Intensive lipid lowering therapies improve LDL-C goal achievement, but does high Lp(a) remain a barrier?

Abstract

Abstract Background LDL-C goal achievement is suboptimal in patients undergoing coronary artery bypass grafting (CABG). We aimed to find factors associated with LDL-C goal achievement in patients under stable lipid-lowering therapy (LLT) at admission for CABG. Methods A prospective, observational study was conducted. Stable LLT was defined as LLT for at least 4 weeks, without any change in intensity and without discontinuation of oral LLT ≥ 1 day prior to laboratory testing. For primary analysis, LLT was categorized according to treatment intensity (author defined categories (low-, moderate-, high intensity) with respect to current ESC/EAS guidelines). Achievement rate (%) of LDL-C < 55 mg/dl were compared within these categories. Results 218/300 (72.7%) were on stable LLT. LDL-C target goal achievement was higher ( p < 0.001) for moderate- and high intensity therapies (70.9%/77.8%) than low-intensity therapies (28.2%). Multivariate regression analysis revealed that the type of LLT was the strongest factor associated with the achievement of LDL-C < 55 mg/dl. Elevated lipoprotein(a) (Lp(a)) (> 125nmol/l) was found to be the strongest factor negatively associated in this analysis. After hypothetical correction of LDL-C for patients with elevated Lp(a) levels, elevated Lp(a) lost its independent association reaching the LDL-C target goal. Only 3.9% of patients (who had not reached the LDL-C target at admission) received intensification of LLT at discharge. Conclusion Since the type of LLT (low-intensity therapies being the least effective) is the most important factor associated with LDL-C target goal achievement in patients with stable LLT and therapy intensification rarely occurs at discharge, admission for CABG should be considered a critical timepoint for lipid-lowering therapy escalation. Higher prescription rates of more intensive LLT are required. Elevated Lp(a) might not be a true independent factor, due to analytical factors related to laboratory LDL-C measurement.