Examines a model where physiological stressors disrupt synchronization across sinoatrial node pacemaker cells, explaining transition-linked arrhythmias and vulnerability.
Key Takeaways
- Model remains a reduced phenomenological framework rather than a calibrated anatomical simulation
- Additional human-relevant substrate-forming context is habitual upright posture
- Stress-related arrhythmogenesis can be framed as an interaction between substrate and perturbation