PATHOPHYSIOLOGIC BASIS OF VENTRICULAR TACHYCARDIA IN MAN

人类室性心动过速的病理生理学基础

• 批准号: 6056260
• 负责人: MICHAEL E CAIN
• 金额: $ 23万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1993
• 资助国家: 美国
• 起止时间: 1993-08-01 至 2001-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6056260
• 关键词: clinical research; computer simulation; disease /disorder proneness /risk; early diagnosis; electrocardiography; electrophysiology; epicardial mapping; heart disorder diagnosis; heart electrical activity; human subject; myocardial infarction; myocardial ischemia /hypoxia; noninvasive diagnosis; tachycardia; ventricular fibrillation

DESCRIPTION (adapted from the applicant's abstract): The goal of the proposed research is to improve the noninvasive identification of patients with ischemi heart disease vulnerable to ventricular tachycardia (VT) or ventricular fibrillation (VF). Analyses of 3-dimensional intraoperative and body surface maps of ventricular activation in patients indicate that current methods of assessing risk fail to detect completely the electrophysiologic abnormalities induced during ventricular infarct healing that increase susceptibility to VT/VF. Recent findings demonstrate that: VT initiates at infarct border zones by intramural reentry and focal mechanisms; tissue generating nonsustained VT is not a surrogate for sustained VT; analysis limited to the terminal QRS complex of signal-averaged ECGs excludes detection of more than 95% of the signals generated by myocardium critical for VT; and during the entire cardiac cycle, there are previously unrecognized spectral, temporal, and spatial features of body surface and inferred epicardial potentials that distinguish patients with VT. Based on these findings, the next step toward improving risk stratification is a focus on bioelectrical signals generated by myocardium enveloping arrhythmogenic tissue. The investigators will characterize the spectral and temporal features that distinguish epicardial potentials inferred over arrhythmogenic loci in infarct zones. They propose then to establish that these bioelectric signals are a more complete fingerprint of the electrophysiologic derangements that increase susceptibility to VT/VF by testing the hypothesis that detection of the uncovered abnormal signals improves identification of patients vulnerable to sustained ventricular arrhythmias. Epicardial potentials subtending arrhythmogenic and non-arrhythmogenic infarct loci (defined ultrasonically and by catheter endocardial mapping) and normal myocardium will be inferred from 190-lead body surface maps, individualized heart-torso models, and echocardiographic images from patients with (n=40) and without (n=40) VT or VF. Magnitude, phase and group-delay spectra of potentials will be analyzed to determine the frequency band(s) and their temporal location(s) in the cardiac cycle that distinguish signals generated locally by myocardium enveloping arrhythmogenic tissue. Fina studies performed in 100 subjects will test whether detection of this fingerprint, developed based on an increased understanding of the pathophysiologic basis of VT in humans, improves identification of patients with prior myocardial infarction inducible into sustained VT.

描述（改编自申请人的摘要）：该项目的目标 拟议的研究是为了提高患者的无创识别 患有缺血性心脏病，易发生室性心动过速 (VT) 或 心室颤动（VF）。 3 维术中和 患者心室激动的体表图表明 当前的风险评估方法无法完全检测到 心室梗塞愈合过程中诱发的电生理异常 增加对 VT/VF 的敏感性。 最近的研究结果表明： VT 通过壁内折返和局灶性在梗塞边界区域启动 机制；产生非持续性室速的组织不能替代 持续性室速；分析仅限于 QRS 波群 信号平均心电图排除了超过 95% 的信号检测 由对 VT 至关重要的心肌产生；并且在整个心脏过程中 周期中，存在以前未识别的光谱、时间和空间 区分体表特征和推断心外膜电位 VT 患者。 基于这些发现，下一步要改进 风险分层的重点是生物电信号 心肌包绕致心律失常组织。 调查人员将 表征区分心外膜的光谱和时间特征 推断梗塞区致心律失常位点的电位。 他们提议 然后确定这些生物电信号是更完整的 增加的电生理紊乱的指纹 通过检验检测 VT/VF 的假设来评估对 VT/VF 的敏感性 发现的异常信号可以提高对易受感染的患者的识别 持续性室性心律失常。 心外膜电位对向 致心律失常和非心律失常梗塞位点（超声定义 并通过导管心内膜标测）和正常心肌将被推断 来自 190 导联体表图、个性化心脏躯干模型，以及 患有 (n=40) 和不患有 (n=40) VT 或不患有 VT 的患者的超声心动图图像 室颤。 将分析电位的幅度、相位和群延迟谱 确定频段及其在时间上的位置 区分心肌局部产生的信号的心动周期 包膜致心律失常组织。 FINA 对 100 名受试者进行的研究 将测试是否检测到该指纹，该指纹是基于 增加对人类 VT 病理生理学基础的了解， 提高对既往心肌梗塞患者的识别 可诱发持续性室速。