Association of serum lipids with arterial stiffness in a population-based study in Beijing

Wang, Fan; Ye, Ping; Luo, Li; Xiao, Wenkai; Qi, Liping; Bian, Su-Yan; Wang, Hongmei; Sheng, Li; Xiao, Tiehui; Xu, Rong

doi:10.1111/j.1365-2362.2011.02481.x

Cited by 62 publications

(53 citation statements)

References 43 publications

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“…50,51 Part of these contradictions can be justified, however, or by the differences between the populations investigated or by the different methods used in the determination of arterial stiffness.…”

Section: 42mentioning

confidence: 99%

Arterial Stiffness: Pathophysiological and Genetic Aspects

Alvim

Santos

Bortolotto

et al. 2017

International Journal of Cardiovascular Sciences

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Cardiovascular diseases (CVD) are the main cause of mortality and it represents a significant percentage of hospitalizations. In the scenario of minimization of costs of the health system, methods that identify subclinical CVD would be important. Some guidelines include the measures of aortic stiffness and intima-media thickness of the carotid artery as methods to identify subclinical CVD in hypertensive patients. The pulse wave velocity (PWV) is the gold standard for the evaluation of arterial stiffness. In this review, we report the pathophysiology, the determinants of arterial stiffness, and justify its inclusion in the assessment of hypertensive patient due its direct association with cardiovascular risk, as show in the I Diretriz Brasileira de Prevenção Cardiovascular. In addition, we raised the main genetic studies of this phenotype, due to its complexity, can be modulated by dozens of genes. However, a better understanding of the relationship genetic-arterial stiffness and, even an intervention based on genotypes, should be achieved in future studies.

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Section: 42mentioning

confidence: 99%

Arterial Stiffness: Pathophysiological and Genetic Aspects

Alvim

Santos

Bortolotto

et al. 2017

International Journal of Cardiovascular Sciences

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“…Our present findings demonstrate that LDLr Ϫ/Ϫ mice, which have increased circulating cholesterol and triglyceride concentrations compared with WT mice, demonstrate arterial stiffness, which, in turn, may increase cardiovascular risk. As such, adults with hypercholesterolemia have greater aortic stiffening compared with individuals with optimal cholesterol levels (27,29,39) and are at a greater risk of an adverse cardiovascular event (21). Notably, despite the increased aortic stiffness in LDLr Ϫ/Ϫ mice, these animals did not have elevated blood pressure.…”

Section: Arterial Stiffnessmentioning

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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“…27,30,31,36,42 A relationship between LDL cholesterol and vascular health has been questioned previously in adults. The findings portray mixed results; some studies in adults showed LDL cholesterol to be a significant independent predictor of endothelial function, 60 PWV, 61 and CIMT, 62 whereas another study demonstrated that improvements in endothelial function because of exercise were not associated with a reduction in LDL cholesterol. 63 A possible alternative for improvement in FMD is a reduction specifically in oxidized LDL rather than general LDL.…”

Section: Discussionmentioning

confidence: 91%