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In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
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Arrhythmogenic Delayed Afterdepolarizations Are Promoted by Severe Hypothermia But Not Therapeutic Hypothermia

Hidehira Fukaya1,2, Joseph S Piktel1,3, Xiaoping Wan1

  • 1The Heart and Vascular Research Center, MetroHealth Campus, Case Western Reserve University.

Circulation Journal : Official Journal of the Japanese Circulation Society
|August 8, 2017
PubMed

Insights

Severe hypothermia (SH) increases arrhythmia risk by enhancing calcium release, unlike therapeutic hypothermia (TH). TH suppresses calcium release, preventing triggered activity and associated arrhythmias.

Area of Science:

  • Cardiology
  • Physiology
  • Biophysics

Background:

  • Severe hypothermia (SH) is arrhythmogenic, but its effect on arrhythmias compared to therapeutic hypothermia (TH) is unclear.
  • Hypothesized that SH, not TH, increases susceptibility to calcium-mediated arrhythmia triggers.

Purpose of the Study:

  • To investigate the effects of SH and TH on calcium handling and arrhythmia triggers.
  • To determine the temperature-dependent mechanisms underlying hypothermia-induced arrhythmias.

Main Methods:

  • Optical mapping of spontaneous calcium release (SCR) and delayed afterdepolarizations (DADs) in canine wedge preparations at normothermia (36°C), TH (32°C), and SH (28°C).
  • Evaluation of isolated myocyte calcium release kinetics and sarcoplasmic reticulum (SR) calcium content.
  • Assessment of calcium spark frequency and ryanodine receptor activity.

Main Results:

  • Therapeutic hypothermia (TH) suppressed multicellular SCR slope and DAD amplitude, preventing triggered activity.
  • Severe hypothermia (SH) significantly increased SCR slope and DAD amplitude, leading to triggered activity.
  • SH markedly increased Ca spark frequency, suggesting increased ryanodine receptor open probability, while SR Ca content remained similar between TH and SH.

Conclusions:

  • Temperature-dependent alterations in calcium release explain the increased susceptibility to arrhythmia triggers in SH.
  • SH increases the risk of lethal arrhythmias due to enhanced calcium release, whereas TH does not.
  • Findings differentiate the arrhythmogenic potential of SH from the protective effects of TH on cardiac electrophysiology.
Abstract

Keywords:
ArrhythmiaOptical mappingTherapeutic hypothermiaTriggered activity

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