VECTOR MAPPING OF MYOCARDIAL ACTIVATION

心脏性猝死通常继发于心室颤动， 是美国人死亡的主要原因室颤 一般认为是次要的再入;然而，几个方面， 室颤的病理生理学机制尚不清楚。在 特别是，心律失常如何可能在不同的实验或 临床情况和室颤期间是否激活 以可量化的方式组织起来，还没有很好地建立起来。的 本研究的总体目标是验证假设， 室颤是由于多个折返回路改变， 随着时间的推移， 心室纤颤可能会有所不同，这取决于潜在的结构或 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期间的激动 将使用计算机化多通道绘图系统记录， 使用标准激活标测和“向量标测”分析 技术.激活波前的大小， 纤颤，搏动到搏动的激活组织（空间和 时间链接），可重入回路的数量和类型以及 功能块的线路位置将用于表征 纤维性颤动不应期测量和病理分析将 也可以在过程中执行并与电激活相关 心室颤动 有待检验的具体假设有：1）启动机制 也许心室颤动的维持 取决于用于诱导心律失常的方法; 2） VF期间的激活将根据实验模型而变化， 基于预先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， 波前的大小）将随着纤颤持续时间的增加而变化; 4）心室颤动是由于多个同时折返 电路.这些电路的数量和特性将有所不同 取决于实验情况，并将取决于 心肌的局部电生理和解剖特性。 一 更好地理解心室颤动的病理生理学 以及它在不同情况下的差异可能会导致更好的治疗方法 来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.