15289-s-bos

4 55 | Rebuttal AoVC in FH caused the higher prevalence and quantity of AoVC that we found in he-FH patients, and particularly those with LDLR-negative mutations. Since the moment of being diagnosed with hypercholesterolemia patients have been treated with statins, which dramatically lowered LDL-C levels, and thereby reduced the predictive value of LDL-C towards AoVC. This could explain why untreated maxLDL and LDLR-negative mutational he-FH were, and the level of statin treated LDL-C was not predictive of AoVC in our study. Diastolic blood pressure was mildly but significantly associated with AoVC in our overall normotensive subjects. One might speculate that the increased diastolic blood pressure promotes stress on the aortic side of the valve leaflets, which is where aortic valve lesions are most commonly found (25). This increased stress on the aortic valve 58 (30%) CENTRAL ILLUSTRATION Severity of AoVC in Patients With he-FH and Control Subjects, and Their Untreated LDL-C Levels Subjects in Each Severity Group of AoVC 22 (51%) 13 (30%) 8 (19%) 6.6 ± 2.5 mmol/L 8.0 ± 2.5 mmol/L 3.7 ± 1.1 mmol/L LDLR Negative Mean Untreated MaxLDL 0 2 4 6 8 104 (55%) 19 (44%) 9 (21%) 15 (35%) 28 (15%) 58 (30%) AoVC Score: 0 AoVC Score: >0-37 AoVC Score: >37 tenKate,G.-J.R.etal. JAmCollCardiol.2015;66(24):2687–95. In this study, 145 asymptomatic patients with heterozygous familial hypercholesterolemia (he-FH) and 131 nonfamilial hypercholesterolemia control subjects underwent computed tomography calcium scoring of the aortic valve. Severity of aortic valve calci cation (AoVC) per group is shown in the pie charts, and the bar graph illustrates the untreated low-density lipoprotein (LDL-C) levels for the groups. LDLR ¼ low-density lipoprotein receptor; MaxLDL ¼ untreated maximum low-density lipoprotein cholesterol. LDLR-Defective Control LDLR Negative LDLR-Defective Control