Virtual electrode polarization leads to reentry in the far field.

INTRODUCTION: Our previous article examined cardiac vulnerability to reentry in the near field within the framework of the virtual electrode polarization (VEP) concept. The present study extends this examination to the far field and compares its predictions to the critical point hypothesis. METHODS AND RESULTS: We simulate the electrical behavior of a sheet of myocardium using a two-dimensional bidomain model. The fiber field is extrapolated from a set of rabbit heart fiber directions obtained experimentally. An S1 stimulus is applied along the top or left border. An extracellular line electrode on the top delivers a cathodal or anodal S2 stimulus. A VEP pattern matching that seen experimentally is observed and covers the entire sheet, thus constituting a far-field effect. Reentry arises from break excitation, make excitation, or a combination of both, and subsequent propagation through deexcited and recovered areas. Reentry occurs in cross-field, parallel-field, and uniform refractoriness protocols. For long coupling intervals (CIs) above CImake(min) (defined as the shortest CI at which make excitation can take place), rotors move away from the cathodal electrode and the S1 site for increases in S2 strength and CI, respectively. For cathodal S2 stimuli, findings are consistent with the critical point hypothesis. For CIs below CImake(min), reentry is initiated by break excitation only, and the resulting reentrant patterns are no longer consistent with those predicted by the critical point hypothesis. CONCLUSION: Shock-induced VEP can explain vulnerability in the far field. The VEP theory of vulnerability encompasses the critical point hypothesis for cathodal S2 shocks at long CIs.

Role of virtual electrodes in arrhythmogenesis: pinwheel experiment revisited.

INTRODUCTION: Recent experimental evidence demonstrates that a point stimulus generates a nonuniform distribution of transmembrane potential (virtual electrode pattern) consisting of large adjacent areas of depolarization and hyperpolarization. This simulation study focuses on the role of virtual electrodes in reentry induction. METHODS AND RESULTS: We simulated the electrical behavior of a sheet of myocardium using a two-dimensional bidomain model with straight fibers. Membrane kinetics were represented by the Beeler-Reuter Drouhard-Roberge model. Simulations were conducted for equal and unequal anisotropy ratios. S1 wavefront was planar and propagated parallel or perpendicular to the fibers. S2 unipolar stimulus was cathodal or anodal. With regard to unequal anisotropy, for both cathodal and anodal stimuli, the S2 stimulus negatively polarizes some portion of membrane, deexciting it and opening an excitable pathway in a region of otherwise unexcitable tissue. Reentry is generated by break excitation of this tissue and subsequent propagation through deexcited and recovered areas of myocardium. Figure-of-eight and quatrefoil reentry are observed, with figure-of-eight most common. Figure-of-eight rotation is seen in the direction predicted by the critical point hypothesis. With regard to equal anisotropy, reentry was observed for cathodal stimuli only at strengths > -95 A/m. CONCLUSION: The key to reentry induction is the close proximity of S2-induced excited and deexcited areas, with adjacent nonexcited areas available for propagation.