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4 57 | Rebuttal AoVC in FH only essential in comprehending the effect of statin treatment, but could also explain the discordant association between AoVC and CAC. As shown in table 4, the absence of CAC was associated with very low prevalence of AoVC. However, the absence of AoVC was not predictive of the absence of CAC. Perhaps, during the early phase of AoVC, risk factors for CAC are preconditions for the development of AoVC. However, if AoVC develops after the initial atherosclerotic phase, its progression seems to be regulated by risk factors that differ from those causing CAC (27,33). We found that the prevalence and extent of subclinical AoVC is clearly increased in he-FH patients, especially in patients carrying LDLR-negative mutations. It should be emphasized that AoVC is generally without symptoms, and only a fraction of patients with AoVC ultimately develop clinical aortic stenosis. The reported prevalence of hemodynamically significant aortic valve stenosis on echocardiography is low in he-FH (15). Since statin therapy became available, the risk of cardiovascular disease mortality has been substantially reduced in he-FH patients (35). Detection and treatment of he-FH patients at young age may not only slow progression of CAD but also could be effective to prevent or slow the development of AoVC during the early phase of disease. This underlines the clinical importance of studies on the effectiveness of statin use for the primary prevention of AoVC, especially in patients with LDLR-negative mutational he-FH. Study limitations This study is a cross-sectional observation of AoVC in patients aged between 40 and 70 years, without clinical outcome data, and without functional assessment of stenosis with echocardiography. The cross-sectional design of our study did not allow for proper evaluation of the effects of statins on AoVC, which would require a prospective study and sequential imaging. Additionally, we do not have sufficient follow-up in our cohort to assess the clinical consequences of the observed AoVC, which a limitation of the observational design of the present study. Only asymptomatic patients were selected and it remains to be seen if patients with AoVC will eventually develop clinical aortic valve disease, since the majority of AoVC will not lead to aortic stenosis (36). The current selection of he-FH patients, whowere referred to our university lipid clinic, may have more severe AoVC as compared to he-FH patients in the general population. This single center study from a tertiary hospital could have resulted in overestimation of the total prevalence and extent of AoVC. However, this potential selection bias should