A ≥20% increase in circulating Lp(a) after the commencement of statins, and subsequent risks of atherosclerotic cardiovascular diseases in patients with coronary artery disease.

BACKGROUND

Lipoprotein(a) [Lp(a)] is an independent and causal risk factor for atherosclerotic cardiovascular disease. While Lp(a) levels are genetically determined and stable, statins have been shown to increase circulating Lp(a).

OBJECTIVE

Whether an increase in Lp(a) following the commencement of statins worsens cardiovascular outcomes remains unknown.

METHODS

The current study prospectively enrolled 100 statin-naïve patients with coronary artery disease (CAD). Lp(a) levels were measured before and 1 month after the commencement of a statin. Major adverse cardiovascular events (MACE) (= all-cause death, nonfatal MI, ischemic stroke, lower extremity artery disease, and clinically driven unplanned revascularization) were compared between patients with and without a percent change in Lp(a) levels of ≥20% following the commencement of a statin.

RESULTS

A percent change in Lp(a) levels of ≥20% occurred in 41.0% of the study population. There were no significant differences in baseline clinical demographics and biochemistry data between patients with and without a percent change in Lp(a) levels of ≥20%. On multivariate analysis, no independent predictors for a percent change in Lp(a) levels of ≥20% were identified, including low-density lipoprotein cholesterol (LDL-C) levels at both baseline and 1 month. During the observational period (65.1 [39.7-75.6] months), a percent change in Lp(a) levels of ≥20% following the commencement of a statin was not associated with a greater risk of subsequent MACE (adjusted hazard ratio = 1.29, 95% CI = 0.52-3.18, P = .586). The association between a percent change in Lp(a) levels of ≥20% and MACE was not observed in any subgroups of the study population.

CONCLUSION

The occurrence of MACE did not differ between patients with and without a percent change in Lp(a) levels of ≥20% after statin use. Our observations indicate that an increase in Lp(a) following the commencement of statins may not necessarily attenuate the antiatherosclerotic effect of LDL-C lowering in patients with CAD.