Kulvinder Kochar Kaur M.D1*, Gautam Allahbadia M.D(Obstt&Gynae) D.N.B2, Mandeep Singh M.D.DM.(Std) (Neurology)3

Earlier we have extensively reviewed the etiopathogenesis of obesity, role of white adipose tissue (WAT), brown AT (BAT), transcription factors involved like PRDM 16 associated with development of beige/brite AT, role of mirabegron and development of therapies for obese patients with or without diabetes. Here we aimed to study how AT impairment might be an anticipator of cardiovascular (CV) processes heart failure (HF), in patient population with obesity, MetS, in addition to known cases of overt type 2 diabetes mellitus (DM) in view of contradictory observations in association with collection of AT of separate kinds in CV risk along with HF-associated clinical results in obese subjects. Thus here we conducted a systematic review utilizing search engine pubmed; google scholar; web of science; embase; Cochrane review library utilizing the MeSH terms like AO; WAT; BAT; Visceral AT; Epicardial AT (EAT); Obesity; BMI; WC; DM; HFpEF; HFrEF; Atrial fibrillation; Adipocytokines; Adiponectin; Leptin; Resistin; Visfatin; Omentin; Zinc—α-2glycoprotein; Angiopoietin like protein 2; Cardiac remodeling; Renin-Angiotensin –aldosterone System (RAAS); Brain natriuretic peptide; Sympathetic nervous system (SNS); Oxidative stress (OS); Insulin resistance (IR) from 1950 to 2021 till date. We found a total of 550 articles out of which we selected 195 articles for this review. No meta-analysis was done. Proof exists that direct influence of epicardial adipocytes into the underlying myocardium resulting in stimulation of worst cardiac remodeling along with modulating HF generation in addition to AF. Further peri vascular collection of adipocytes, leads to liberation of proinflammatory adipocytokines (adiponectin, leptin, resistin) OS stimulation, switching of phenotypes of macrophages in addition to poor vascular repair, all of which result in microvascular inflammation, endothelial impairment, Atherosclerosis exaggeration, and finally escalation of CV mortality. Nevertheless, systemic actions of WAT and BAT might be separate, with adipogenesis in addition to browning of AT and deficient antiinflammatory adipocytokines (visfatin, omentin, zinc—α-2glycoprotein, glypican 4) were usually correlated withadipose triglyceride lipase escalation, changed glucose homeostasis, IR of skeletal muscles, escalation of cardiomyocyte apoptosis, decreased survival and poor progenitor endothelial cell function that could have a significant Impact on HF generation along with cardiac fibrosis. Thus here we have summarized all these along with how better diagnosis of HFpEF might be feasible with echocardiography. The pro and anti-inflammatory profiles act as good biomarkers for HF risk stratification.

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