Guo H, Hecker S, Lévy S, Olshansky B
Department of Medicine, Loyola University Medical Center, Maywood, Illinois, USA.
Europace. 2001 Apr;3(2):115-23. doi: 10.1053/eupc.2001.0151.
Tachycardia with a QRS configuration which resembles that in sinus rhythm is usually thought to be supraventricular. Ventricular tachycardia, with a similar QRS configuration to that in sinus rhythm on the 12-lead ECG, can occur. The mechanisms of this form of ventricular tachycardia have not been previously reported.
The mechanism of ventricular tachycardia was defined during electrophysiological study in five patients. During sinus rhythm, all patients had a wide QRS complex (>0.12 s) on the 12-lead ECG. The morphology remained grossly unchanged during spontaneous, symptomatic tachycardia. Four of the five patients had coronary artery disease and left ventricular dysfunction. The remaining patient had idiopathic dilated cardiomyopathy. The relationship between the His bundle, deflection, the right bundle branch and the QRS complex was evaluated during tachycardia. Atrial and ventricular pacing, and ventricular activation mapping were performed during tachycardia to define the tachycardia mechanism. The tachycardia induced at electrophysiological testing, which was similar to the clinical tachycardia, was proven to be ventricular tachycardia in each patient. The morphology of ventricular tachycardia was right bundle branch block in two patients and left bundle branch block in three patients. The median tachycardia cycle length was 300 ms (range: 260-480 ms). His bundle activation occurred in a 1:1 relationship with ventricular activation during tachycardia in all patients at least intermittently. The tachycardias were thought initially to be bundle branch reentry tachycardia. With further intervention and continued observation, it became clear that His bundle activation was passive and was not required for the tachycardia to sustain. During tachycardia, His bundle activation appeared to precede the local ventricular activation. Instead, the His bundle was activated slowly from the previous ventricular beat causing a long ventricular-His (VH) interval. This was shown by: (1) activation patterns, (2) response to pacing, (3) intermittent VH dissociation, and (4) termination of ventricular tachycardia.
A unique form of ventricular tachycardia is described. The QRS complex morphology on the 12-lead ECG during tachycardia was grossly similar to that during sinus rhythm. The His bundle activation was passive and occurred with a long activation time from the ventricle to the His bundle. Although it mimics usual bundle branch reentry, this form of ventricular tachycardia appears to be due to a different mechanism in which the His bundle is not obligatory for the continuation of the reentrant phenomenon.
QRS波形态与窦性心律相似的心动过速通常被认为是室上性的。然而,12导联心电图上QRS波形态与窦性心律相似的室性心动过速也可能发生。此前尚未报道过这种形式的室性心动过速的机制。
在对5例患者进行电生理研究期间明确了室性心动过速的机制。在窦性心律时,所有患者12导联心电图上均有宽QRS波群(>0.12秒)。在自发的有症状心动过速期间,其形态基本保持不变。5例患者中有4例患有冠状动脉疾病和左心室功能障碍。其余1例患者患有特发性扩张型心肌病。在心动过速期间评估希氏束、偏转、右束支与QRS波群之间的关系。在心动过速期间进行心房和心室起搏以及心室激动标测以确定心动过速机制。在电生理检查中诱发的与临床心动过速相似的心动过速,经证实每例患者均为室性心动过速。室性心动过速的形态在2例患者中为右束支传导阻滞,在3例患者中为左束支传导阻滞。心动过速的中位周期长度为300毫秒(范围:260 - 480毫秒)。在所有患者中,至少在心动过速期间希氏束激动与心室激动至少间歇性地呈1:1关系。这些心动过速最初被认为是束支折返性心动过速。随着进一步干预和持续观察,很明显希氏束激动是被动的,对于心动过速的维持并非必需。在心动过速期间,希氏束激动似乎先于局部心室激动。相反,希氏束是从前一个心室搏动缓慢激活的,导致心室 - 希氏束(VH)间期延长。这通过以下几点得以证明:(1)激动模式,(2)起搏反应,(3)间歇性VH分离,以及(4)室性心动过速的终止。
描述了一种独特形式的室性心动过速。心动过速期间12导联心电图上的QRS波群形态与窦性心律期间的形态大致相似。希氏束激动是被动的,且从心室到希氏束的激活时间较长。尽管它模仿了常见的束支折返,但这种形式的室性心动过速似乎是由于一种不同机制导致的,其中希氏束对于折返现象的持续并非必需。