Hormonal
Perivascular adipose tissue (PVAT) and epicardial adipose tissue (EAT) exert local paracrine effects on cardiovascular health, functioning as protective in lean states via adiponectin and prostacyclin release, but becoming pathogenic in obesity by shifting to a pro-inflammatory state that promotes vasoconstriction, smooth muscle proliferation, and atherosclerosis.
Epicardial and perivascular fat are biologically active tissues that influence heart health. In lean individuals, they release protective substances like adiponectin that keep blood vessels flexible and healthy. In obesity, these depots become inflamed, releasing harmful substances that stiffen arteries and promote plaque buildup. While imaging these fats is useful for research, current evidence suggests that overall visceral fat reduction (via weight management) is the most effective way to mitigate these risks, as local fat measurements do not significantly add to risk prediction beyond standard visceral fat metrics.
In this setting, the beneficial paracrine effects of EAT (i.e., ADIPOQ release, fatty acid uptake) are abrogated, and a causative role in local inflammation and CV pathophysiology may be assumed... PVAT-derived prostacyclin prevented acetylcholine-induced endothelial dysfunction, which is a precursor to atherosclerosis.
Why this rating
The paper synthesizes extensive animal models (knockouts, transplantation) and human observational/imaging studies, though it acknowledges a lack of definitive human causality trials.
Source
Epicardial and Perivascular Adipose Tissues and Their Influence on Cardiovascular Disease: Basic Mechanisms and Clinical Associations
Timothy P. Fitzgibbons et al. · Journal of the American Heart Association · 2014
DOI 10.1161/jaha.113.000582
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