Can We Decrease Epicardial and Pericardial Fat in Patients With Diabetes?

Diabetes mellitus (DM) is a chronic and complex metabolic disorder and also an important cause of cardiovascular (CV) disease (CVD). Patients with type 2 DM (T2DM) and obesity show a greater propensity for visceral fat deposition (and excessive fat deposits elsewhere) and the link between adiposity...

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Bibliographic Details
Published in:Journal of Cardiovascular Pharmacology and Therapeutics 2021-09, Vol.26 (5), p.415-436
Main Authors: Muzurović, Emir M., Vujošević, Snežana, Mikhailidis, Dimitri P.
Format: Article
Language:English
Subjects:
Adipose Tissue - drug effects
Adipose Tissue - physiopathology
Cardiovascular Diseases - complications
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - physiopathology
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - drug therapy
Exercise
Humans
Hypoglycemic Agents - pharmacology
Obesity - complications
Obesity - physiopathology
Pericardium - drug effects
Pericardium - physiopathology
Risk Factors
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Summary:Diabetes mellitus (DM) is a chronic and complex metabolic disorder and also an important cause of cardiovascular (CV) disease (CVD). Patients with type 2 DM (T2DM) and obesity show a greater propensity for visceral fat deposition (and excessive fat deposits elsewhere) and the link between adiposity and CVD risk is greater for visceral than for subcutaneous (SC) adipose tissue (AT). There is growing evidence that epicardial AT (EAT) and pericardial AT (PAT) play a role in the development of DM-related atherosclerosis, atrial fibrillation (AF), myocardial dysfunction, and heart failure (HF). In this review, we will highlight the importance of PAT and EAT in patients with DM. We also consider therapeutic interventions that could have a beneficial effect in terms of reducing the amount of AT and thus CV risk. EAT is biologically active and a likely determinant of CV morbidity and mortality in patients with DM, given its anatomical characteristics and proinflammatory secretory pattern. Consequently, modification of EAT/PAT may become a therapeutic target to reduce the CV burden. In patients with DM, a low calorie diet, exercise, antidiabetics and statins may change the quantity of EAT, PAT or both, alter the secretory pattern of EAT, improve the metabolic profile, and reduce inflammation. However, well-designed studies are needed to clearly define CV benefits and a therapeutic approach to EAT/PAT in patients with DM.
ISSN:1074-2484
1940-4034
DOI:10.1177/10742484211006997