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152 | Chapter 9 What was already known • Carotid plaques are a better cardiovascular disease (CVD) risk predictor than carotid intima-media thickness (C-IMT) in the general population (13,22,23) • Carotidplaque progression andC-IMT are reducedby highdose statin treatment (24,25) • Premature aortic valve disease is highly present in patients with homozygous Familial Hypercholesterolemia (FH) (26-28) • Lipoprotein (a) is an independent risk factor of CVD and Aortic valve calcification (AoVC) (2,29,30) What this thesis adds • The prevalence of carotid plaques and the C-IMT are similar in long-term statin- treated FH patients and healthy controls (Chapter 3) • The prevalence and extent of AoVC are increased in statin-treated heterozygous FH patients compared to controls (Chapter 4) • The dose response relation found in the prevalence of AoVC in non-FH patients, compared to FH patients with LDLR-defective mutations compared to FH patients with LDLR-negative mutations which reflects increasing LDL-C levels, suggests a causal role for cholesterol in the initiation of AoVC (chapter 4) • Lp(a) levels are independently associated with AoVC in statin-treated FH patients (Chapter 5) • Possible residual risk of Lp(a) is not detected via carotid ultrasonography outcomes (C-IMT and carotid plaque) in FH patients (Chapter 6) • Novel plasma proteins: leucine-rich alpha-2-glycoprotein (LRG1), inter-alpha- trypsin inhibitor heavy chain H3 (ITIH3), complement C4-B (C4B), complement C1q subcomponent subunit B (C1QB), monocyte differentiation antigen (CD14) and histidine-rich glycoprotein (HRG) associated with previous CVD events and coronary atherosclerosis in FH patients (Chapter 8)