VECTOR MAPPING OF MYOCARDIAL ACTIVATION

心源性猝死通常继发于室颤残留 这是美国人死亡的主要原因。室颤 通常被认为是次于再入的；然而，有几个方面 室颤的病理生理学机制尚不清楚。在……里面 具体地说，心律失常在不同的实验或 室颤时的临床表现和是否激活 都是以可量化的方式组织起来的，还没有得到很好的确立。这个 本研究的总体目标是验证以下假设 室颤是由于多个折返回路改变所致 随着时间推移以及启动和维持的模式 室颤可能因潜在的结构或结构而异 心肌的电生理特性，并取决于 亚急性和慢性心肌梗死模型的启动方式 和扩张型心肌病。室颤时的激活 将使用计算机化的多通道测绘系统进行记录 使用标准激活映射和“矢量映射”进行分析 技巧。激活波前的大小，周期长度 纤颤，节拍到节拍的激活组织(空间和 时间链接)、重入电路的数量和类型以及 将使用功能块线的位置来表征 纤颤。不应期测量和病理分析将 也可以执行，并与电激活相关 室颤。 需要检验的具体假设是：L)启蒙机制 也许维持室颤的方法会有所不同 取决于诱发心律失常的方法；2)模式 VF期间的激活将根据实验模型和 基于先前存在的局部电生理和解剖特性；3) VF的特征(空间和时间链接、周期长度和 波前的大小)将随着纤颤持续时间的增加而变化； 4)室颤是由多个同时折返者引起的 电路。这些电路的数量和特性会有所不同 取决于实验情况，并将依赖于 心肌的局部电生理和解剖特性。一个 更好地了解室颤的病理生理学机制 它在不同情况下的不同可能会带来更好的治疗方法 用于预防和终止这种致命的心律失常。

Sudden cardiac death usually secondary to ventricular fibrillation remains a major cause of mortality in the United States. Ventricular fibrillation is generally believed to be secondary to reentry; however, several aspects of the pathophysiology of ventricular fibrillation remain unknown. In particular, how the arrhythmia may differ in different experimental or clinical situations and whether activation during ventricular fibrillation is organized in a quantifiable fashion has not been well established. The overall goal of the present study is to verify the hypothesis that ventricular fibrillation is due to multiple reentrant circuits that change over time and that patterns of the initiation and maintenance of ventricular fibrillation may vary depending upon underlying structural or electrophysiologic properties of the myocardium and depending upon the mode of initiation of models of subacute and chronic myocardial infarction and dilated cardiomyopathy. Activation during ventricular fibrillation will be recorded using a computerized multi-channel mapping system and analyzed using standard activation mapping and "vector mapping" techniques. The size of activation wavefronts, the cycle length of fibrillation, the beat to beat organization of activation (spatial and temporal linking), the number and types of reentrant circuits and the location of lines of functional block will be used to characterize fibrillation. Refractory period measurements and pathologic analysis will also be performed and correlated with electrical activation during ventricular fibrillation. The specific hypotheses to be tested are: l) the mechanism of initiation and perhaps the maintenance of ventricular fibrillation will differ depending upon the method used to induce the arrhythmia; 2) patterns of activation during VF will vary depending on the experimental model and based on pre-existing local electrophysiologic and anatomic properties; 3) characteristics of VF (spatial and temporal linking, cycle length, and size of wavefronts) will vary as the duration of fibrillation increases; and 4) ventricular fibrillation is due to multiple simultaneous reentrant circuits. The number and characteristics of these circuits will vary depending upon the experimental situation and will be dependent upon of local electrophysiologic and anatomic properties of the myocardium. A better understanding of the pathophysiology of ventricular fibrillation and how it differs in different situations may lead to better therapies for the prevention and termination of this lethal arrhythmia.