Shuhei Fujita, Yu Kataoka, Naoto Kuyama, Stephen J Nicholls, Kentaro Mitsui, Kota Murai, Takamasa Iwai, Kenichiro Sawada, Hideo Matama, Satoshi Honda, Masashi Fujino, Shuichi Yoneda, Fumiyuki Otsuka, Kensuke Takagi, Kazuhiro Nakao, Yasuhide Asaumi, Ken-Ichi Tsujita, Teruo Noguchi
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.
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.