Abstract
Background and Aims: Familial Hypercholesterolemia (FH) patients have an increased cardiovascular risk due to high TC or LDL-C levels. Lp(a) is a lipoprotein rich in cholesterol and is an independent risk factor for CVD due to prothrombotic/anti-fibrinolytic effects or/and by promoting accelerated atherogenesis. We aim to determine if elevated Lp(a) concentrations can contribute to clinical phenotype of FH.
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