15289-s-bos

3 33 | Carotid ultrasonography in statin treated FH Introduction Familial hypercholesterolemia (FH) is the most common genetic disorder associated with premature atherosclerotic cardiovascular disease (ASCVD), and is caused by pathogenic mutations in the LDLR, APOB or PCSK-9 gene (1-3). The risk of premature ASCVD is increased due to high low-density lipoprotein cholesterol (LDL-C) levels (4), which can be lowered by statin treatment. Statin therapy can reduce ASCVD risk in heterozygous FH patients to the same risk as in the general population (5). However, there are still FH patients who develop ASCVD despite statin treatment (5). To identify these FH patients, imaging modalities that detect subclinical atherosclerosis may be useful. Carotid ultrasonography can be used the detect plaques and estimate carotid intima media thickness (C-IMT). Increased C-IMT and the presence of carotid artery plaques in particular, are significant predictors of ASCVD in the general population(6-9). Previously it was shown that treatment with a high potency statin during 2 years inhibited progression of C-IMT in FH patients (10,11). Sivapalaratnam, et al. showed that the C-IMT of statin treated FH patients is comparable to that of their healthy spouses (12), suggesting a normalization of risk of ASCVD in the former group. However, C-IMT is not as strongly associated with ASCVD as the presence of carotid plaques (9,13,14), which was not investigated in the aforementioned study. Whether the prevalence of carotid plaques is normalized in FH patients by long-term statin treatment, and whether normalized carotid parameters indeed reflect subclinical coronary atherosclerosis, remains unknown. We therefore compared carotid plaque prevalence and C-IMT between FH patients and healthy controls. Moreover, in a subgroup of FH patients we correlated these parameters with coronary artery calcification. Patients and methods Study Population Between May 2012 and May 2015, asymptomatic heterozygous FH patients were recruited from the outpatient cardiogenetics clinic at the Erasmus Medical Centre in Rotterdam. FH was defined as a score ≥6 on ‘The Dutch Lipid Clinic Network criteria’ (addendum 1) (15). All patients were on statin treatment. All patients were screened for mutations in the LDLR , APOB and PCSK-9 genes. Patients with twomutations, compound heterozygous FH and homozygous FH, were excluded as were patients with symptoms