The structure and functioning of the atrioventricular (AV) node has remained mysterious owing to its high degree of complexity. In this review article, we integrate advances in knowledge regarding connexin expression in the AV node. Complex patterning of 4 different connexin isoforms with single channel conductances ranging from ultralow to high explains the dual pathway electrophysiology of the AV node, the presence of 2 nodal extensions, longitudinal dissociation in the penetrating bundle, and, most importantly, how the AV node maintains slow conduction between the atria and the ventricles. It is shown that the complex patterning of connexins is the consequence of the embryonic development of the cardiac conduction system. Finally, it is argued that connexin dysregulation may be responsible for AV node dysfunction.
Effects of brief postganglionic vagal nerve stimulation on the activation sequence of the rabbit sinoatrial (SA) node were investigated. Activation sequences in a small area (7 mm × 7 mm) on the epicardial surface were measured in a beat‐to‐beat manner using an extracellular potential mapping system composed of 64 modified bipolar electrodes with high‐gain and low‐frequency band‐pass filtering. The leading pacemaker site was recognised clearly from both the activation sequence and the characteristic morphology of the potentials. Vagal stimulation resulted in a short‐lasting initial slowing of spontaneous rate followed by a long‐lasting secondary slowing; a brief period of relative or absolute acceleration was interposed between the two slowing phases. During these changes of spontaneous rate, the leading pacemaker site shifted in a complex beat‐to‐beat manner by 1‐6 mm alongside the crista terminalis in the superior or inferior direction. For the first spontaneous excitation following stimulation, the greater the slowing, the larger the distance of the pacemaker shift. There was no such linear relationship between the extent of slowing and the distance of pacemaker shift for the subsequent beats. These changes in the leading pacemaker site in response to vagal stimulation may be the result of the functional and morphological heterogeneity of the mammalian SA node in terms of innervation, receptor distribution and ion channel densities.
Ventricular fibrillation (VF) is currently a major cause of sudden cardiac death (SCD). To cure VF, electrical defibrillation is the only therapy. However, strong energy is required. Thus, to reduce the energy or develop a new method is desired. The mechanism of how the electric shock sweeps VF is still controversial. In this article, we summarize evidence and remaining problems of this topic. There are three issues in time sequence of VF: how to initiate, how to continue, and how to terminate. Many investigations to achieve VF-free heart have been reported, but there are currently no definite methods to prevent VF. Thus, to terminate VF is one of the big challenges to prevent SCD. There are two strategies to improve electrical defibrillation: elucidate the substantial mechanism and reduce the energy. (1) Substantial mechanism proposed: In a failed defibrillation episode, at the energy level of the near defibrillation threshold, the initial activation site is related to the repolarization phase of the location. However, it is still not clear whether it is part of the continuous VF activity or initiation of re-VF. It is well known that strong field electric shock (including cathodal and anodal stimuli) has many effects on the cardiac tissue, such as electroporation, virtual electrode effects, and electrophysiological responses, which are influenced by tissue geometry (including fiber orientation and bifurcation of tissues). These phenomena should modify the defibrillation effect. Finally, the characteristics of dynamic spiral wave (SW; the sources of continuity of re-entries) influence the continuity of VF. (2) Efforts to reduce the defibrillation energy: To reduce the defibrillation energy, biphasic pulse, regional cooling, modified stimuli programs, and automated local stimuli to SW are proposed. The superiority of biphasic pulse to monophasic pulse was established in the late 20th century; however, the mechanism is still not well understood. Cooling of some region of the heart ventricles widens the route of SW trajectory and terminates SW. Programming high frequency stimulus or double stimuli according to computer simulation of the heart model could reduce the defibrillation threshold. Automated local stimulus to the site between the tail of SW activation and the next activation front could terminate the SW.
'%3e%3cpath fill='%23012169' d='M0 0v30h60V0z'/%3e%3cpath stroke='%23fff' stroke-width='6' d='m0 0 60 30m0-30L0 30'/%3e%3cpath stroke='%23C8102E' stroke-width='4' d='m0 0 60 30m0-30L0 30' clip-path='url(%23b)'/%3e%3cpath stroke='%23fff' stroke-width='10' d='M30 0v30M0 15h60'/%3e%3cpath stroke='%23C8102E' stroke-width='6' d='M30 0v30M0 15h60'/%3e%3c/g%3e%3c/svg%3e)
