Abstract
Initiation of ventricular tachycardia (VT) or ventricular fibrillation (VF) requires heterogeneity of the substrate. This heterogeneity has a stable/fixed component (structural or functional) and a dynamic component. The latter explains the random and sudden destabilization of the substrate and the initiation of VT or VF by a ventricular extra stimulus trigger. The main mechanisms of dynamic heterogeneity are discussed at the cellular level (action potential duration alternans and restitution and intracellular calcium cycling instability) and at the tissue level (conduction velocity restitution and concordant and discordant alternans). Better knowledge of dynamic factors in arrhythmogenesis has an overwhelming impact on both predicting malignant arrhythmias and changing the antiarrhythmic drug paradigm from suppressing triggers to modifying dynamic instability factors.
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