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Arrhythmia Vulnerability in Diabetic Cardiac Tissue is Species-Dependent: Effects of I KATP, Uncoupling, and Connexin

A Ghazanfari1, E Vigmond2, A Nygren3

  • 1Department of Electrical and Computer Engineering, University of Calgary, Calgary, AB, Canada. a.ghazanfari@ucalgary.ca.

Cardiovascular Engineering and Technology
|June 29, 2017
PubMed

Insights

Diabetes complicates the heart, increasing arrhythmia risk. Simulations reveal species-dependent vulnerability, with rabbit models aligning with human data, unlike rat models.

Area of Science:

  • Cardiovascular Physiology
  • Computational Biology
  • Diabetology

Background:

  • Diabetes mellitus is a known risk factor for cardiac complications, including arrhythmias.
  • The precise mechanisms underlying diabetes-associated arrhythmia risk remain incompletely understood.
  • Factors such as ATP-sensitive potassium channel (IKATP) activity and gap junction coupling are implicated in cardiac electrical stability.

Purpose of the Study:

  • To investigate the impact of diabetes on ischemia-induced arrhythmia vulnerability.
  • To explore the roles of ATP-sensitive potassium current (IKATP) and gap junction uncoupling in diabetic hearts.
  • To assess species-specific differences in arrhythmia risk using computational models.

Main Methods:

  • Computational simulations of ventricular electrophysiology in healthy and diabetic rat and rabbit models.
  • Modeling of ATP-sensitive potassium channel (IKATP) opening during ischemia.
  • Simulation of gap junction uncoupling and its effect on reentrant arrhythmia vulnerability.
  • Analysis of conduction reserve using 1D simulations.

Main Results:

  • The diabetic rat model exhibited decreased vulnerability to reentrant arrhythmia compared to the healthy rat model.
  • Conversely, the diabetic rabbit model showed increased vulnerability to reentrant arrhythmia relative to the healthy rabbit model.
  • Decreased gap junctional coupling exacerbated arrhythmia vulnerability in both rabbit models.
  • Opening of IKATP during ischemia widened the window of vulnerability for arrhythmias.

Conclusions:

  • Arrhythmia vulnerability in the diabetic heart is significantly species-dependent.
  • Rabbit models demonstrate greater similarity to human clinical observations regarding diabetic arrhythmia risk than rat models.
  • Computational modeling highlights the critical roles of IKATP and gap junction coupling in modulating arrhythmia susceptibility in diabetes.
Keywords:
ATP-dependent potassium channelConnexin lateralizationDiabetesIschemiaReentrant cardiac arrhythmiaWindow of vulnerability

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