Key Points
- To examine how microstructural alterations and redistribution of gap junctions produce discontinuous conduction disturbances that trigger reentrant arrhythmias in structural heart disease.
- Evaluated the biophysical impact of irregular gap junction distribution and microscopic cellular load variations during longitudinal and transverse myocardial propagation.
- Modeled how the loss of side-to-side coupling between fibers creates cell isolation and reduces propagation diversity.
- Normal cardiac propagation relies on stochastic microscopic load variations that protect against arrhythmias by naturally smoothing the macroscopic wavefront.
- Loss of lateral cell connections in microfibrosis eliminates this protective microscopic diversity, creating severe spatial load variations that precipitate conduction block and reentry.
Structured PICO
PPopulationMyocardial microstructure / cardiac muscle cells
IInterventionMicrofibrosis (loss of side-to-side cell connections)
CComparatorNormal mature cardiac muscle
OOutcomeConduction block and reentry arrhythmias
Microfibrosis and the resulting loss of side-to-side cellular connections provide a mechanistic explanation for the development of conduction block and reentrant arrhythmias in structural heart disease.