MECHANOELECTRIC FEEDBACK IN CARDIAC DEFIBRILLATION

心脏除颤中的机电反馈

• 批准号: 8362802
• 负责人: Andrew D. McCulloch
• 金额: $ 3万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8362802
• 关键词: Algorithms; Anatomic Models; Anatomy; Arrhythmia; Behavior; Biomedical Computing; Canis familiaris; Cardiac; Collaborations; Development; Electric Countershock; Electrocardiogram; Electrophysiology (science); Feedback; Funding; Grant; Heart; Human; Investigation; Knowledge; Life; Mechanics; Modeling; Mus; Muscle Contraction; National Center for Research Resources; Play; Principal Investigator; Process; Research; Research Infrastructure; Resources; Role; Shock; Source; Structure; Techniques; United States National Institutes of Health; Universities; cost; effective therapy; heart rhythm; improved; mechanical behavior

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. (A) OBJECTIVES Cardiac fibrillation is disorganized electrical behavior of the heart, and its consequence is the loss of coordinated muscle contraction. Electrical defibrillation by timely application of a strong electric shock to the heart has long been used as an effective therapy for this otherwise lethal disturbance of cardiac rhythm. In recent years defibrillation therapy has dramatically expanded due to its improved accessibility and functionality. Despite the critical role that the technique plays in saving human life, the fundamental mechanisms by which electrical shocks halt life-threatening disturbances in cardiac rhythm are not completely understood. Mechanical contraction follows the electrical activation of the heart. However, it has long been known that there is a cross-talk between the electrical and mechanical processes which could play a role in anti-arrhythmia therapy. Owing to the complexities in cardiac structure and behavior, mechanical contributions have never before been considered in the investigation of cardiac defibrillation mechanisms. The objective of this research is to determine the contribution of mechanoelectrical feedback in the process of cardiac defibrillation, and thus, to increase our knowledge of the mechanisms by which the exposure of the heart to strong electric shocks terminates fibrillation. This application seeks to continue the collaboration between the Computational Cardiac Electrophysiology Group at Johns Hopkins University and the National Biomedical Computation Resource. As a collaborative project of the NBCR this research will promote extensions to the development of Continuity and its anatomic, electrical and mechanical models and algorithms that will permit greater integration with bidomain models of the heart and torso, opening it up to the large array of applications in cardiac pacing, shock and electrocardiography. The following specific aims are proposed: + Specific Aim 1: To develop an anatomically-accurate three-dimensional electromechanical model of defibrillation in dog and mouse hearts building on the existing anatomic models developed at UCSD. + Specific Aim 2: Using the dog and mouse defibrillation models to analyze the mechanisms responsible for the increase in defibrillation threshold in volume overloaded hearts.

该副本是利用资源的众多研究子项目之一 由NIH/NCRR资助的中心赠款提供。对该子弹的主要支持 而且，副投影的主要研究员可能是其他来源提供的 包括其他NIH来源。 列出的总费用可能 代表subproject使用的中心基础架构的估计量， NCRR赠款不直接向子弹或副本人员提供的直接资金。 （a）目标 心脏纤颤是心脏杂乱无章的电气行为，其结果是 失去协调的肌肉收缩。通过及时应用电气除颤 长期以来，对心脏的强烈电击一直被用作有效的疗法 否则心律的致命障碍。近年来，除颤疗法已有 由于其可访问性和功能提高，因此大大扩展。尽管很关键 该技术在挽救人类生命中扮演的角色，即基本机制 电击阻止心律下威胁生命的障碍 理解。 机械收缩遵循心脏的电动激活。但是，它有很长的 众所周知，电气和机械过程之间存在串扰 可以在抗心律失常疗法中发挥作用。由于心脏结构的复杂性 和行为，机械贡献从未在 心脏除颤机制的研究。 这项研究的目的是 在心脏过程中确定机械电反馈的贡献 除颤，从而增加我们对暴露的机制的了解 强烈电击的心脏终止了纤颤。本申请寻求 继续在计算心脏电生理组之间的合作 约翰·霍普金斯大学和国家生物医学计算资源。作为 NBCR的协作项目这项研究将促进发展的扩展 连续性及其解剖学，电气和机械模型和算法 允许与心脏和躯干的双域模型更大的整合，将其打开到 心脏起搏，休克和心电图中的大量应用。 提出了以下具体目标： +特定目标1：开发解剖学精确的三维 在现有的狗和鼠标心中除颤的机电模型 UCSD开发的解剖模型。 +特定目标2：使用狗和小鼠除颤模型分析 导致体积超载除颤阈值增加的机制 心。