COMPUTER ASSISTED MAPPING OF VENTRICULAR FIBRILLATION

描述（改编自申请人的描述）：精确的机制 在心室颤动（VF）期间维持折返的方法以及它如何 缺血、梗塞和心力衰竭的改变是未知的。这 信息对于预防心脏性猝死至关重要。本申请提出 评估几种不同的VF维护机制， 在动物身上进行透壁标测。除了绘制和量化 室颤期间的激活序列，壁内单相动作电位（MAP） 将使用电极来量化复极化。具体目标1：使用3D 激活标测以量化VF期间的壁内折返。将映射VF 同时从多达870个壁内电极和484个心外膜电极， 开胸猪，以量化正常心脏和 缺血和梗塞。假设将被测试，（1）传导 当波前平行传播时，阻塞发生的频率更高， 垂直于肌纤维的长轴，（2）一定的最小长度， 传导阻滞是开始折返所必需的，（3）在VF期间发生局灶性激动， 由涉及浦肯野-肌肉连接的折返引起，（4）折返回路 由转子细丝的分叉、“发芽”或快速漂移形成，（5） 再入可以通过在一个 梗死瘢痕和（6）急性缺血区域不会导致VF 上维护具体目标2：穿刺针的MAP记录。地图 记录将与微电极和光学记录进行比较。它将 确定MAP电极是否可以测量激活和动作电位 在豚鼠和兔子中持续时间不改变它们。具体目标3：使用 3-D MAP映射，比较非均匀分散的相对作用， 恢复和心室的恢复特性， 心室颤动时折返三个假设的相对重要性 将在犬中评价VF维持的机制：（1）不均匀的 当波前在较小的区域中时，恢复的分散导致阻塞。 耐火性遇到相邻的耐火性更大的区域;（2） 恢复特性，其中激活发生在 恢复曲线在耦合间隔中引起振荡， 更大时发生阻塞;（3）在波前传播处发生折返 垂直于前一波阵面的折射率的波尾。的 将检验斑片状纤维化引起的心力衰竭 减少VF组织，而快速起搏导致的心力衰竭增加 了

DESCRIPTION (adapted from the applicant's description): The precise mechanisms by which reentry is maintained during ventricular fibrillation (VF) and how it is altered by ischemia, infarction and heart failure are unknown. This information is vital to prevent sudden cardiac death. This application proposes to evaluate several different mechanisms proposed for VF maintenance by performing transmural mapping in animals. Besides mapping and quantifying activation sequences during VF, intramural monophasic action potential (MAP) electrodes will be used to quantify repolarization. Specific Aim 1: Use 3-D activation mapping to quantify intramural reentry during VF. VF will be mapped simultaneously from up to 870 intramural and 484 epicardial electrodes in open-chest pigs to quantify 3-D reentry in normal hearts and hearts with ischemia and infarction. The hypotheses will be tested that (1) conduction block occurs more frequency when wavefronts travel parallel rather than perpendicular to the long axis of myofibers, (2) a certain minimal length of block is necessary to initiate reentry, (3) focal activation occurs during VF, caused by reentry involving the Purkinje-muscle junction, (4) reentry circuits are formed by bifurcation, "sproing," or rapid drift of rotor filaments, (5) reentry can be initiated by vortex shedding at the sharp boundaries of an infarct scar and (6) an acute ischemic region does not contribute to VF maintenance. Specific Aim 2: Validate MAP recordings from plunge needles. MAP recordings will be compared with microelectrode and optical recordings. It will be determined if the MAP electrodes can measure activation and action potential duration without altering them in guinea pigs and rabbits. Specific Aim 3: Use 3-D MAP mapping to compare the relative roles of the non-uniform dispersion of recovery and the restitution properties of the ventricles in causing block and reentry during VF. The relative importance of three hypotheses for the mechanism of VF maintenance will be evaluated in dogs: (1) the non-uniform dispersion of recovery causes block when a wavefront in an area of lesser refractoriness encounters an adjacent region of greater refractoriness; (2) restitution properties where activation occurs on a steep portion of the restitution curve causes oscillation in coupling intervals which becomes so great that block occurs; and (3) reentry occurs where a wavefront propagates perpendicular to the wavetail of refractoriness of the previous wavefront. The hypotheses will be tested that heart failure caused by patchy fibrosis decreases VF organization while heart failure cause by rapid pacing increases it.