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DB13 Lipoprotein(a) and cardiovascular events in patients with familial hypercholesterolemia

Aug 2026 · European Journal of Endocrinology · Vol 195 · 0 citations

TL;DR

Elevated Lp(a) is a significant predictor of cardiovascular risk in patients with FH, independent of LDL-C lowering achieved by statin therapy, and consideration of targeted lipid-lowering therapy is needed to optimize cardiovascular risk management in this population.

Abstract

Familial hypercholesterolemia (FH) is associated with significantly elevated risk for premature atherosclerotic cardiovascular disease (ASCVD), with a substantial number of patients experiencing cardiovascular events despite statin therapy. Lipoprotein(a) (Lp(a)), a mostly genetically determined statin-resistant lipoprotein, is recognized as an independent cardiovascular risk factor, but its contribution to cardiovascular outcomes in clinical FH cohorts remains insufficiently studied. This retrospective cohort study included 214 patients diagnosed with FH from January 2008 to January 2026 at the Department of Lipid Disorders and Lipoprotein Apheresis, University Clinical Centre of Serbia (62.6% women, age 50.4±13.5 years). Lp(a), lipid parameters, and therapy were analyzed at baseline and during follow-up. Chi-square, Mann-Whitney U test, and Wilcoxon test were applied as appropriate. During follow-up, 16.4% of patients experienced a new cardiovascular event. Elevated Lp(a) (≥50 mg/dL) was present in 35.8% of patients. Patients with elevated Lp(a) were significantly more likely to have a history of cardiovascular event (OR 3.45, 95% CI 1.39-8.54, p=0.005) and to experience a new cardiovascular event during follow-up (OR 3.84, 95% CI 1.62-9.06, p=0.001). Lp(a) values did not significantly change during statin therapy (p=0.842), while LDL-C, total cholesterol, and triglycerides significantly decreased (p<0.001). Most commonly prescribed therapeutics included atorvastatin (44%), rosuvastatin (30%), and statin-ezetimibe combination (7%). Elevated Lp(a) is a significant predictor of cardiovascular risk in patients with FH, independent of LDL-C lowering achieved by statin therapy. Routine Lp(a) measurement and consideration of targeted lipid-lowering therapy are needed to optimize cardiovascular risk management in this population.

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