Lipoprotein(a) [Lp(a)] is a well-established, genetically determined risk factor for atherosclerotic cardiovascular disease, but its short-term response to aggressive lipid-lowering therapy after acut Show more
Lipoprotein(a) [Lp(a)] is a well-established, genetically determined risk factor for atherosclerotic cardiovascular disease, but its short-term response to aggressive lipid-lowering therapy after acute coronary syndrome (ACS) remains unclear. To evaluate 1-month changes in Lp(a) and assess whether baseline Lp(a) levels are associated with low-density lipoprotein cholesterol (LDL-C) goal achievement in statin-naive ACS patients undergoing triple oral lipid-lowering therapy. We retrospectively analyzed 345 patients with ACS treated with rosuvastatin (20-40 mg), ezetimibe (10 mg), and bempedoic acid (180 mg) for 1 month after percutaneous coronary intervention. Lp(a) and LDL-C were measured at baseline and 1 month. Multivariable logistic regression identified predictors of achieving the LDL-C goal (<50 mg/dL). Despite a 59.1 ± 17.3% reduction in the mean LDL-C, the average Lp(a) increased by 91% (from 42.2 ± 39.2 mg/dL to 80.5 ± 66.3 mg/dL, P < .001). LDL-C targets of <50 mg/dL and <55 mg/dL were achieved in 68.9% and 78.6% patients, respectively. Baseline Lp(a) independently predicted failure to reach LDL-C goals (adjusted odds ratio [OR] 0.97; 95% CI 0.96-0.98; P < 0.001), while diabetes mellitus increased the likelihood of achieving targets (adjusted OR 2.69; 95% CI 1.36-5.61; P = .006). A strong inverse relationship was observed between Lp(a) change and LDL-C goal achievement (ρ = -0.38, P < 10⁻¹²). In Indian patients with ACS, aggressive triple oral lipid-lowering therapy quickly reduces LDL-C, while being accompanied by a substantial rise in Lp(a) levels, likely reflecting an acute-phase response. Baseline Lp(a) may independently limit LDL-C target attainment. Early Lp(a) testing may improve residual risk assessment and help guide the use of emerging Lp(a)-focused treatments. Show less