Correlation between epicardial adipose tissue and atrial fibrillation burden in coronary artery bypass graft surgery.

AIMS: Recent studies suggest an association between epicardial adipose tissue (EAT) and atrial fibrillation. The aim of the study is to evaluate the quantitative and qualitative characteristics of EAT in relation to atrial fibrillation burden after coronary artery bypass graft (CABG). METHODS: This prospective single-centre study included patients undergoing CABG. The patients underwent transthoracic echocardiography and collection of a bioptic sample containing right appendage and EAT during CABG for histological characterization. After surgery, clinical and telemetry data were collected. RESULTS: Fifty-six consecutive patients were enrolled. The mean postsurgical hospitalization was 7.9 ±â€Š3.7 days. Twenty-two patients had at least one episode of atrial fibrillation. In the atrial fibrillation group, there was a bigger atrial volume, a higher degree of diastolic disfunction, a thicker layer of EAT and an older median age in comparison with the group that did not develop it. EAT with a cut-off of 4 mm was a predictor of atrial fibrillation with an odds ratio (OR) of 1.49 (confidence interval (CI) 1.09-2.04), 73% of sensibility and 89% of specificity. From the histological analyses, the patients with atrial fibrillation had a significantly higher percentage of fibrosis. At univariate analysis, atrial volume [OR 1.05, CI 1.01-1.09, P = 0.022], E/A rate (OR 0.04, CI 0.02-0.72 P = 0.29), the percentage of fibrosis (OR 1.12, CI 1.00-1.25, P = 0.045) and age (OR 1.17, CI 1.07-1.28, P = 0.001) were predictors of atrial fibrillation. At multivariate analysis, atrial volume (P = 0.027), fibrosis (P = 0.003) and age (P = 0.039) were independent predictors of atrial fibrillation. CONCLUSION: Postcardiac surgical atrial fibrillation is frequent. EAT thickness, atrial volume, fibrosis and age are predictors of postcardiac surgical atrial fibrillation.

Senolytic effects of quercetin in an in vitro model of pre-adipocytes and adipocytes induced senescence.

The dysfunction of adipose tissue with aging and the accumulation of senescent cells has been implicated in the pathophysiology of chronic diseases. Recently interventions capable of reducing the burden of senescent cells and in particular the identification of a new class of drugs termed senolytics have been object of extensive investigation. We used an in vitro model of induced senescence by treating both pre-adipocytes as well as mature adipocytes with hydrogen peroxide (H2O2) at a sub-lethal concentration for 3 h for three consecutive days, and hereafter with 20 uM quercetin at a dose that in preliminary experiments resulted to be senolytic without cytotoxicity. H2O2 treated pre-adipocytes and adipocytes showed typical senescence-associated features including increased beta-galactosidase activity (SA-ß-gal) and p21, activation of ROS and increased expression of pro-inflammatory cytokines. The treatment with quercetin in senescent pre-adipocytes and adipocytes was associated to a significant decrease in the number of the SA-ß-gal positive cells along with the suppression of ROS and of inflammatory cytokines. Besides, quercetin treatment decreased miR-155-5p expression in both models, with down-regulation of p65 and a trend toward an up-regulation of SIRT-1 in complete cell extracts. The senolytic compound quercetin could affect AT ageing by reducing senescence, induced in our in vitro model by oxidative stress. The downregulation of miRNA-155-5p, possibly through the modulation of NF-κB and SIRT-1, could have a key role in the effects of quercetin on both pre-adipocytes and adipocytes.

Brown and Beige Adipose Tissue and Aging.

Across aging, adipose tissue (AT) changes its quantity and distribution: AT becomes dysfunctional with an increase in production of inflammatory peptides, a decline of those with anti-inflammatory activity and infiltration of macrophages. Adipose organ dysfunction may lead to age-related metabolic alterations. Aging is characterized by an increase in adiposity and a decline in brown adipose tissue (BAT) depots and activity, and UCP1 expression. There are many possible links to age-associated involution of BAT, including the loss of mitochondrial function, impairment of the sympathetic nervous system, age-induced alteration of brown adipogenic stem/progenitor cell function and changes in endocrine signals. Aging is also associated with a reduction in beige adipocyte formation. Beige adipocytes are known to differentiate from a sub-population of progenitors resident in white adipose tissue (WAT); a defective ability of progenitor cells to proliferate and differentiate has been hypothesized with aging. The loss of beige adipocytes with age may be caused by changes in trophic factors in the adipose tissue microenvironment, which regulate progenitor cell proliferation and differentiation. This review focuses on possible mechanisms involved in the reduction of BAT and beige activity with aging, along with possible targets for age-related metabolic disease therapy.