15289-s-bos

5 81 | Lp(a) and AoVC in FH Limitation The capability of the CT scan to detect small calcifiedplaques is limited [37], therefore the presence of AVC might be underestimated. Moreover, we included only middle-aged, asymptomatic statin-treated FH patients. The results may be different in symptomatic, elderly or untreated patients. Replication in a larger group of FH patients is required to confirm and extend our findings. Clinical implication AVC and aortic valve stenosis are a major risk factor for CVD. However, no efficient treatment other than aortic valve replacement is available. With this study, we provide evidence that plasma Lp(a) concentrations may be a clinically useful risk factor of AVC and subsequent residual CVD risk assessment in heterozygous FH patients. Although statin treatment has been found to reduce AVC in vitro and in vivo [38, 39], it does not affect the clinical outcome of AVC [40, 41], and we speculated that this might be explained by the fact that statins do not reduce Lp(a) concentrations [29, 42]. In contrast, the progression of CAC is attenuated by statins, which is mainly the result of the cholesterol-lowering effect of statins [43, 44]. As the association between Lp(a) and AVC found in this study was independent of cholesterol-year score (CYS), therapeutic strategies to lower plasma Lp(a) concentration may be a potential treatment for AVC in FH patients. Notably, the commonly used Lp(a) cut-off points of 30 and 50 mg/dL (80th percentile) were not independently associated with AVC. These cut-off values were suggested based on the association between Lp(a) and myocardial infarction [45, 46]. However, data to support a clear Lp(a) cut-off point associated with increased AVC are not available and need further investigation. In addition, FH patients have higher plasma Lp(a) levels than the general population [47, 48]. Therefore, thresholds have to be validated in this particular high risk group to be discriminative. In our population, an Lp(a) higher than the 80th percentile (~80 mg/dL) was independently associated with an increased risk of AVC presence (data not shown). On the other hand, based on our results, lowering Lp(a) concentration is expected to have a limited effect on the development of CAC in asymptomatic FH patients. In conclusion, we report a significant association between plasma Lp(a) concentration and AVC in asymptomatic statin-treated FH patients, independently of age and other CVD-related risk factors. Although AVC and CAC were strongly mutually associated, Lp(a) concentration was not correlated with CAC, suggesting a specific role of Lp(a) in AVC in these patients.