WAVELET FORMATION IN EXCITABLE CARDIAC TISSUE - THE ROLE OF WAVE-FRONT OBSTACLE INTERACTIONS IN INITIATING HIGH-FREQUENCY FIBRILLATORY-LIKEARRHYTHMIAS

High-frequency arrhythmias leading to fibrillation are often associate d with the presence of inhomogeneities (obstacles) in cardiac tissue a nd reduced excitability of cardiac cells. Studies of antiarrhythmic dr ugs in patients surviving myocardial infarction revealed an increased rate of sudden cardiac death compared with untreated patients. These d rugs block the cardiac sodium channel, thereby reducing excitability, which may alter wavefront-obstacle interactions. In diseased atrial ti ssue, excitability is reduced by diminished sodium channel availabilit y secondary to depolarized rest potentials and cellular decoupling sec ondary to intercellular fibrosis. Excitability can also be reduced by incomplete recovery between successive excitations. In all of these ca ses, 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. T o probe the relationship between excitability and arrhythmogenesis, we explored conditions for new wavelet formation after collision of a pl ane wave with an obstacle in an otherwise homogeneous excitable medium . Formulating our approach in terms of the balance between charge avai lable in the wavefront and the excitation charge requirements of adjac ent medium, we found analytically the critical medium parameters that defined conditions for wavefront-obstacle separation. Under these cond itions, when a parent wavefront collided with a primitive obstacle, th e resultant fragments separated from the obstacle boundaries, subseque ntly curled, and spawned new ''daughter'' wavelets. We identified spat ial arrangements of obstacles such that wavefront-obstacle collisions leading to spawning of new wavelets could produce high-frequency wavel et trains similar to fibrillation-like arrhythmias.