Why the study?
How antiarrhythmic drugs modify spatiotemporal factors involved in ventricular fibrillation, such as spatial alternans and conduction velocity, is poorly understood.
Does verapamil alter spatial electrophysiological properties to prevent ventricular fibrillation initiation in isolated rabbit hearts?
Does verapamil alter spatial electrophysiological properties to prevent ventricular fibrillation initiation in isolated rabbit hearts?
In isolated rabbit hearts, calcium spatial alternans and slow conduction velocity drive VF initiation, which can be postponed by the calcium blocker verapamil.
Answers are grounded in this paper and cite their sources.
Calcium spatial alternans predominate in VF initiation; leaves open whether targeted calcium modulation prevents clinical arrhythmias.
BACKGROUND: Alternans have been associated with the development of ventricular fibrillation and its control has been proposed as antiarrhythmic strategy. However, cardiac arrhythmias are a spatiotemporal phenomenon in which multiple factors are involved (e.g. calcium and voltage spatial alternans or heterogeneous conduction velocity) and how an antiarrhythmic drug modifies these factors is poorly understood. OBJECTIVE: The objective of the present study is to evaluate the relation between spatial electrophysiological properties (i.e. spatial discordant alternans and conduction velocity) and the induction of ventricular fibrillation (VF) when a calcium blocker is applied. METHODS: The mechanisms of initiation of VF were studied by simultaneous epicardial voltage and calcium optical mapping in isolated rabbit hearts using an incremental fast pacing protocol. The additional value of analyzing spatial phenomena in the generation of unidirectional blocks and reentries as precursors of VF was depicted. Specifically, the role of action potential duration (APD), calcium transients (CaT), spatial alternans and conduction velocity in the initiation of VF was evaluated during basal conditions and after the administration of verapamil. RESULTS: Our results enhance the relation between (1) calcium spatial alternans and (2) slow conduction velocities with the dynamic creation of unidirectional blocks that allowed the induction of VF. In fact, the administration of verapamil demonstrated that calcium and not voltage spatial alternans were the main responsible for VF induction. CONCLUSIONS: VF induction at high activation rates was linked with the concurrence of a low conduction velocity and high magnitude of calcium alternans, but not necessarily related with increases of APD. Verapamil can postpone the development of cardiac alternans and the apparition of ventricular arrhythmias.
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Hernández‐Romero et al. (2019) studied this question.
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