LDL-C and hs-CRP Jointly Modify the Effect of Lp(a) on 5-Year Death in Patients With Percutaneous Coronary Intervention.

Abstract

Recent studies have suggested that adverse events associated with lipoprotein(a) [Lp(a)] might be modified by low-density lipoprotein cholesterol (LDL-C) or high-sensitivity C-reactive protein (hs-CRP) levels, but whether LDL-C and hs-CRP jointly mediate the outcome of Lp(a) remains unknown in patients with coronary artery disease. A prospective study was conducted, enrolling consecutive 10 724 patients with percutaneous coronary intervention (PCI) in 2013. The endpoint event was all-cause death. A total of 10 000 patients with complete baseline data were finally included. During a median follow-up of 5.1 years, Lp(a) ≥ 30 mg/dL was an independent risk factor of all-cause death in the overall population, LDL-C ≥ 70 mg/dL, and hs-CRP ≥ 2 mg/L population, respectively. According to concurrent LDL-C (70 mg/dL) and hs-CRP (2 mg/L) levels, further analysis revealed that when LDL-C < 70 mg/dL regardless of hs-CRP levels, Lp(a) ≥ 30 mg/dL was not an independent predictor of all-cause death. However, when LDL-C ≥ 70 mg/dL, Lp(a) ≥ 30 mg/dL was independently associated with a higher risk of all-cause death in hs-CRP ≥ 2 mg/L (HR: 1.488, 95% CI: 1.059‒2.092), but not in hs-CRP < 2 mg/L (HR: 1.303, 95% CI: 0.914‒1.856). Among PCI patients, Lp(a)-associated outcome was jointly affected by LDL-C and hs-CRP. As long as LDL-C is well controlled, the adverse effects of increased Lp(a) on cardiovascular risk seem to be weakened, and only when LDL-C and hs-CRP increase at the same time, elevated Lp(a) is associated with poorer long-term outcome.