Kottkamp H, Chen X, Hindricks G, Willems S, Borggrefe M, Breithardt G
Department of Cardiology and Angiology, Hospital of the Westfälische Wilhelms-University, Münster, Germany.
J Cardiovasc Electrophysiol. 1994 Mar;5(3):268-73. doi: 10.1111/j.1540-8167.1994.tb01163.x.
Idiopathic left ventricular tachycardia with a QRS pattern of right bundle branch block and left-axis deviation constitutes a rare but electrophysiologically distinct arrhythmia entity. The underlying mechanism of this tachycardia, however, is still a matter of controversy. This report describes findings in a 42-year-old man who underwent successful radiofrequency catheter ablation of idiopathic left ventricular tachycardia.
On electrophysiologic study, the tachycardia was reproducibly induced and terminated with double ventricular extrastimuli. Intravenous verapamil terminated the tachycardia whereas adenosine did not. Detailed left ventricular catheter mapping during sinus rhythm revealed a fragmented delayed potential at the mid-apical region of the inferior site near the posterior fascicle of the left bundle branch. At the same site, continuous electrical activity throughout the entire cardiac cycle was recorded during ventricular tachycardia. Repeated spontaneous termination of this continuous electrical activity in late diastole was followed immediately by termination of the tachycardia. Single application of radiofrequency current for 20 seconds at this site completely abolished inducibility of the tachycardia. After catheter ablation, at the identical site of preablation recording of the fractionated potential during sinus rhythm, no fragmented delayed activity could be recorded. There was no complication from the ablation procedure.
The preablation recordings of fragmented delayed potentials during sinus rhythm and continuous diastolic electrical activity during tachycardia, together with ablation characteristics and previously reported electrophysiologic properties of this arrhythmia, may further support microreentry as the underlying mechanism in idiopathic left ventricular tachycardia.
QRS波呈右束支传导阻滞及左轴偏移模式的特发性左心室心动过速是一种罕见但在电生理方面有独特表现的心律失常类型。然而,这种心动过速的潜在机制仍存在争议。本报告描述了一名42岁男性患者成功接受特发性左心室心动过速射频导管消融术的相关发现。
在电生理研究中,通过双心室期外刺激可重复性地诱发并终止心动过速。静脉注射维拉帕米可终止心动过速,而腺苷则无效。窦性心律时进行的详细左心室导管标测显示,在左束支后分支附近下壁的心尖中部区域存在碎裂延迟电位。在室性心动过速期间,在同一部位记录到整个心动周期的连续电活动。舒张晚期这种连续电活动反复自发终止后,紧接着心动过速也终止。在此部位单次施加20秒射频电流可完全消除心动过速的可诱发性。导管消融术后,在窦性心律时记录到碎裂电位的消融前相同部位,未记录到碎裂延迟活动。消融过程无并发症发生。
窦性心律时碎裂延迟电位的消融前记录以及心动过速期间舒张期连续电活动,连同消融特征及此前报道的这种心律失常的电生理特性,可能进一步支持微折返是特发性左心室心动过速的潜在机制。