P1547The impact of high baseline lipoprotein(a) level on coronary artery calcification progression determined with CT: sub-analysis of a prospective multicenter trial

Abstract

Introduction: Lipoprotein(a), or Lp(a), is a low‐density lipoprotein (LDL)‐like particle. Apolipoprotein B is covalently linked to apolipoprotein(a) by a single disulfide bond. Lp(a) is independent of known risk factors for, and predictive of, cardiovascular disease (CVD). Coronary artery calcification (CAC), which is determined by CT, is an excellent marker for the clinical measurement of the burden of CVD risk. In addition, after serial assessments, the progression of CAC scores has been proposed as a useful predictor of cardiac outcome. We recently reported the results of a prospective multicenter study that examined the effects of intensive and standard pitavastatin treatment with or without eicosapentaenoic acid on the annual progression of CAC we found that the overall CAC progression rate over 1 year was 40% and that the CAC progression in each patient group was not affected by the allocated treatments. A determination of the factors involved in CAC progression is of interest. Purpose: We investigated the association between baseline Lp(a) levels and the progression of CAC in patients with hypercholesterolemia undergoing statin therapy in data from the multicenter randomized controlled study. Methods: The principal study evaluated the annual progression of CAC in patients with an Agatston score of 1 to 999, and hypercholesterolemia treated with statins. Serum concentration of Lp(a) was measured using an enzyme‐linked immunosorbent assay Results: A total of 147 patients (mean age, 67 years; men, 54%) were analyzed. The median baseline Lp(a) level was 10.2 mg/dL, and 9.5% of participants (n=14) had an Lp(a) level >30 mg/dL. Linear regression analysis showed that the baseline Lp(a) level was positively correlated with age (r=0.28, p<0.01) and negatively correlated with triglyceride (r =‐0.22, p<0.01) When patients were classified into three groups according to CAC progression, the proportion of patients with Lp(a) >30 mg/dL significantly increased as CAC progressed (non‐progression; 5.4%, 0100; 26.3%). Logistic regression analysis showed that Lp(a) >30 mg/dL was an independent predictor of the annual change in Agatston score >100 (OR: 5.51; 95% CI: 1.28‐23.68; p=0.02), even after adjusting for age, sex, hypertension, diabetes mellitus, current smoking, body mass index, and lipid‐lowering medications. Conclusion: Baseline Lp(a) >30 mg/dL was a predictor of CAC progression in this population of patients with hypercholesterolemia undergoing statin therapy. Our findings suggest that measuring Lp(a) levels will help in the risk assessment for CVD events as well as treatment options.