Key result
Epicardial and pericardial adipose tissue exert a direct metabolic impact by secreting proinflammatory adipokines and free fatty acids, promoting cardiovascular disease locally in the context of T2DM.
This review highlights the pathophysiological role of epicardial and pericardial adipose tissue in promoting cardiovascular disease among patients with Type-2 diabetes mellitus.
EAT/PAT may mediate T2DM-driven coronary disease; leaves open whether depot-specific therapies alter outcomes.
Type-2 diabetes mellitus (T2DM) plays a central role in the development of cardiovascular disease (CVD). However, its relationship to epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) in particular is important in the pathophysiology of coronary artery disease. Owing to its close proximity to the heart and coronary vasculature, EAT exerts a direct metabolic impact by secreting proinflammatory adipokines and free fatty acids, which promote CVD locally. In this review, we have discussed the relationship between T2DM and cardiac fat deposits, particularly EAT and PAT, which together exert a big impact on the cardiovascular health.
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Adam M. Noyes (2014) conducted a review in Type-2 diabetes mellitus and cardiovascular disease. Cardiac adipose tissue (epicardial and pericardial) was evaluated. Epicardial and pericardial adipose tissue exert a direct metabolic impact by secreting proinflammatory adipokines and free fatty acids, promoting cardiovascular disease locally in the context of T2DM.
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