Mechanisms and treatment of polymorphic ventricular tachycardia

1.在本研究中，我们研究了直流电击诱发多形性室性心动过速(PVT)的机制以及不同药物对体外灌流的兔心PVT的影响。用自制的光学记录系统，用电压敏感染料(di-4-ANEPPS)对8-32个脑室外膜部位的荧光动作电位信号进行记录。常规记录具有高S/N比(&gt；50db)的稳定光信号，具有-3.6%/min的小基线漂移。在动作电位复极期施加直流电击(10-40V)可引起动作电位延长和心室复极空间离散度增加，从而引起兴奋的迂回运动，导致室上性心动过速。与单相电击相比，双相电击引起的心室复极离散度较小，PVT发生率和持续时间较短。10μM异丙吡胺延长心室动作电位…而30μM异丙吡胺则显著降低心室传导速度。在10μM二丙吡胺存在下，对直流电击诱发的室上性心动过速的敏感性略有降低。相反，在30μM二丙基吡胺存在下，对PVT的易感性大大增加，并且诱导性PVT的持续时间比对照组长得多。E-4031(0.1μM)可引起室性动作电位的逆频率依赖性延长，且持续时间较短，对室上性心动过速的易感性明显降低。β肾上腺素能受体被异丙肾上腺素(0.1μM)刺激后，动作电位明显缩短，且有明显的地区差异。在异丙肾上腺素存在的情况下，PVT表现出比对照组更长的保存时间。综上所述，直流电击通过增强室壁复极的空间不均一性，启动PVT下兴奋的迂回运动，药物诱导的ADP弥散可能促进和夸大直流电击诱发的折返性快速性心律失常。较少

1. In this study, we investigated mechanisms underlying DC shock-induced polymorphic ventricular tachycardia (PVT) and effects of various drugs on PVT in rabbit hearts perfused in vitro.2. Fluorescent action potential signals were recorded from 8-32 epicardial sites of ventricles stained with a voltage-sensitive dye (di-4-ANEPPS) with the use of our custom-built optical recording system. Stable optical signals with a high S/N ratio (>50dB) were routinely recorded with a small base-line drift of -3.6%/min.3. Application of DC shocks (10-40V) during the repolarization phase of action potentials caused a prolongation of action potentials and an enhancement of spatial dispersion of ventricular repolarization, giving rise to an initiation of circuitous movement of excitation leading to PVT.4. Biphasic shocks caused less dispersion of ventricular repolarization and lower incidence and shorter duration of PVT than monophasic shocks.5. 10μM disopyramide prolonged ventricular action potentials … More with minimal effects on conduction velocity, whereas 30 μM disopyramide decreased significantly ventricular conduction velocity. In the presence of 10μM disopyramide, vulnerability to PVT induction by DC shock was slightly reduced. In contrast, in the presence of 30μM disopyramide, vulnerability to PVT was greatly increased and induced PVT showed much longer perpetuation than controls. E-4031 (0.1μM) caused a reverse-frequency dependent prolongation of ventricular action potentials and a marked decrease in vulnerability to PVT with shorter perpetuation.6. Stimulation of β adorenergic receptor by isoproterenol (0.1μM) resulted in a shortening of action potentials with considerable regional differences. In the presence of isoproterenol, PVT showed longer perpetuation than controls.7. In conclusion, DC shocks initiate circuitous movement of excitation underlying PVT through an enhancement of spatial inhomogeneity of ventricular repolarization, and drug-induced in ADP dispersion may facilitate and exaggerate DC shock-induced reentrant tachyarrhythmias. Less