To propose a hypothesis centered on the sinoatrial node (SAN) that explains stress-related arrhythmogenic vulnerability due to transient loss of synchronization within the pacemaker population.
Approach:
Key Findings:
The SAN operates as a heterogeneous population of pacemaker cells.
Increased pacemaker-dispersion vulnerability can result from stress and autonomic loading.
Abrupt physiological transitions may reveal latent instability in the SAN.
Interpretation:
The function of the SAN should be understood in terms of population-level coherence.
Limitations:
The model is a phenomenological framework and lacks a calibrated anatomical simulation.
Validation of the proposed predictions requires further empirical testing.
Conclusion:
The study highlights the significance of synchronization reserve in the SAN during physiological challenges.
