Boersma L, Brugada J, Kirchhof C, Allessie M
Department of Physiology, University of Limburg, Maastricht, The Netherlands.
Circulation. 1994 Feb;89(2):852-62. doi: 10.1161/01.cir.89.2.852.
Premature stimulation is used to characterize the reentrant circuit during ventricular tachycardia (VT) in patients. The goal of this study was to compare the effects of premature stimulation on functional and anatomic reentrant VT.
In 18 Langendorff-perfused rabbit hearts, thin layers of anisotropic left ventricular subepicardium were created by a cryoprocedure. In 8 hearts, rapid pacing induced reentry around a line of functional conduction block; in 10 hearts, reentry occurred around a fixed epicardial obstacle created by a cryoprobe. The cycle lengths (CL) of functional and anatomic VT were 110 +/- 10 and 167 +/- 17 milliseconds, respectively. During anatomic VT, the excitable gap measured 43% of the CL and premature stimuli could always reset VT (44 +/- 12 milliseconds). During early premature beats, conduction of the orthodromic wave was slightly depressed, but anatomic VT was never terminated. Reset curves at different sites in the ventricle revealed three different response types, both determined by and characterizing the spatial and temporal relation between pacing and recording sites. Premature stimulation during functional VT revealed a local excitable gap at the pacing site measuring 27% of the cycle length of VT. However, in only 3 of 8 hearts, premature stimuli could reset functional VT by 8%. In 5 VTs, advancement of the paced activation was fully compensated by prolongation of the return cycle, and VT was not reset. Due to slow conduction both toward and inside the circuit, the paced orthodromic wave lost its prematurity already within a distance of 6 to 10 mm from the pacing site.
Both during anatomic and functional reentry, an excitable gap is present in the reentrant circuit. Three different response curves reveal the localization of the pacing and recording sites in the circuit. Anatomic VT can always be reset by premature stimuli, whereas in 5 of 8 hearts, functional VT could not be reset. In the other 3 hearts, VT could only be reset for less than 7% to 11% of the VT interval. Therefore, it seems very unlikely that clinical VT based on functional reentry can be reset.
过早刺激用于表征患者室性心动过速（VT）期间的折返环路。本研究的目的是比较过早刺激对功能性和解剖性折返性室性心动过速的影响。
在18个Langendorff灌注兔心脏中，通过冷冻程序创建各向异性左心室心外膜下层的薄层。在8个心脏中，快速起搏诱发围绕功能性传导阻滞线的折返；在10个心脏中，折返发生在由冷冻探头造成的固定心外膜障碍物周围。功能性和解剖性室性心动过速的周长（CL）分别为110±10和167±17毫秒。在解剖性室性心动过速期间，可兴奋间隙为周长的43%，过早刺激总能重置室性心动过速（44±12毫秒）。在早期过早搏动期间，顺向波的传导略有抑制，但解剖性室性心动过速从未终止。心室不同部位的重置曲线显示出三种不同的反应类型，这既由起搏和记录部位之间的空间和时间关系决定，也对其进行了表征。功能性室性心动过速期间的过早刺激显示起搏部位存在局部可兴奋间隙，其为室性心动过速周长的27%。然而，在8个心脏中只有3个，过早刺激可将功能性室性心动过速重置8%。在5次室性心动过速中，起搏激动的提前被折返周期的延长完全代偿，室性心动过速未被重置。由于向环路内和环路内的传导缓慢，起搏的顺向波在距起搏部位6至10毫米的距离内就已失去其提前性。
在解剖性和功能性折返期间，折返环路中均存在可兴奋间隙。三种不同的反应曲线揭示了环路中起搏和记录部位的定位。解剖性室性心动过速总能被过早刺激重置，而在8个心脏中有5个，功能性室性心动过速不能被重置。在另外3个心脏中，室性心动过速只能在室性心动过速间期的不到7%至11%的时间内被重置。因此，基于功能性折返的临床室性心动过速似乎极不可能被重置。
