Abstract
(1) Sodium–glucose cotransporter-2 inhibitors (SGLT2-i) reduce adipose tissue and cardiovascular events in patients with type 2 diabetes (T2D). Accumulation of epicardial adipose tissue (EAT) is associated with increased cardio-metabolic risks and obstructive coronary disease events in patients with T2D. (2) We performed a systematic review and meta-analysis of SGLT2-i therapy on T2D patients, reporting data on changes in EAT after searching the PubMed/MEDLINE, Embase, Science Direct, Scopus, Google Scholar, and Cochrane databases. A random effects or fixed effects model meta-analysis was then applied. (3) Results: A total of three studies (n = 64 patients with SGLT2-i, n = 62 with standard therapy) were included in the final analysis. SGLT2 inhibitors reduced EAT (SMD: −0.82 (−1.49; −0.15); p < 0.0001). An exploratory analysis showed that HbA1c was significantly reduced with SGLT2-i use, while body mass index was not significantly reduced with this drug. (4) Conclusions: This meta-analysis suggests that the amount of EAT is significantly reduced in T2D patients with SGLT2-i treatment.
Highlights
A close link exists between type 2 diabetes (T2D) and cardiovascular disease
The search included 107 potentially relevant articles after title screening, and 84 studies were excluded after abstract screening, as these were non-human or preclinical studies, or did not assess the treatment of interest
Three studies examined the effect of Sodium–glucose cotransporter-2 inhibitors (SGLT2-i) on Epicardial adipose tissue (EAT) compared to a control group and were considered eligible for the quantitative analyses
Summary
A close link exists between type 2 diabetes (T2D) and cardiovascular disease. Cardiovascular disease is the most prevalent cause of morbidity and mortality among people with type 2 diabetes [1].There is growing evidence concerning the importance of epicardial adiposity in cardiometabolic risk. A close link exists between type 2 diabetes (T2D) and cardiovascular disease. Cardiovascular disease is the most prevalent cause of morbidity and mortality among people with type 2 diabetes [1]. Studies suggest that excessive EAT plays an important role in the genesis of coronary heart disease through potential paracrine or endocrine mechanisms by exerting inflammatory mediators, such as TNF-alpha, IL-6, adipocytokines, and leptin, which predispose to atherosclerosis [2,3]. Studies have shown that EAT is closely related to the extent and severity of coronary artery disease [4]. It is associated with high-risk atherosclerotic plaque composition [5]
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