Physicians' Academy for Cardiovascular Education

High Lp(a) levels associated with increased CV risk despite statin treatment

Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials

Literature - Willeit P, Ridker PM, Nestel PJ et al. - The Lancet 2018; published online ahead of print

Introduction and methods

Existing data show that elevated lipoprotein(a) (Lp[a]) levels are associated with increased risk of CHD, stroke, peripheral arterial disease, and calcific aortic valve stenosis [1-3]. However, the contribution of high Lp(a) levels to CV events in patients with established CVD with or without statin therapy is unclear.

This meta-analysis of the Lipoprotein(a) Studies Collaboration used 7 randomized, placebo-controlled trials [4-10] of statins with individual patient-level data for CVD outcomes and Lp(a) measurements at baseline and follow-up (under statin treatment), and evaluated the associations of baseline and on-treatment Lp(a) levels with CV risk.

In each study, CV outcomes, including fatal or non-fatal CHD, stroke, or revascularization procedures, were stratified by predefined Lp(a) groups (15 to <30 mg/dL, 30 to <50 mg/dL, and ≥50 mg/dL, vs <15 mg/dL).

Main results


Elevated Lp(a) levels of 50 mg/dL or higher, at baseline or on-treatment, were associated with an increased risk of CV events, independent of other CV risk factors. The effect was evident on treatment with either statin or placebo. These data suggest existence of a residual risk in patients with elevated Lp(a) that is not addressed by statins and support the rationale for outcomes trials to test specific therapies to lower Lp(a).


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