Peng-Sheng Chen

Idiopathic paroxysmal atrial fibrillation induced by a focal discharge mechanism in the left superior pulmonary vein: possible roles of the ligament of Marshall.

Ablation of Atrial Fibrillation. Introduction: The origin of double potentials inside the left superior pulmonary vein and their relation to the mechanisms of idiopathic paroxysmal focal atrial fibrillation (AF) are unclear.

Mesenchymal Stem Cell Injection Induces Cardiac Nerve Sprouting and Increased Tenascin Expression in a Swine Model of Myocardial Infarction

Introduction: Mesenchymal stem cell (MSC) transplantation is a promising technique to improve cardiac function. Whether MSC can increase cardiac nerve density and contribute to the improved cardiac function is unclear.

New Perspectives on the Role of Autonomic Nervous System in the Genesis of Arrhythmias

Sudden cardiac death (SCD) is a major cause of morbidity and mortality in patients with coronary artery diseases and myocardial infarction (MI). There is a circadian variation of the frequency of SCD. Beta‐blocker therapy significantly reduces the incidence of SCD after MI. These clinical observations suggest a close association between ventricular arrhythmia and sympathetic activity in patients with MI. Following injury, peripheral nerves undergo Wallerian degeneration, which may be followed by neurilemma cell proliferation and axonal regeneration (nerve sprouting), resulting in sympathetic hyperinnervation. It is possible that the increased innervation after myocardial injury may result in increased sympathetic nerve density, which in turn increases the propensity for cardiac arrhythmia. While this Nerve Sprouting Hypothesis seemed to be intuitive, there was no experimental proof of a causal link between sympathetic nerve sprouting and arrhythmogenesis. We therefore performed several studies to determine the relationship between nerve sprouting and cardiac arrhythmia. We also performed direct sympathetic nerve recording in an animal model of SCD. We found that cardiac sympathetic nerves are highly plastic. In addition to MI and rapid pacing, nerve sprouting and heterogeneous sympathetic hyperinnervation may also be induced by radiofrequency ablation, hypercholesterolemia, and stem cells transplantation. The coexistence of denervated and hyperinnervated area in the diseased myocardium could result in increased electrophysiological heterogeneity during sympathetic activation, leading to ventricular arrhythmia and SCD.

Modulation of QT interval by cardiac sympathetic nerve sprouting and the mechanisms of ventricular arrhythmia in a canine model of sudden cardiac death

QT Interval and Sudden Cardiac Death. Introduction: We previously reported that there is a high incidence of sudden cardiac death (SCD) in dogs with myocardial infarction (MI), complete AV block (CAVB), and nerve growth factor (NGF) infusion to the left stellate ganglion (LSG). Whether or not QT interval prolongation underlines the mechanism of SCD was unclear.

Current Concepts of Ventricular Defibrillation

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.

THE ZONE OF VULNERABILITY TO T WAVE SHOCKS IN HUMANS

Vulnerability to VF in Humans. Introduction: Shocks during the vulnerable period of the cardiac cycle induce ventricular fibrillation (VF) if their strength is above the VF threshold (VFT) and less than the upper limit of vulnerability (ULV). However, the range of shock strengths that constitutes the vulnerable zone and the corresponding range of coupling intervals have not been defined in humans. The ULV has been proposed as a measure of defibrillation because it correlates with the defibrillation threshold (DFT), but the optimal coupling interval for identifying it is unknown.

Spatiotemporal Correlation Between Phase Singularities and Wavebreaks During Ventricular Fibrillation

Introduction: Phase maps and the detection of phase singularities (PSs) have become a well‐developed method for characterizing the organization of ventricular fibrillation (VF). How precisely PS colocalizes with wavebreak (WB) during VF, however, is unknown.

Demonstration of Electrical and Anatomic Connections Between Marshall Bundles and Left Atrium in Dogs: Implications on the Generation of P Waves on Surface Electrocardiogram

Marshall Bundle and P Wave. Introduction: The muscle bundles within the ligament of Marshall (LOM) are electrically active. The importance of these muscle bundles (Marshall bundle [MB]) to atrial activation and the generation of the ECG P wave is unclear.

Prevalence of retrograde accessory pathway conduction during atrial fibrillation.

Retrograde Conduction in Atrial Fibrillation. Introduction: Although atrial fibrillation occurs frequently in patients with the preexcitation syndrome, its pathogenesis remains controversial. The purpose of this study was to test the hypothesis that retrograde conduction over the accessory pathway occurs during atrial fibrillation and can serve as an important source of new wavefronts in atrial fibrillation.

Fibrillation and defibrillation: the odd couple?

The mechanism(s) of ventricular defibrillation by an electrical shock still remain(s) elusive and somewhat enigmatic. Attempts to understand how the flow of electrical current through the fibrillating ventricles succeeds in terminating multiple and irregular activation wavefronts are confounded by a host of formidable methodologic and, at times, conceptual impediments. The relatively large size. and complicated anatomy of the ventricles often preempt the use of high-resolution, three-dimensional activation maps with a reasonable degree of accuracy. The greater than anticipated complexity with which the charge of the electrical shock distributes itself in the three-dimensional ventricular myocardium (real and virtual electrode effects) further complicates the task of precise delineation and tracking of defibrillation mechanism(s). In the final analysis, the accepted tenet of defibrillation rests solely on understanding how depolarizing and hyperpolarizing currents (produced by real and virtual electrode effects) interact with cells in differing stages of excitability and refractoriness to terminate reentrant and nonreentrant activation wavefronts. Because shocks with critical strengths (equivalent to critical S2 stimulus) induce ventricular fibrillation (VF) when applied during a critical recovery time (vulnerable period), it is highly probable that these two critical factors coexist during VF, promoting the formation of reentry. Therefore, it is clear that a shock can produce two seemingly opposing effects: it can terminate reentrant and nonreentrant activation at certain sites by premature depolarization; but the same shock can induce de novo reentry in vulnerable sites by the same mechanism that an S2 stimulus of critical strength and timing induces reentry during regular pacing. It must be emphasized that, in the currently accepted tenets of defibrillation, the potential role of automatic foci, either induced by the shock or present intrinsically, generally are not considered to be important determinants of failed defibrillation shocks of a VF. However, this may not be the case with AF, as automatic foci originating from the