Notes: In support of the spiral wave theory of reentry, simulation studies and animal models have been utilized to show various patterns of spiral wave tip motion such as meandering and drifting. However, the demonstration of these or any other patterns in cardiac tissues have been limited. Whether such patterns of spiral tip motion are commonly observed in fibrillating cardiac tissues is unknown, and whether such patterns form the basis of ventricular tachycardia or fibrillation remain debatable. Using a computerized dynamic activation display, 108 episodes of atrial and ventricular tachycardia and fibrillation in isolated and intact canine cardiac tissues, as well as in vitro swine and myopathic human cardiac tissues, were analyzed for patterns of nonstationary, spiral wave tip motion. Among them, 46 episodes were from normal animal myocardium without pharmacological perturbations, 50 samples were from normal animal myocardium, either treated with drugs or had chemical ablation of the subendocardium, and 12 samples were from diseased human hearts. Among the total episodes, 11 of them had obvious nonstationary spiral tip motion with a life span of 〉2 cycles and with consecutive reentrant paths distinct from each other. Four patterns were observed: (1) meandering with an inward petal flower in 2; (2) meandering with outward petals in 5; (3) irregularly concentric in 3 (core moving about a common center); and (4) drift in 1 (linear core movement). The life span of a single nonstationary spiral wave lasted no more than 7 complete cycles with a mean of 4.6±4.3, and a median of 4.5 cycles in our samples. Conclusion: (1) Patently evident nonstationary spiral waves with long life spans were uncommon in our sample of mostly normal cardiac tissues, thus making a single meandering spiral wave an unlikely major mechanism of fibrillation in normal ventricular myocardium. (2) A tendency toward four patterns of nonstationary spiral tip motion was observed. © 1998 American Institute of Physics.

Notes: It is well known that the ability to fibrillate is intrinsic to a normal ventricle that exceeds a critical mass. The questions we address are how is ventricular fibrillation (VF) initiated and perpetuated in normal myocardium, and why is VF not seen more often in the general population if all ventricles have the ability to fibrillate. To study the mechanisms of VF, we used computerized mapping techniques with up to 512 channels of simultaneous multisite recordings for data acquisition. The data were then processed for dynamic display of the activation patterns and for mathematical analyses of the activation intervals. The results show that in normal ventricles, VF can be initiated by a single strong premature stimulus given during the vulnerable period of the cardiac cycle. The initial activations form a figure-eight pattern. Afterward, VF will perpetuate itself without any outside help. The self-perpetuation itself is due to at least two factors. One is that single wave fronts spontaneously break up into two or more wavelets. The second is that when two wavelets intersect perpendicular to each other, the second wavelet is broken by the residual refractoriness left over from the first wavelet. Mathematical analyses of the patterns of activation during VF revealed that VF is a form of chaos, and that transition from ventricular tachycardia (VT) to VF occurs via the quasiperiodic route. In separate experiments, we found that we can convert VF to VT by tissue size reduction. The physiological mechanism associated with the latter transition appears to be the reduction of the number of reentrant wave fronts and wandering wavelets. Based on these findings, we propose that the reentrant wave fronts and the wandering wavelets serve as the physiological equivalent of coupled oscillators. A minimal number of oscillators is needed for VF to perpetuate itself, and to generate chaotic dynamics; hence a critical mass is required to perpetuate VF. We conclude that VF in normal myocardium is a form of reentrant cardiac arrhythmia. A strong electrical stimulus initiates single or dual reentrant wave fronts that break up into multiple wavelets. Sometimes short-lived reentry is also generated during the course of VF. These organized reentrant and broken wavelets serve as coupled oscillators that perpetuate VF and maintain chaos. Although the ability to support these oscillators exists in a normal ventricle, the triggers required to generate them are nonexistent in the normal heart. Therefore, VF and sudden death do not happen to most people with normal ventricular myocardium. © 1998 American Institute of Physics.

Notes: Mechanisms of Deflbhllation. The aim of this article is to review the current concepts of ventricular defibrillation. We studied the interaction between strong electrical stimulas and cardiac responses in both animal models and in humans. We found that a premature stimulus (S2) of appropriate strength results in figure-eight reentry in vitro by inducing propagated graded responses. The same stimulation protocol induces figure-eight reentry and ventricular fibrillation (VF) in vivo. When the S2 strength and the magnitude of graded responses increase beyond a critical level, the increase in refractoriness at the site of the stimulus becomes so long that the unidirectional block becomes bidirectional block, preventing the formation of reentry (upper limit of vulnerability [DLV]). In other studies, we found that the effects of an electrical stimulation on reentry is in part determined by the timing of the stimulus. A protective zone is present after the induction of VF and after an unsuccessful defibrillation shock during which an electrical stimulus can terminate reentry and protect the heart from VF. These results indicate that the effects of a defibrillation shock is dependent on both the strength and the timing of the shock. Timing is not important in areas where the shock field strength is 〈 ULV because the shock terminates all reentry hut cannot reinitiate new ones. However, in areas where shock field strength is 〈 ULV, the effects of the shock are determined by the timing of the shock relative to local VF activations. This ULV hypothesis of defibrillation explains the probablistic nature of ventricular defibrillation. It also indicates that, to achieve a high probability of successful defibrillation, a shock must result in a shock field strength of 〈 ULV throughout the ventricles.

Notes: Restitution and Fibrillation. Combined experimental and theoretical work has shown that restitution properties of the cardiac action potential duration and conduction velocity contribute to breakup of reentrant wavefronts during cardiac fibrillation independent of preexisting electrophysiologic heterogeneities in the tissue. Developing therapies that favorably alter these cardiac electrical restitution properties are a promising new approach to preventing fibrillation.