Lipoprotein (a) and Low-density lipoprotein apolipoprotein B metabolism following apheresis in patients with elevated lipoprotein(a) and coronary artery disease

Abstract

<b>Background:</b> Lipoprotein apheresis effectively lowers lipoprotein(a) [Lp(a)] and low‐density lipoprotein (LDL) by approximately 60%‐70%. The rebound of LDL and Lp(a) particle concentrations following lipoprotein apheresis allows the determination of fractional catabolic rate (FCR) and hence production rate (PR) during non‐steady state conditions. We aimed to investigate the kinetics of Lp(a) and LDL apolipoprotein B‐100 (apoB) particles in patients with elevated Lp(a) and coronary artery disease undergoing regular apheresis.<br/> <b>Patients and methods:</b> A cross‐sectional study was carried out in 13 patients with elevated Lp(a) concentration (>500 mg/L) and coronary artery disease. Lp(a) and LDL‐apoB metabolic parameters, including FCR and PR were derived by the fit of a compartment model to the Lp(a) and LDL‐apoB concentration data following lipoprotein apheresis.<br/> <b>Results:</b> The FCR of Lp(a) was significantly lower than that of LDL‐apoB (0.39 [0.31, 0.49] vs 0.57 [0.46, 0.71] pools/day, <i>P</i> = 0.03) with no significant differences in the corresponding PR (14.80 [11.34, 19.32] vs 15.73 [11.93, 20.75] mg/ kg/day, <i>P</i> = 0.80). No significant associations were observed between the FCR and PR of Lp(a) and LDL‐apoB.<br/> <b>Conclusions:</b> In patients with elevated Lp(a), the fractional catabolism of Lp(a) is slower than that of LDL‐apoB particles, implying that different metabolic pathways are involved in the catabolism of these lipoproteins. These findings have implications for new therapies for lowering apolipoprotein(a) and apoB to prevent atherosclerotic cardiovascular disease.