVD) risk (n=27,658). Lp(a) level >50 mg/dL vs. Lp(a) level ≤50 mg/dL was evaluated on Fatal or nonfatal coronary heart disease events, stroke, or any coronary or carotid revascularization (ASCVD) (HR 1.38, 95% CI 1.06-1.79). Among statin-treated patients with the lowest achieved LDL-C, Lp(a) >50 mg/dL was associated with higher ASCVD risk compared to Lp(a) ≤50 mg/dL (HR 1.38; 95% CI 1.06-1.79).
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