Vascular stiffness in familial hypercholesterolaemia is associated with C‐reactive protein and cholesterol burden

Cheng, Hao Min; Ye, Z. X.; Chiou, Kuan Rau; Lin, Shing‐Jong; Charng, Min Ji

doi:10.1111/j.1365-2362.2007.01772.x

Cited by 37 publications

(44 citation statements)

References 35 publications

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“…In our study, as shown in Fig. 1a, the cholesterol-year score was positively correlated with the carotid IMT ( r = 0.389, p < 0.05), which is consistent with the findings in a previous study [11]. In addition, the serum sulfatide levels were also positively correlated with the carotid IMT ( r = 0.838, p < 0.001) (Fig.…”

Section: Resultssupporting

confidence: 92%

Association between serum sulfatide and carotid intima media thickness in patients with familial hypercholesterolemia

2014

Glycoconj J

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There is a positive association between sulfatide and atherosclerosis in an animal model for human familial hypercholesterolemia. Carotid intima–media thickness (IMT) is thought to be a marker of atherosclerosis in humans. We investigated the relationship between sulfatide and carotid IMT in heterozygous familial hypercholesterolemia (FH) patients. Thirty-five genetically-verified heterozygous patients with FH and 34 healthy controls were recruited into our study. We measured serum sulfatide levels, the carotid IMT, and conventional cardiovascular risk factors including obesity parameters, blood pressure, fasting blood glucose, and lipid profiles. Subjects with heterozygous FH had significantly elevated serum sulfatide, elevated total cholesterol, low-density lipoprotein cholesterol, and increased carotid IMT compared with control subjects. In patients with FH, univariate analysis showed that serum sulfatide was significantly correlated with carotid IMT. Multiple linear regression analysis indicated that serum sulfatide was the only independent predictor of carotid IMT in patients with FH. Patients with heterozygous FH had significantly higher carotid IMT and the level of serum sulfatide was independently associated with atherosclerotic progression. (R: 0.720, R2: 0.503, p < 0.001).

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Section: Resultssupporting

confidence: 92%

Association between serum sulfatide and carotid intima media thickness in patients with familial hypercholesterolemia

2014

Glycoconj J

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“…Here, in HeFH subjects, we showed an independent association between TCB and calcified coronary atherosclerotic burden that expands previous results on arterial stiffening and thickening (23). In young patients under 45 years we report the high prevalence of CAC presence in correlation with the cholesterol burden at diagnosis suggesting a potential role of early exposure to elevated cholesterol levels.…”

supporting

confidence: 88%

Early coronary calcifications are related to cholesterol burden in heterozygous familial hypercholesterolemia

Gallo

Giral

Carrié

et al. 2017

Journal of Clinical Lipidology

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“…Recent meta-analysis data have indicated that the increased risk for CVD and related events are, in part, attributable to stiffening of the aorta as assessed by aortic pulse wave velocity (aPWV) (3). Importantly, nearly 50% of Americans have total cholesterol values above the desirable level (21), which, in turn, promotes aortic stiffening (13,23,42). Thus, gaining insights for the mechanisms by which traditional risk factors, such as hypercholesterolemia, promote aortic stiffening is of clinical importance.…”

mentioning

confidence: 99%

Aortic perivascular adipose-derived interleukin-6 contributes to arterial stiffness in low-density lipoprotein receptor deficient mice

Ouyang

Eng

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Du B, Ouyang A, Eng JS, Fleenor BS. Aortic perivascular adipose-derived interleukin-6 contributes to arterial stiffness in lowdensity lipoprotein receptor deficient mice. Am J Physiol Heart Circ Physiol 308: H1382-H1390, 2015. First published April 3, 2015 doi:10.1152/ajpheart.00712.2014.-We tested the hypothesis that aortic perivascular adipose tissue (PVAT) from young low-density lipoprotein receptor-deficient (LDLr Ϫ/Ϫ ) mice promotes aortic stiffness and remodeling, which would be mediated by greater PVAT-derived IL-6 secretion. Arterial stiffness was assessed by aortic pulse wave velocity and with ex vivo intrinsic mechanical properties testing in young (4 -6 mo old) wild-type (WT) and LDLr Ϫ/Ϫ chow-fed mice. Compared with WT mice, LDLr Ϫ/Ϫ mice had increased aortic pulse wave velocity (407 Ϯ 18 vs. 353 Ϯ 13 cm/s) and intrinsic mechanical stiffness (5,308 Ϯ 623 vs. 3,355 Ϯ 330 kPa) that was associated with greater aortic protein expression of collagen type I and advanced glycation end products (all P Ͻ 0.05 vs. WT mice). Aortic segments from LDLr Ϫ/Ϫ compared with WT mice cultured in the presence of PVAT had greater intrinsic mechanical stiffness (6,092 Ϯ 480 vs. 3,710 Ϯ 316 kPa), and this was reversed in LDLr Ϫ/Ϫ mouse arteries cultured without PVAT (3,473 Ϯ 577 kPa, both P Ͻ 0.05). Collagen type I and advanced glycation end products were increased in LDLr Ϫ/Ϫ mouse arteries cultured with PVAT (P Ͻ 0.05 vs. WT mouse arteries), which was attenuated when arteries were cultured in the absence of PVAT (P Ͻ 0.05). PVAT from LDLr Ϫ/Ϫ mice secreted larger amounts of IL-6 (3.4 Ϯ 0.1 vs. 2.3 Ϯ 0.7 ng/ml, P Ͻ 0.05), and IL-6 neutralizing antibody decreased intrinsic mechanical stiffness in LDLr Ϫ/Ϫ aortic segments cultured with PVAT (P Ͻ 0.05). Collectively, these data provide evidence for a role of PVAT-derived IL-6 in the pathogenesis of aortic stiffness and remodeling in chow-fed LDLr Ϫ/Ϫ mice. periaortic fat; aorta; cholesterol; inflammation; triglycerides DEATHS DUE TO CARDIOVASCULAR DISEASES (CVD) are the leading cause of mortality in the United States and in other modern societies worldwide (21). Recent meta-analysis data have indicated that the increased risk for CVD and related events are, in part, attributable to stiffening of the aorta as assessed by aortic pulse wave velocity (aPWV) (3). Importantly, nearly 50% of Americans have total cholesterol values above the desirable level (21), which, in turn, promotes aortic stiffening (13,23,42). Thus, gaining insights for the mechanisms by which traditional risk factors, such as hypercholesterolemia, promote aortic stiffening is of clinical importance. Aortic stiffness is, in part, due to changes in the expression of extracellular matrix proteins within the arterial wall and increased cross-linking of these proteins (15, 44). Collagen type I is a key load-bearing collagen isoform with increased expression in arteries with greater aortic stiffness (18). In contrast, elastin, a protein that provides elasticity to arteries, has an attenuated expression that also ...

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Vascular stiffness in familial hypercholesterolaemia is associated with C‐reactive protein and cholesterol burden

Abstract: Both high cholesterol burden and vascular inflammation are not only associated with atherosclerosis, but also contribute to the development of arterial stiffness in FH patients. Early detection of hypercholesterolaemia in FH patients is warranted to prevent the untoward pathophysiologies.

Cited by 37 publications

References 35 publications

Association between serum sulfatide and carotid intima media thickness in patients with familial hypercholesterolemia

Association between serum sulfatide and carotid intima media thickness in patients with familial hypercholesterolemia

Early coronary calcifications are related to cholesterol burden in heterozygous familial hypercholesterolemia

Aortic perivascular adipose-derived interleukin-6 contributes to arterial stiffness in low-density lipoprotein receptor deficient mice

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