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A novel approach to identifying antiarrhythmic drug targets
1Dept of Biomedical Sciences, T7 012C VRT, Cornell University, Ithaca, NY 14853-6401, USA. rfg2@cornell.edu
Insights
Sudden cardiac death from ventricular fibrillation (VF) may be caused by spiral wave re-entry. Targeting electrical restitution may offer a new antiarrhythmic therapy by suppressing VF.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
- Medical Science
Background:
- Sudden cardiac death (SCD) is the leading cause of mortality in the USA.
- Ventricular fibrillation (VF) is a primary cause of SCD.
- VF may originate from spiral wave re-entry in cardiac tissue.
Purpose of the Study:
- To investigate the link between electrical alternans and VF.
- To explore the role of cardiac electrical restitution in VF.
- To identify potential antiarrhythmic targets for VF.
Main Methods:
- Experimental and theoretical studies of cardiac tissue.
- Analysis of spiral wave dynamics.
- Investigating the effects of agents modulating the restitution slope.
Main Results:
- VF initiation and break-up correlate with electrical alternans.
- Electrical alternans are associated with a steeply sloped restitution relation.
- Agents reducing the restitution slope suppress alternans and terminate VF.
Conclusions:
- Electrical restitution is a potential mechanism driving VF.
- Modulating electrical restitution may serve as a novel antiarrhythmic strategy.
- Targeting electrical restitution offers a promising therapeutic approach for VF.
Abstract:
Sudden cardiac death, secondary to ventricular fibrillation (VF), remains the leading cause of death in the USA. Recent experimental and theoretical studies suggest that VF could be caused by spiral wave re-entry. The initiation and subsequent break-up of spiral waves has been linked to electrical alternans, a phenomenon produced in cardiac tissue that has a steeply sloped restitution relation. Agents that reduce the slope of the restitution relation have been shown to suppress alternans and, presumably by that mechanism, terminate VF. These results suggest that electrical restitution could be a promising new target for antiarrhythmic therapies.