Diabesity in Elderly Cardiovascular Disease Patients: Mechanisms and Regulators

Area of Science:

• Cardiology
• Endocrinology
• Metabolic Syndrome

Background:

• Cardiovascular disease (CVD) is a leading global cause of mortality, with high fasting glucose and obesity as significant risk factors.
• Diabesity, the co-occurrence of type 2 diabetes and obesity, exacerbates CVD risk through cardiac, metabolic, inflammatory, and neurohumoral alterations.
• Epicardial adipose tissue (EAT) dysfunction in diabesity promotes myocardial inflammation and fibrosis, linked to heart failure, atrial fibrillation, and atherosclerosis.

Purpose of the Study:

• To review the pathophysiological mechanisms linking diabesity to cardiovascular disease development and progression.
• To explore the therapeutic implications of understanding these diabesity-associated CVD mechanisms.
• To highlight the need for improved knowledge for comprehensive patient management.

Main Methods:

• Literature review of studies on diabesity, cardiovascular disease, and epicardial adipose tissue.
• Analysis of pathophysiological pathways connecting metabolic dysfunction to cardiac changes.
• Synthesis of current therapeutic strategies and their impact on diabesity-related CVD.

Main Results:

• Diabesity significantly contributes to cardiac dysfunction (diabesity-related cardiomyopathy) via inflammation and fibrosis.
• Epicardial adipose tissue plays a crucial role in mediating diabesity's adverse cardiovascular effects.
• Hypoglycemic drugs show potential in reducing EAT volume and improving its metabolic profile.

Conclusions:

• A deeper understanding of diabesity's cardiovascular mechanisms is essential for effective patient management.
• Targeting metabolic and inflammatory pathways in diabesity offers therapeutic opportunities for CVD prevention and treatment.
• Optimizing glucometabolic control is critical in managing diabesity-related cardiovascular complications.