Atrial defibrillation voltage: Falling to a new low

Abstract

The mechanisms by which an electric shock terminates cardiac arrhythmias have been the subject of a large body of research (for review, see 1 ). These studies have been driven by the understanding that a significant reduction in shock energy can only be achieved by full appreciation of the mechanisms by which a shock interacts with the heart and then exploiting them to devise novel low-voltage therapeutic approaches.The research has demonstrated that the response of the myocardium to the shock involves simultaneous occurrence of positive and negative membrane polarization [2][3][4] . Detailed analysis of the etiology of this "virtual electrode polarization" (VEP) has demonstrated that tissue structure is responsible for its formation of VEP as well as for its shape, location, polarity, and intensity. The effect of tissue structure is two-fold. First, discontinuities in tissue structure (i.e. conductivities) force current to cross the membranes of neighboring cells, giving rise to VEP. Intercellular and interlaminar clefts 5,6 , or tissue lesions 7 are possible factors in this process. Second, continuous tissue structure such as ventricular shape and fiber architecture also give rise to VEP 8 .Action potential duration in the myocardium can be either extended by positive VEP or shortened by negative VEP, and strong negative VEP can completely abolish the action potential, creating a new, post-shock excitable area 9 . Propagation through the post-shock excitable area has proven to directly determine the outcome of a defibrillation shock. A shock succeeds in extinguishing fibrillatory wavefronts if excitations manage to traverse the newly-created post-shock excitable area before the rest of the myocardium recovers from refractoriness. Decreasing the post-shock excitable area could thus increase the likelihood of defibrillation success and lower the defibrillation voltage 10 ; however, this has proven difficult since the post-shock excitable areas are often hidden deep in the ventricular wall 10,11 .When the shock happens to affect resting cells (those that are part of the pre-shock, fibrillatory wavefront's excitable gap), positive VEPs immediately depolarize these cells; these cells become "secondary sources" emitting new wavefronts, rapidly overwhelming any effects of negative VEP. The targeted activation of cells in the fibrillatory wavefront's excitable gap by electric shocks thus has the potential to eliminate the reentrant circuit by rendering tissue refractory. Furthermore, since this is an excitation process (by positive VEP), the external current needs to only bring cells to the excitation threshold, requiring less energy as compared to de-excitation (by negative VEP) where an activated cell is forced into premature recovery.Address for correspondence: Johns Hopkins University, 3400 N. Charles St., Hackerman Hall Room 216, Baltimore, MD 21218, office phone: 410-516-4375, office fax: 410-516-5294, ntrayanova@jhu.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted...

Terminating ventricular tachyarrhythmias using far-field low-voltage stimuli: Mechanisms and delivery protocols

“…Consistent with our preliminary results, 17 earliest endocardial activations after a field stimulus occurred at the trabecular grooves (Suppl.Fig.S1B). These observations underscore the significance of the endocardial structures—in particular, the trabecular grooves—in the tissue response to low-voltage far-field stimuli.…”

“…The formation of VEPs in the myocardium was crucial for both of these mechanisms, even if these stimulus-induced polarizations were below the activation threshold. Confirming our preliminary findings, 17 the strongest VEPs occurred in the trabecular grooves.…”

Modeling Defibrillation of the Heart: Approaches and Insights

“…The recent efforts towards low-voltage defibrillation [112], [113] have also benefitted from insights obtained by ventricular modeling studies. Trayanova [114] demonstrated that small-scale virtual electrode polarization underlying the appearance of new wave-fronts following a repeated low-voltage field stimuli can arise not only from the coronary vasculature, but also from the presence of trabeculations on the endocardial surface.…”