15289-s-bos

6 89 | Lp(a) is not associated with carotid plaques and C-IMT in FH Introduction Familial hypercholesterolemia (FH) is the most common genetic disorder associated with premature cardiovascular disease (CVD). FH is caused by mutations in the LDLR, APOB or PCSK-9 gene [2-4]. FH patients have raised low-density lipoprotein (LDL)- cholesterol levels, which strongly increases the risk of premature CVD [5]. To reduce CVD risk, preventive statin therapy is indicated, but despite statin treatment some FHpatients still develop CVD [6-8]. This residual risk might be partly explained by alternative risk factors like lipoprotein (a), also called Lp(a). Lp(a) is a LDL-like protein with an apo(a) moiety, and Lp(a) levels are predominantly genetically determined [9]. High Lp(a) levels have been shown to explain residual CVD risk in FH patients as well as in the general population[10, 11], and are unaffected by statin therapy[12]. Atherosclerosis can be visualized by carotid ultrasonography as the presence of plaques and the intima media thickness (C-IMT), which are both associated with CVD[13-16]. Previous studies have shown an association between Lp(a) levels and C-IMT in subjects in the general population and in those with severe hypercholesterolemia [17, 18]. However, it is unknown whether Lp(a) levels are associated with carotid plaque presence and C-IMT in statin-treated patients. The aim of this study is to assess whether Lp(a) levels are related to atherosclerosis depicted by carotid ultrasonography in statin-treated FH patients. Methods Study Population Between May 2012 and October 2014, FH patients were included from the outpatient cardio-genetics clinic at the Erasmus Medical Center in Rotterdam. FH was defined as a score ≥6 on ‘The Dutch Lipid Clinic Network criteria’ [19]. All patients were screened for mutations in the LDLR , APOB and PCSK-9 genes. Patients with homozygous and compound heterozygous FH were excluded. Written informed consent for blood storage and the use of clinical data was obtained and approved by the local ethical committee (MEC-2012-309).