Impact of obesity on cardiac metabolism, fibrosis, and function

Rajiv Mahajan1, Dennis H Lau1, Prashanthan Sanders1

  • 1Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.

Insights

Obesity causes cardiac dysfunction and fibrosis, increasing atrial fibrillation risk. Weight loss strategies can reverse these harmful effects on the heart.

Area of Science:

  • Cardiology
  • Metabolic Syndrome
  • Pathophysiology

Background:

  • Obesity is a global pandemic impacting healthcare systems.
  • Obesity is linked to atherosclerotic vascular disease, ventricular hypertrophy, heart failure, atrial fibrillation, and stroke.
  • Obesity contributes to cardiac dysfunction, adipokine dysregulation, and pro-fibrotic pathways.

Purpose of the Study:

  • To review cardiac metabolic and functional alterations in obesity.
  • To explore mechanisms of cardiac fibrosis in obesity.
  • To focus on atrial substrate changes predisposing to atrial fibrillation.

Main Methods:

  • Review of experimental and clinical studies.
  • Analysis of signaling pathways involved in cardiac fibrosis.
  • Examination of metabolic and functional changes in the obese heart.

Main Results:

  • Obesity is associated with cardiac dysfunction and fibrosis.
  • Cardiac fibrosis is a key factor in obesity-related atrial fibrillation.
  • Obesity-induced cardiac changes are potentially reversible with weight reduction.

Conclusions:

  • Obesity significantly impacts cardiac metabolism and function.
  • Cardiac fibrosis, driven by obesity, underlies atrial fibrillation.
  • Weight reduction offers a potential therapeutic strategy for reversing obesity-related cardiac pathology.

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