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

Emir M Muzurović1, Snežana Vujošević1, Dimitri P Mikhailidis2,3

  • 1Department of Internal Medicine, Endocrinology Section, 274294Clinical Centre of Montenegro, Faculty of Medicine, University of Montenegro, Podgorica, Montenegro.

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|April 12, 2021
PubMed
Summary

Epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) are linked to cardiovascular disease in diabetes. Lifestyle changes and medications may reduce EAT/PAT, potentially lowering cardiovascular risk in diabetic patients.

Keywords:
antidiabeticscardiovascular diseasecardiovascular riskdiabetes mellitusepicardial fatpericardial fat

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Area of Science:

  • Cardiology
  • Endocrinology
  • Metabolic Disorders

Background:

  • Diabetes mellitus (DM) is a chronic metabolic disorder and a significant risk factor for cardiovascular disease (CVD).
  • Visceral adiposity, particularly epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT), is increasingly recognized for its role in DM-related cardiovascular complications.
  • EAT and PAT are biologically active and implicated in atherosclerosis, atrial fibrillation, myocardial dysfunction, and heart failure in diabetic patients.

Purpose of the Study:

  • To review the significance of pericardial adipose tissue (PAT) and epicardial adipose tissue (EAT) in patients with diabetes mellitus (DM).
  • To explore therapeutic interventions targeting EAT and PAT to mitigate cardiovascular risk in DM.
  • To highlight the potential of EAT/PAT modification as a therapeutic strategy for reducing cardiovascular burden.

Main Methods:

  • This review synthesizes existing evidence on the role of EAT and PAT in DM-related cardiovascular outcomes.
  • It examines the impact of various therapeutic interventions on EAT/PAT quantity and secretory patterns.
  • The review discusses the potential of EAT/PAT as a modifiable target for cardiovascular risk reduction.

Main Results:

  • EAT is biologically active and a key determinant of cardiovascular morbidity and mortality in DM due to its anatomical location and inflammatory profile.
  • Adiposity, especially visceral fat, is strongly linked to increased CVD risk.
  • Therapeutic interventions including diet, exercise, antidiabetics, and statins may influence EAT/PAT quantity and quality, improve metabolic profiles, and reduce inflammation.

Conclusions:

  • Modification of EAT and PAT represents a promising therapeutic target for reducing the cardiovascular burden in patients with DM.
  • While lifestyle modifications and certain medications show potential in altering EAT/PAT, further well-designed studies are required.
  • Defining clear cardiovascular benefits and optimal therapeutic approaches for EAT/PAT management in DM is crucial.