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Related Experiment Video

Updated: May 7, 2026

Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection

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Simulating cell apoptosis induced sinus node dysfunction.

Sanjay Kharche, John Beling, Irina V Biktasheva

Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference

|October 11, 2013

Summary

Apoptosis of sinoatrial node (SAN) pacemaker cells significantly disrupts atrial electrical activity, leading to bradycardia and sinus arrest. This study quantifies how increasing cell death in the SAN impacts heart rhythm.

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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

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Published on: July 5, 2021

Area of Science:

Computational electrophysiology
Cardiac cell modeling
Arrhythmia mechanisms

Background:

Sinus node dysfunction (SND) is a clinical condition affecting heart rhythm.
Sinoatrial node (SAN) pacemaker cell apoptosis is linked to SND.
Understanding the impact of SAN dysfunction on atrial pacing is crucial.

Purpose of the Study:

To investigate the effect of sinoatrial node (SAN) pacemaker cell apoptosis on electrical propagation in atrial tissue.
To develop and utilize a computational model to simulate these effects.
To quantify the relationship between pacemaker cell apoptosis and cardiac rhythm disturbances.

Main Methods:

Extended the Fenton Karma model to simulate mouse SAN and atrial cell action potentials.
Incorporated cell models into a 2D computational model of the SAN and surrounding atrial tissue.
Simulated varying proportions of apoptotic pacemaker cells and quantified effects on atrial cycle length (ACL) and pacing.

Main Results:

Determined SAN size (0.6 mm radius) for a basal mouse atrial cycle length (ACL) of 295 ms.
Observed drastic ACL increase at low pacemaker cell apoptosis levels.
Documented bradycardia and high incidence of sinus arrest with increasing apoptosis; 10% apoptosis led to complete pacing arrest.

Conclusions:

Pacemaker cell apoptosis is a significant mechanism underlying sinus node dysfunction (SND).
Computational modeling confirms the detrimental impact of apoptotic cells on atrial electrophysiology.
Results highlight the critical role of SAN integrity in maintaining normal heart rhythm.