Stress-induced pacemaker desynchronization in the sinoatrial node

1

The sinoatrial node (SAN) consists of a heterogeneous population of pacemaker cells rather than a single dominant oscillator.
2

Stress-related arrhythmogenic vulnerability may arise from transient loss of synchronization within the SAN pacemaker population.
3

Sustained autonomic stress and structural remodeling can amplify intrinsic-frequency dispersion, reducing synchronization reserve.
4

Abrupt physiological transitions can expose latent instability in the SAN, leading to arrhythmogenic events.
5

The proposed model emphasizes the importance of population-level coherence in the SAN for maintaining normal rhythm.