About this Research Topic
The His-Purkinje System (HPS) is responsible for the rapid electrical activation of the heart. It is a branching network embedded within the myocardium, although electrically insulated from it, except at its terminal ends. The HPS has been implicated as being arrhythmogenic under certain pathological conditions. First, it has been shown to be a major source of ectopy, and second, it may provide conduction pathways which form part of a reentrant circuit. Despite its importance and profound effect on ventricular activation, many basic aspects of it remain woefully unelucidated, including how the HPS couples to the myocardium to overcome the source-sink mismatch, its physical structure, and key electrophysiological differences with the working myocardium.
The goal of this Frontiers Research Topic is to shed light on the functioning and structure of the HPS so that treatment strategies for arrhythmias arising from within the HPS or external to it, can be developed. We would also like to identify the effects of the HPS on normal ventricular conduction so that its effects can be recognized experimentally. Ideally, we would like to know its structure, from the cellular to the network level. Additionally, it is desired to explore HPS specific strategies to prevent the occurrence of cardiac arrhythmias, especially ventricular fibrillation which is immediately lethal. It is hoped that the data gathered from various spatial scales and by various techniques are integrated to form a more complete vision of the HPS.
This topic is open to any articles which elucidate the functioning of the HPS, from intracellular processes, to junctional behavior, to network activation, under normal and pathological conditions. Articles describing structure and how it relates to function are also encouraged. Additionally, articles are welcome which explore antiarrhythmic treatments targeting the HPS, including but not limited to ablative, pharmacological, device, and genetic approaches. Submissions of a computational, basic science, or clinical nature are welcome as long as they provide mechanistic insight.
Topic Editor Dr. Edward Joseph Vigmond is a co-founder of Numericor GmbH, a private company which performs cardiac simulations and licenses simulation software. Both Dr. Vigmond and Dr. Jason D Bayer declares no conflict of interest with regard to the Research Topic subject.
The goal of this Frontiers Research Topic is to shed light on the functioning and structure of the HPS so that treatment strategies for arrhythmias arising from within the HPS or external to it, can be developed. We would also like to identify the effects of the HPS on normal ventricular conduction so that its effects can be recognized experimentally. Ideally, we would like to know its structure, from the cellular to the network level. Additionally, it is desired to explore HPS specific strategies to prevent the occurrence of cardiac arrhythmias, especially ventricular fibrillation which is immediately lethal. It is hoped that the data gathered from various spatial scales and by various techniques are integrated to form a more complete vision of the HPS.
This topic is open to any articles which elucidate the functioning of the HPS, from intracellular processes, to junctional behavior, to network activation, under normal and pathological conditions. Articles describing structure and how it relates to function are also encouraged. Additionally, articles are welcome which explore antiarrhythmic treatments targeting the HPS, including but not limited to ablative, pharmacological, device, and genetic approaches. Submissions of a computational, basic science, or clinical nature are welcome as long as they provide mechanistic insight.
Topic Editor Dr. Edward Joseph Vigmond is a co-founder of Numericor GmbH, a private company which performs cardiac simulations and licenses simulation software. Both Dr. Vigmond and Dr. Jason D Bayer declares no conflict of interest with regard to the Research Topic subject.
Keywords: cardiac conduction system, cardiac arrhythmias, cardiac ectopy, cardiac reentrant mechanisms, antiarrhythmic therapy
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
