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.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 （一） 目标 心脏纤维性颤动是心脏的紊乱的电行为，其后果是 失去协调的肌肉收缩。通过及时应用电除颤器 对心脏的强电击长期以来一直被用作治疗这种疾病的有效疗法 否则会导致心脏节律紊乱近年来，除颤治疗已经 由于其改进的可访问性和功能性而急剧扩展。尽管批评 该技术在拯救人类生命方面发挥的作用， 电击停止危及生命的心律紊乱并不完全 明白 机械收缩跟随心脏的电激活。然而，长期以来， 众所周知，在电气和机械过程之间存在串扰， 可能在抗心律失常治疗中发挥作用。由于心脏结构复杂 和行为，机械的贡献从来没有被认为是在 心脏除颤机制的研究。 本研究的目的是 确定机械电反馈在心脏过程中的作用， 除颤，从而增加我们对暴露机制的了解， 强电击可以终止心脏纤颤。本申请旨在 继续与计算心脏电生理学小组合作， 约翰霍普金斯大学和国家生物医学计算资源。作为 NBCR的合作项目，这项研究将促进扩展到发展 连续性及其解剖，电气和机械模型和算法， 允许与心脏和躯干的bidomain模型更大的整合， 广泛应用于心脏起搏、电击和心电图。 建议的具体目标如下： + 具体目标1：开发解剖学上精确的三维 狗和小鼠心脏除颤的机电模型建立在现有的 在加州大学圣地亚哥分校开发的解剖模型。 + 具体目标2：使用犬和小鼠除颤模型分析 容量过载时除颤阈值增加的机制 心中