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A Dynamical Threshold for Cardiac Delayed Afterdepolarization-Mediated Triggered Activity.

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Hypokalemia lowers the dynamic threshold for action potential (AP) excitation in ventricular myocytes, promoting triggered activity. This effect is linked to ion channel dynamics, particularly IK1 and INCX.

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Area of Science:

  • Cardiovascular Physiology
  • Computational Biology
  • Electrophysiology

Background:

  • Ventricular myocytes require a specific voltage threshold (around -60 mV) for action potential (AP) excitation, primarily driven by sodium current (INa).
  • Hypokalemia shifts the resting potential further from this threshold, typically requiring stronger stimuli for AP initiation.
  • However, hypokalemia has been observed to promote triggered activity, a phenomenon not fully explained by the direct effect on the INa threshold.

Purpose of the Study:

  • To investigate the mechanisms underlying hypokalemia-induced triggered activity in ventricular myocytes.
  • To identify the factors contributing to altered excitation thresholds in hypokalemia.
  • To elucidate the role of ion channel dynamics in cardiac excitability during low potassium conditions.

Main Methods:

  • Computer simulations of rabbit ventricular myocyte electrophysiology.
  • Experimental studies on rabbit ventricular myocytes.
  • Bifurcation analyses to identify dynamical thresholds and underlying mechanisms.

Main Results:

  • A dynamical threshold, distinct from the INa threshold, was identified, primarily determined by IK1 and INCX.
  • This dynamical threshold is lower in hypokalemia, facilitating spontaneous depolarization and triggered APs, especially in conjunction with calcium release.
  • The system can achieve depolarization above the ICa,L threshold even with INa block due to this dynamical threshold.
  • Sodium channel (INa) block is less effective in suppressing hypokalemia-induced triggered activity in tissue compared to normokalemia.

Conclusions:

  • Hypokalemia lowers a critical dynamical excitation threshold in ventricular myocytes, explaining its pro-arrhythmic effects by promoting triggered activity.
  • This threshold is governed by a saddle-node bifurcation involving IK1 and INCX, and is particularly sensitive to calcium dynamics.
  • Understanding this dynamical threshold is crucial for explaining arrhythmogenesis in hypokalemia and developing targeted therapies.