3 results match your criteria: "UCLA School of Medicine and Cedars Sinai Medical Center[Affiliation]"

Ventricular fibrillation: how do we stop the waves from breaking?

Circ Res

December 2000

Cardiovascular Research Laboratory and the Departments of Medicine (Cardiology), Physiology and Physiological Science, UCLA School of Medicine and Cedars-Sinai Medical Center, Los Angeles, CA 90095-1760, USA.

Combined experimental and theoretical developments have demonstrated that in addition to preexisting electrophysiological heterogeneities, cardiac electrical restitution properties contribute to breakup of reentrant wavefronts during cardiac fibrillation. Developing therapies that favorably alter electrical restitution properties have promise as a new paradigm for preventing fibrillation.

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Sudden cardiac death resulting from ventricular fibrillation can be separated into 2 components: initiation of tachycardia and degeneration of tachycardia to fibrillation. Clinical drug studies such as CAST and SWORD demonstrated that focusing exclusively on the first component is inadequate as a therapeutic modality. The hope for developing effective pharmacological therapy rests on a comprehensive understanding of the second component, the transition from tachycardia to fibrillation.

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