Epicardial Adiposopathy and Atrial Fibrillation

Atrial fibrillation (AF) is the most frequent heart rhythm disorder in clinical practice. Many conditions could predispose the development of AF such as hypertension, heart failure, valvular heart disease, aging, coronary artery disease, diabetes mellitus, and sleep apnoea.

Kocyigit and colleagues reported a study to investigate the association between epicardial adipose tissue (EAT) thickness and AF recurrence after cryoballoon-based pulmonary vein isolation (PVI). A total of 249 patients (55.6 ± 10.7 years; 48.2% male; 18.5% persistent AF were followed-up for 29 months (8 months-48 months). AF after the ablation procedure was 75.9% at a median follow-up of 29 months.

Total periatrial EAT thickness (18.1 ± 6.2 vs. 14.7 ± 4.7 mm; P<0.001) was greater in patients with late AF recurrence when compared to those without. Periventricular or total EAT thickness measurements did not differ between both groups (P>0.05). Multivariate Cox proportional hazard regression analysis showed that periatrial EAT thickness (hazard ratio, 1.086; P=0.001) and left atrial volume index (hazard ratio, 1.144; P<0.001) were independent predictors for late AF recurrence. EAT thickness may serve as a beneficial parameter for prediction of AF recurrence after cryoballoonbased PVI.Read more.....

The Role of NLRP3 Inflammasome in Cardiovascular Diseases

Introduction:

NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome is a cytosolic protein complex involved in the pathogenesis of atherosclerosis . After the endothelial NLRP3 inflammasome is activated by intracellular cholesterol crystals, it directly produces endothelial dysfunction and may initiate or exacerbate vascular injuryduring hypercholesterolemia. In addition, an assembled inflammasome promotes the maturation and release of proinflammatory cytokines interleukin-1β (IL-1 β) and IL-18 .

IL-1β and IL-18 act as mediators that promote the cascade release of other cytokines. These interleukins have been previously implicated in the pathogenesis of atherosclerosis . 

Wang et al found that NLRP3 and downstream cytokines are correlated with the severity of coronary artery disease (CAD).The NLRP3 inflammasome is up-regulated within the myocardium after myocardial infarction(MI), primarily in non-cardiomyocytes (i.e. fibroblasts). Its deficiency markedly improves myocardial function and reduces infarct size after ex vivo myocardial ischaemia–reperfusion (I/R) injury. It was Sandanger  who suggested that the NLRP3 inflammasome is up-regulated in myocardial fibroblasts after MI, potentially contributing to infarct size after myocardial I/R.