Local adipose tissue depots as cardiovascular risk factors

Thalmann, Sébastien; Meier, Christoph A.

doi:10.1016/j.cardiores.2007.03.008

Cited by 137 publications

(117 citation statements)

References 115 publications

(121 reference statements)

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“…There have been a few reports on cytokines in epicardial adipose tissue. 5,[18][19][20][21][22][23] Iacobellis, et al reported that mRNA expression of adiponectin in epicardial adipose tissue was significantly lower in subjects with severe CAD than in those without CAD. 21) Our data suggest that enhanced infiltration of inflammatory cells into EAT may account for inflammatory cytokine expression in EAT of CAD patients, although our sample size was too small to draw a definitive conclusion.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Inflammation in Epicardial Fat in Patients With Coronary Artery Disease

et al. 2011

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SummaryIt has been hypothesized that epicardial fat, a local visceral fat depot with close proximity to coronary arteries, may serve as a source of inflammatory cytokines and cells in coronary atherosclerotic lesions. Here, we characterized infiltration of inflammatory cells and expression of adipocytokines in epicardial adipose tissue in patients with and without coronary artery disease (CAD). Pare samples were obtained from epicardial and subcutaneous adipose tissue during elective cardiac surgery (CAD, n = 8; non-CAD, n = 9). Inflammatory cell infiltration was investigated by immunohistochemical staining using antibodies against CD3, CD4, CD8 and CD68. Expression of adipocytokines was evaluated by real-time quantitative reverse transcription-polymerase chain reaction. Infiltration of macrophages and CD8-positive T cells in the epicardial adipose tissue in the CAD group was greater than that in the non-CAD group. In contrast, there was no significant difference between the two groups in the number of inflammatory cells in subcutaneous adipose tissue. No statistical difference could be found between the CAD group and the non-CAD group in the expression levels of adiponectin and inflammatory cytokines in epicardial adipose tissue. Our findings suggest that inflammatory cell infiltration is enhanced in epicardial adipose tissue, but not in subcutaneous fat, in patients with coronary artery disease. Chronic inflammation in epicardial fat may influence the pathogenesis of coronary atherosclerosis. (Int Heart J 2011; 52: 139-142)

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Section: Discussionmentioning

confidence: 99%

Enhanced Inflammation in Epicardial Fat in Patients With Coronary Artery Disease

et al. 2011

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“…52 Increased epicardial fat pads associated with intramyocardial lipid deposition may lead to both systolic and diastolic dysfunctions, whereas accumulation of fat around blood vessels (perivascular fat) may affect vascular function in a paracrine manner, as perivascular fat cells secrete vascular relaxing factors, proatherogenic cytokines and smooth muscle cell growth factors. 54,55 High amounts of perivascular fat could also mechanically contribute to the increased vascular stiffness observed in obesity, whereas accumulation of fat within the renal sinus associated with the increased intraabdominal pressure of visceral obesity may compress the renal papilla, the renal vein and lymphatics vessels, altering intrarenal physical forces that favor sodium reabsorption and arterial hypertension. 52 Finally, the accumulation of adipose tissue surrounding skeletal muscle bundles, that is, intermuscular adipose tissue (IMAT), albeit in the thigh region, also has a strong association with insulin resistance.…”

Section: Ectopic Fatmentioning

confidence: 99%

Body composition phenotypes in pathways to obesity and the metabolic syndrome

et al. 2010

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Dynamic changes in body weight have long been recognized as important indicators of risk for debilitating diseases. While weight loss or impaired growth can lead to muscle wastage, as well as to susceptibility to infections and organ dysfunctions, the development of excess fat predisposes to type 2 diabetes and cardiovascular diseases, with insulin resistance as a central feature of the disease entities of the metabolic syndrome. Although widely used as the phenotypic expression of adiposity in population and gene-search studies, body mass index (BMI), that is, weight/height 2 (H 2 ), which was developed as an operational definition for classifying both obesity and malnutrition, has considerable limitations in delineating fat mass (FM) from fat-free mass (FFM), in particular at the individual level. After an examination of these limitations within the constraints of the BMI-FM% relationship, this paper reviews recent advances in concepts about health risks related to body composition phenotypes, which center upon (i) the partitioning of BMI into an FM index (FM/H 2 ) and an FFM index (FFM/H 2 ), (ii) the partitioning of FFM into organ mass and skeletal muscle mass, (iii) the anatomical partitioning of FM into hazardous fat and protective fat and (iv) the interplay between adipose tissue expandability and ectopic fat deposition within or around organs/tissues that constitute the lean body mass. These concepts about body composition phenotypes and health risks are reviewed in the light of race/ethnic variability in metabolic susceptibility to obesity and the metabolic syndrome.

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“…Adipocytes expand during normal aging, promoting visceral obesity and dysfunctional elevations of circulating AngII (Pacholczyk et al 2013). Chronic increases in AngII production mechanically damage the vascular wall (Zieman et al 2005), resulting in arterial stiffness and blood pressure variability (Thalmann and Meier 2007;Natale et al 2009). Arterial stiffness and elevated body mass are both significant predictors of white matter abnormalities and risk for ischemic stroke in older individuals (Safar et al 2000;Kuo et al 2010;Strazzullo et al 2010;Verstynen et al 2012), suggesting that abnormal activation of the peripheral RAS may influence cerebrovascular mechanisms of age-related white matter degeneration.…”

Section: Introductionmentioning

confidence: 99%

Impact of the AGTR1 A1166C polymorphism on subcortical hyperintensities and cognition in healthy older adults

Salminen

Schofield

Pierce

et al. 2014

AGE

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Vascular aging consists of complex and multifaceted processes that may be influenced by genetic polymorphisms of the renin-angiotensin system. A polymorphism in the angiotensin II type 1 receptor gene (AGTR1/rs5186) has been associated with an increased risk for arterial stiffness, hypertension, and ischemic stroke. Despite these identified relationships, the impact of AGTR1 A1166C on white matter integrity and cognition is less clear in a healthy aging population. The present study utilized indices of neuroimaging and neuropsychological assessment to examine the impact of the A1166C polymorphism on subcortical hyperintensities (SH) and cognition in 49 healthy adults between ages 51-85. Using a dominant statistical model (CC + CA (risk) vs. AA), results revealed significantly larger SH volume for individuals with the C1166 variant (p<0.05, partial eta 2 = 0.117) compared with those with the AA genotype. Post hoc analyses indicated that increased SH volume in C allele carriers could not be explained by vascular factors such as pulse pressure or body mass index. In addition, cognitive performance did not differ significantly between groups and was not significantly associated with SH in this cohort. Results suggest that presence of the C1166 variant may serve as a biomarker of risk for suboptimal brain integrity in otherwise healthy older adults prior to changes in cognition.

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Local adipose tissue depots as cardiovascular risk factors

Cited by 137 publications

References 115 publications

Enhanced Inflammation in Epicardial Fat in Patients With Coronary Artery Disease

Enhanced Inflammation in Epicardial Fat in Patients With Coronary Artery Disease

Body composition phenotypes in pathways to obesity and the metabolic syndrome

Impact of the AGTR1 A1166C polymorphism on subcortical hyperintensities and cognition in healthy older adults

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