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52 | Chapter 4 Risk factors for AoVC Risk factors for AoVC are shown in table 3. The AoVC burden by Agatston score was associated with age, untreated maxLDL, LDLR-negative mutational he-FH, CAC and diastolic blood pressure. Gender, smoking, hypertension, diabetes mellitus and obesity were not associated with the extent of AoVC. In the multivariable ordinal regression model, all variables explained 27% of the variance of AoVC and all remained significantly associated with AoVC. Among the variables, LDLR-negative mutation carrier status was a strong predictor of the extent of AoVC (OR: 4.81; 95%CI: 2.22-10.40; p= <0.001). Analyses restricted to the he-FH patients, LDLR-defective, and LDLR-negative had similar results (data not shown). Association between coronary and aortic valve calcification The presence of CAC was associated with a higher prevalence of AoVC, both in he-FH and control patients (table 4). Of the patients without CAC, no more than 4% showed AoVC. However, in the absence of AoVC, still more than 39% of patients exhibited CAC. Aortic valve calcification and LDL receptor mutational status Out of 145 he-FH patients, fifty-nine patients (41%) had an LDLR-negative mutation. Compared to he-FH patients with LDLR-defective mutations, LDLR-negative mutational he-FH was associated with: higher total cholesterol (5.8 ± 1.6 and 5.3 ± 1.3 mmol/L, p=0.026), LDL-C (3.9 ± 1.4 and 3.2 ±1.1 mmol/L, p=0.002) and untreated maxLDL (8.0 ± 2.5 and 6.6 ± 1.7 mmol/L, p= <0.001). In addition, he-FH patients with LDLR-negative mutations were younger (51 ± 7 and 53 ± 8 years, p=0.040), started using statins at younger age (40 ± 9.8 and 46 ± 9.4 years, p=<0.001), and used statins for a longer period of time (10. ± 7 and 7 ± 7 years, p=0.010). All other variables from table 1 were not statistically different between groups. He-FH patients with LDLR-negative mutations had higher prevalence of AoVC (31 (53%)) as compared to LDLR-defective mutations (28 (33%); p< 0.001) and controls (27 (21%); p = 0.016). The difference in AoVC prevalence between LDLR-defective mutational he-FH and the controls was also significant (p = 0.048). Additionally, AoVC- scores increase faster with age in LDLR-negative he-FH than in LDLR-defective he-FH (data not shown).