doi: 10.1161/CIRCULATIONAHA.108.190525
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(Circulation. 2008;118:1113-1114.)
© 2008 American Heart Association, Inc.
Clinical Summaries
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Dynamic Mechanism for Initiation of Ventricular Fibrillation In Vivo |
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Our study demonstrates a novel mechanism of induction of ventricular fibrillation in vivo in intact normal beagle dogs. This work may contribute to our understanding of the mechanisms leading to the development of ventricular fibrillation in the structurally normal heart. For example, in patients with idiopathic ventricular fibrillation, focal ectopic ventricular activity originating in the Purkinje network is thought to trigger the onset of ventricular fibrillation. Our work also may be clinically relevant to patients with channelopathies, ie, long-QT syndrome, in which typically a short-long-short sequence of premature stimuli induces ventricular tachycardia and fibrillation. We showed in our study that such specific patterns (called CLVF, cycle lengths inducing VF) can indeed lead to ventricular fibrillation by creating conduction block and wave break, depending on the restitution properties of the action potential duration and conduction velocity. In that regard, a potential therapeutic application of our work is to specifically target the restitution parameters with drugs so that CLVF would no longer lead to ventricular fibrillation. We showed that the calcium channel blocker verapamil exerts antifibrillatory effects by altering restitution parameters but not at clinically relevant dosages. However, we postulate that other drugs may prove to have antiarrhythmic effects by altering the restitution parameters of a patient and thus may prevent the induction of ventricular fibrillation rather than by suppressing the premature stimuli. See p 1123.
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Longitudinal Strain Delay Index by Speckle Tracking Imaging: A New Marker of Response to Cardiac Resynchronization Therapy |
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Recent results from the PROSPECT and RETHINQ trials might suggest that a relatively limited and simple quantification of left ventricular dyssynchrony has suboptimal accuracy
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