Okazaki O, Yamauchi Y, Kashida M, Izumo K, Akatsuka N, Ohnishi S, Shoda M, Nirei T, Kasanuki H, Ebato M, Mashima S, Harumi K, Wei D
Division of Cardiology, International Medical Center of Japan, Tokyo.
J Electrocardiol. 1998;30 Suppl:98-104. doi: 10.1016/s0022-0736(98)80051-4.
The possible contribution of localized conduction delay and abnormal action potentials to ventricular fibrillation (VF) was studied by applying an anisotropic cardiac computer model to clinical cases of the Brugada-type electrocardiogram (ECG), which shows right bundle branch block (RBBB), a normal QT interval, ST-segment elevation, and late r' in leads V1 and V2. The anisotropic heart model was composed of 50,000 discrete units with a spatial resolution of 1.5 mm and was mounted in a human torso model. The longitudinal/transverse conduction velocity ratio was 3:1. For the normal ECG, a conduction velocity of 0.75 m/s was required. In the abnormal area of the right anterior epicardial wall, the conduction velocity was set at 0.2 m/s, with decreasing action potential amplitude and 10% prolonged action potential duration. The ECG features of ST-segment elevation and Brugada-type right bundle branch block pattern were simulated. The action potential duration was able to change dynamically with coupling interval of stimulation, with a ratio of 9% for normal ventricular muscle and 50% for Purkinje fibers. Five successive stimuli were applied to the left lateral epicardium 300 ms after the first sinus excitation, and sustained VF was induced with the transmural conduction delay at the right anterior ventricle as a block increasing the vulnerability. At the initiation of VF, reentry circuits were shown around the border zone of the right epicardium and were very heterogeneous around the conduction delayed area and septal area. In an area with the characteristics of nontransmural conduction delay, sustained VF was prevented, and the pattern of transient right bundle branch block appeared on the simulated ECG and body surface potential maps. The late r' wave was calculated in the precordial leads and right anterior site on the body surface potential maps. These results suggest that increased multipolarity in the border zone between the Purkinje fibers and delayed conduction area in the right ventricle might play an important role as a functional block for the persistence of VF.
通过将各向异性心脏计算机模型应用于Brugada型心电图(ECG)的临床病例,研究了局部传导延迟和异常动作电位对心室颤动(VF)的可能作用。Brugada型心电图表现为右束支传导阻滞(RBBB)、正常QT间期、ST段抬高以及V1和V2导联出现晚期r'波。各向异性心脏模型由50,000个离散单元组成,空间分辨率为1.5毫米,并安装在人体躯干模型中。纵向/横向传导速度比为3:1。对于正常心电图,需要0.75米/秒的传导速度。在右前心外膜壁的异常区域,传导速度设定为0.2米/秒,同时动作电位幅度降低,动作电位持续时间延长10%。模拟了ST段抬高和Brugada型右束支传导阻滞模式的心电图特征。动作电位持续时间能够随刺激的耦合间期动态变化,正常心室肌的变化率为9%,浦肯野纤维为50%。在第一次窦性激动后300毫秒,对左外侧心外膜施加5次连续刺激,以右前心室的透壁传导延迟作为增加易损性的阻滞,诱发持续性VF。在VF起始时,折返环出现在右心外膜的边界区域,并且在传导延迟区域和间隔区域周围非常不均匀。在具有非透壁传导延迟特征的区域,持续性VF被阻止,并且在模拟心电图和体表电位图上出现短暂性右束支传导阻滞模式。在胸前导联和体表电位图上的右前部位计算了晚期r'波。这些结果表明,浦肯野纤维与右心室延迟传导区域之间边界区域的多极程度增加可能作为VF持续存在的功能性阻滞发挥重要作用。