The role of statin therapy in atherosclerotic plaque stabilization in a patient with elevated Lp(a): A clinical case

Abstract

Background and Aims: A 50-year-old female was referred to the lipid clinic due to elevated lipoprotein(a) [Lp(a)]. Her medical history also included hypertension and peripheral vascular disease. The treatment regimen consisted of rosuvastatin 20 mg, ezetimibe 10 mg, bisoprolol 5 mg, amlodipine 5 mg, and hydrochlorothiazide 12.5 mg. Methods: A routine cardiac computed tomography (CT) scan identified non-obstructive coronary artery disease with soft and mixed (calcified and noncalcified) atherosclerotic plaques in the left anterior descending artery (LAD), with an initial calcium score of 12 AU (Figure 1A). Preliminary laboratory analyses (Table 1) confirmed hyperlipidemia, with the following lipid levels: total cholesterol 156 mg/dL, low-density lipoprotein cholesterol 70 mg/dL, high-density lipoprotein cholesterol (HDL-C) 75 mg/dL, Non-HDL-C 81 mg/dL, triglycerides 53 mg/dL, and Lp(a) 70 mg/dL. Results: Rosuvastatin therapy was intensified to 40 mg following detection of soft atherosclerotic plaques in the LAD. Over 52 weeks, significant improvements were observed in most lipid markers, including a slight reduction in Lp(a) levels, which remained elevated (Table 1), and an increase in HDL-C. Post-intervention cardiac CT scans revealed notable improvements, with mixed atherosclerotic plaques in the LAD evolving into fully calcified plaques (Figure 1B). These findings were corroborated by a second coronary angiotomography, which demonstrated an increase in the calcium score to 46 AU. Conclusions: Elevated Lp(a) significantly contributes to plaque formation. While statins are widely used to manage lipid levels and reduce cardiovascular risk by stabilizing plaques and slowing atherosclerosis progression, their impact on plaque stability in patients with elevated Lp(a) remains uncertain. Statins are not intended to lower Lp(a) levels and may increase them by up to 15%. However, combined with exercise and a healthy diet, their primary goal is to reduce inflammation and atherogenicity, thereby lowering thrombosis risk.