Dataset Information

The impact of obesity on the relationship between epicardial adipose tissue, left ventricular mass and coronary microvascular function.

ABSTRACT:

Purpose

Epicardial adipose tissue (EAT) has been linked to coronary artery disease (CAD) and coronary microvascular dysfunction. However, its injurious effect may also impact the underlying myocardium. This study aimed to determine the impact of obesity on the quantitative relationship between left ventricular mass (LVM), EAT and coronary microvascular function.

Methods

A total of 208 (94 men, 45 %) patients evaluated for CAD but free of coronary obstructions underwent quantitative [(15)O]H2O hybrid positron emission tomography (PET)/CT imaging. Coronary microvascular resistance (CMVR) was calculated as the ratio of mean arterial pressure to hyperaemic myocardial blood flow.

Results

Obese patients [body mass index (BMI) > 25, n = 133, 64 % of total] had more EAT (125.3 ± 47.6 vs 93.5 ± 42.1 cc, p < 0.001), a higher LVM (130.1 ± 30.4 vs 114.2 ± 29.3 g, p < 0.001) and an increased CMVR (26.6 ± 9.1 vs 22.3 ± 8.6 mmHg×ml(-1)×min(-1)×g(-1), p < 0.01) as compared to nonobese patients. Male gender (β = 40.7, p < 0.001), BMI (β = 1.61, p < 0.001), smoking (β = 6.29, p = 0.03) and EAT volume (β = 0.10, p < 0.01) were identified as independent predictors of LVM. When grouped according to BMI status, EAT was only independently associated with LVM in nonobese patients. LVM, hypercholesterolaemia and coronary artery calcium score were independent predictors of CMVR.

Conclusion

EAT volume is associated with LVM independently of BMI and might therefore be a better predictor of cardiovascular risk than BMI. However, EAT volume was not related to coronary microvascular function after adjustments for LVM and traditional risk factors.

SUBMITTER: Bakkum MJ

PROVIDER: S-EPMC4521095 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background Inflammation in epicardial adipose tissue (EAT) may contribute to coronary atherosclerosis. Myocardial bridge is a congenital anomaly in which the left anterior descending coronary artery takes a "tunneled" course under a bridge of myocardium: while atherosclerosis develops in the proximal left anterior descending coronary artery, the bridged portion is spared, highlighting the possibility that geographic separation from inflamed EAT is protective. We tested the hypothesis that inflammation in EAT was related to atherosclerosis by comparing EAT from proximal and bridge depots in individuals with myocardial bridge and varying degrees of atherosclerotic plaque. Methods and Results Maximal plaque burden was quantified by intravascular ultrasound, and inflammation was quantified by pericoronary EAT signal attenuation (pericoronary adipose tissue attenuation) from cardiac computed tomography scans. EAT overlying the proximal left anterior descending coronary artery and myocardial bridge was harvested for measurement of mRNA and microRNA (miRNA) using custom chips by Nanostring; inflammatory cytokines were measured in tissue culture supernatants. Pericoronary adipose tissue attenuation was increased, indicating inflammation, in proximal versus bridge EAT, in proportion to atherosclerotic plaque. Individuals with moderate-high versus low plaque burden exhibited greater expression of inflammation and hypoxia genes, and lower expression of adipogenesis genes. Comparison of gene expression in proximal versus bridge depots revealed differences only in participants with moderate-high plaque: inflammation was higher in proximal and adipogenesis lower in bridge EAT. Secreted inflammatory cytokines tended to be higher in proximal EAT. Hypoxia-inducible factor 1a was highly associated with inflammatory gene expression. Seven miRNAs were differentially expressed by depot: 3192-5P, 518D-3P, and 532-5P were upregulated in proximal EAT, whereas miR 630, 575, 16-5P, and 320E were upregulated in bridge EAT. miR 630 correlated directly with plaque burden and inversely with adipogenesis genes. miR 3192-5P, 518D-3P, and 532-5P correlated inversely with hypoxia/oxidative stress, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PCG1a), adipogenesis, and angiogenesis genes. Conclusions Inflammation is specifically elevated in EAT overlying atherosclerotic plaque, suggesting that EAT inflammation is caused by atherogenic molecular signals, including hypoxia-inducible factor 1a and/or miRNAs in an "inside-to-out" relationship. Adipogenesis was suppressed in the bridge EAT, but only in the presence of atherosclerotic plaque, supporting cross talk between the vasculature and EAT. miR 630 in EAT, expressed differentially according to burden of atherosclerotic plaque, and 3 other miRNAs appear to inhibit key genes related to adipogenesis, angiogenesis, hypoxia/oxidative stress, and thermogenesis in EAT, highlighting a role for miRNA in mediating cross talk between the coronary vasculature and EAT.

Project description:ObjectiveWe sought to investigate the correlation of pericoronary adipose tissue with coronary artery disease and left ventricular (LV) function.MethodsParticipants with clinically suspected coronary artery disease were enrolled. All participants underwent coronary computed tomography angiography (CCTA) and echocardiography followed by invasive coronary angiography (ICA) within 6 months. Pericoronary adipose tissue (PCAT) was extracted to analyze the correlation with the Gensini score and LV function parameters, including IVS, LVPW, LVEDD, LVESD, LVEDV, LVESV, FS, LVEF, LVM, and LVMI. The correlation between PCAT and the Gensini score was assessed using Spearman's correlation analysis, and that between the PCAT volume or FAI and LV function parameters was determined using partial correlation analysis.ResultsOne hundred and fifty-nine participants (mean age, 64.55 ± 10.64 years; men, 65.4% [104/159]) were included in the final analysis. Risk factors for coronary artery disease, such as hypertension, diabetes, dyslipidemia, and a history of smoking or drinking, had no significant association with PCAT (P > 0.05), and there was also no correlation between PCAT and the Gensini score. However, the LAD-FAI was positively correlated with the IVS (r = 0.203, P = 0.013), LVPW (r = 0.218, P = 0.008), LVEDD (r = 0.317, P < 0.001), LVESD (r = 0.298, P < 0.001), LVEDV (r = 0.317, P < 0.001), LVESV (r = 0.301, P < 0.001), LVM (r = 0.371, P < 0.001), and LVMI (r = 0.304, P < 0.001). Also, the LCX-FAI was positively correlated with the LVEDD (r = 0.199, P = 0.015), LVESD (r = 0.190, P = 0.021), LVEDV (r = 0.203, P = 0.013), LVESV (r = 0.197, P = 0.016), LVM (r = 0.220, P = 0.007), and LVMI (r = 0.172, P = 0.036), and the RCA-FAI was positively correlated with the LVEDD (r = 0.258, P = 0.002), LVESD (r = 0.238, P = 0.004), LVEDV (r = 0.266, P = 0.001), LVESV (r = 0.249, P = 0.002), LVM (r = 0.237, P = 0.004), and LVMI (r = 0.218, P = 0.008), respectively. Finally, the total volume was positively correlated with FS (r = 0.167, P = 0.042).ConclusionThe FAI was positively correlated with the LV function but was not associated with the severity of coronary artery disease.