A logical state model of reentrant ventricular activation.
The ventricular surface of the heart was modeled as two-dimensional, 4096 element, network of cells connected logically to each other. An ischemic area was represented by a central core of prolonged refractoriness, distributed into eccentrically-layered elliptical contours such that refractoriness declined along varying gradients to the surrounding normal area. Propagation of cardiac action potentials was stimulated by five sequential states ranging from activation to inactivation. Reentrant activation was induced by premature stimulation of the network and resembled a "figure 8" type reentry seen experimentally. Activation patterns of reentry appeared as two propagation wavefronts which traveled around the ends of a continuous line of functional conduction block, merged into a single wavefront, then conducted slowly along a retrograde path to reactivate a region proximal to the block. Reentry could be prevented by modifying the distribution of recovery of excitability through stimulation at two strategically located sites during basic rhythm. Prevention occurred when the second site was situated in an area of prolonged refractoriness, just distal to the line of block. These simulations indicate that reentrant activation is characterized by the formation of long lines of conduction block which occur along a border of steeply graded refractoriness, and retrograde slow conduction which occurs along a more shallow refractory gradient. The occurrence of reentry is dependent on: 1) the coupling interval of the premature stimulus, 2) the location of the stimulus relative to the maximum refractory gradient, and 3) the activation sequence of the basic paced beats. Thus, this paper presents an efficient logical state model of cardiac activation which simulates experimentally observed activation patterns of reentry and its prevention.
Restivo
M
M
Brooklyn Veteran's Administration, NY 11209.
Craelius
W
W
Gough
W B
WB
el-Sherif
N
N
D000200:Action Potentials; D000465:Algorithms; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000503:physiopathology*; D011381:Programming Languages; D013610:Tachycardia / Q000503:physiopathology