title: Wavelet formation in excitable cardiac tissue: the role of wavefront-obstacle interactions in initiating high-frequency fibrillatory-like arrhythmias.
abstract: High-frequency arrhythmias leading to fibrillation are often associated with the presence of inhomogeneities (obstacles) in cardiac tissue and reduced excitability of cardiac cells. Studies of antiarrhythmic drugs in patients surviving myocardial infarction revealed an increased rate of sudden cardiac death compared with untreated patients. These drugs block the cardiac sodium channel, thereby reducing excitability, which may alter wavefront-obstacle interactions. In diseased atrial tissue, excitability is reduced by diminished sodium channel availability secondary to depolarized rest potentials and cellular decoupling secondary to intercellular fibrosis. Excitability can also be reduced by incomplete recovery between successive excitations. In all of these cases, wavefront-obstacle interactions in a poorly excitable medium may reflect an arrhythmogenic process that permits formation of reentrant wavelets leading to flutter, fibrillation, and sudden cardiac death. To probe the relationship between excitability and arrhythmogenesis, we explored conditions for new wavelet formation after collision of a plane wave with an obstacle in an otherwise homogeneous excitable medium. Formulating our approach in terms of the balance between charge available in the wavefront and the excitation charge requirements of adjacent medium, we found analytically the critical medium parameters that defined conditions for wavefront-obstacle separation. Under these conditions, when a parent wavefront collided with a primitive obstacle, the resultant fragments separated from the obstacle boundaries, subsequently curled, and spawned new "daughter" wavelets. We identified spatial arrangements of obstacles such that wavefront-obstacle collisions leading to spawning of new wavelets could produce high-frequency wavelet trains similar to fibrillation-like arrhythmias.
authors.affiliation: Department of Medicine (Cardiology), Duke University Medical Center, Durham, North Carolina 27710, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: Starobin
authors.forename: Y I
authors.initials: YI
authors.lastname: Zilberter
authors.forename: E M
authors.initials: EM
authors.lastname: Rusnak
authors.forename: C F
authors.initials: CF
authors.lastname: Starmer
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D055592:Biophysical Phenomena; D001703:Biophysics; D004594:Electrophysiology; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008433:Mathematics; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D012964:Sodium / Q000378:metabolism; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology
chemical_list: D000889:Anti-Arrhythmia Agents; D012964:Sodium