摘要
目的 用三维标测方法观察急性冠状动脉血栓性心肌缺血室性心律失常的机制。方法向左冠状动脉回旋支 (leftcircumflexartery,LCX)近端释放阳极电流刺激血栓形成。结果 9例发生非持续性室性心动过速 (nonsustainedventriculartachycardia ,NSuVT) ,其激动的起源和维持在心室的不同部位。6例发生持续性室性心动过速 (sustainedventriculartachycardiaSuVT) ,其诱发是由于局灶性机制。SuVT的维持在 3/ 6例是由于局灶性机制 ,另 3例SuVT的维持 ,是由于心肌内的一个大折返径路 ,即以前壁缺血区心内膜下经间隔作为快径 ,而左心室后壁心外膜并经心肌内返回心内膜下作为慢径。 4/ 6例SuVT在 10～ 41s内蜕变成心室颤动 (室颤 ,ventricularfibrillation ,VF)。 1例SuVT自行终止 ,但于 14min后出现 4个连续的室性搏动诱发VF。VF诱发是由于多发的折返波形成。平均总的心肌激动时间 (acti vationtime ,AT)在缺血前是 (40± 4)ms,缺血后增加达 2 7～ 10 2ms。SuVT发作前AT值 (10 1± 2 8)ms比 1min前的AT值 (79± 15 )ms明显延长 (P <0 0 1)。VF前 10个SuVT搏动的平均AT值为 (16 9± 2 9)ms,比SuVT没有发展为VF的犬的AT值明显延长。结论 LCX的血栓可导致 90 %的犬出现NSuVT ,6 0 %的SuVT及 5 0 %的VF。局灶性机制?
Objective Spontaneous sustained ventricular tachycardia(SuVT)and its progression to ventricular fibrillation(VF)induced by coronary artery thrombotic occlusion were characterized using three dimensional mapping in ten open chest dogs.Methods Regional ischemia was induced by thrombotic occlusion using a wire electrode to deliver a 200～300 μA anodic current to the intima of the proximal left circumflex artery(LCX).Results Total occlusion occurred 47 minutes after onset of the current as indicated by a Doppler flowmeter.In nine dogs,nonsustained VT(NSuVT)was initiated and maintained from numerous,different focal sites of origin.VT occurred in six dogs(group A)and was also initiated by focal mechanisms located near the ischemic border in four dogs and within the ischemic region in the other two.In three dogs,the SuVT was maintained primarily through a focal mechanism,which arose in the ischemic border region.In the other three dogs,VT was maintained by macroreentry that extended form the subendocardium of the ischemic region anteriorly through the septum as the fast pathway,towards the epicardium of the posterior area of LV and then intramurally back to the subendocardium as the slow pathway.VT degenerated into VF in 10～41 seconds in four of these six dogs.In one case,VT stopped spontaneously but was followed 14 min later by 4 cycles of VT that initiated VF.The transition from VT to VF was due exclusively to intramural reentry with multiple wavefronts involving the nonischemic region in three dogs,the ischemic border region in one,and the ischemic region in one.The mean total activation time(AT)in the control state was (40±4) ms,AT started to increase near the time of total LCX occlusion.The maximal increase was 27～102 ms.The AT of the ten sinus cycles before VT(101±28)ms was significantly longer than 1 minute before VT[(79±15)ms,[WTBX]P<0 01].In four dogs,.In four dogs,VT occurred 3～7 minutes after total occlusion when the AT increased to 98～146 ms.The AT in the four dogs without VT(group B)was always less than 98 ms.The mean AT of the first ten cycles of VT in those dogs in which VT degenerated into VF(169±29)ms was significantly longer than that in the two dogs in which VT remained stable without degenerating into VF.Conclusion Thrombotic occlusion of the LCX induced NSuVT in 90%,VT in 60%,and VF in 50% of the dogs.Focal mechanisms underlay most NSuVT and the initiation of VT.VT was maintained either by a focal origin near the ischemic border or by reentry,which propagated intramurally from the epicardium to the subendocardium in the ischemic region.VF was maintained exclusively by intramural reentry involving the ischemic region,border,and nonischemic regions.AT is positively correlated with malignant ventricular arrhythmias and may differentiate VT that remains stable from that progresses to VF.
出处
《中华心律失常学杂志》
2001年第4期221-228,共8页
Chinese Journal of Cardiac Arrhythmias
