Ouyang Feifan, Bänsch Dietmar, Schaumann Anselm, Ernst Sabine, Linder Christian, Falk Peter, Hachiya Hitoshi, Kuck Karl-Heinz, Antz Matthias
2nd Medical Department, General Hospital St. Georg, Hamburg, Germany.
Herz. 2003 Nov;28(7):591-7. doi: 10.1007/s00059-003-2494-8.
In patients with left ventricular tachycardia (VT) and failed endocardial ablation, a subepicardial substrate may be considered.
Seven patients with drug-refractory VT of right bundle branch block morphology were investigated to identify the arrhythmogenic substrate using three-dimensional (3-D) electroanatomic endocardial and epicardial mapping.
In three patients with repetitive monomorphic VT, endocardial and epicardial mapping during tachycardia showed a focal pattern with an earliest activation preceding the onset of the QRS complex by 20 and 28 ms in the lateral aspect of the epicardial outflow tract in two patients and by 24 ms near the posterolateral mitral annulus in one patient; in two patients with sustained VT, endocardial mapping during tachycardia displayed a focal pattern with a wide breakthrough, and epicardial mapping showed a macroreentrant VT with an isthmus located in the left anterior wall in one patient and in the left inferolateral wall in the other. In the remaining two patients, endocardial and epicardial mapping were performed during sinus rhythm. An area with fragmented and late potentials as well as low amplitude was only identified in the epicardial left inferolateral wall. During tachycardia, a diastolic potential was only recorded on the epicardium and coincided with the late potential during sinus rhythm in the same area. A focal or linear epicardial irrigated lesion terminated the VT and resulted in noninducibility in all seven patients. During a median follow-up of 16 months, VT recurred in two patients without antiarrhythmic drugs. The recurrent VT was successfully reablated in one patient and treated with oral amiodarone in the other.
Subepicardial left focal and macroreentrant VT may present as focal origin on endocardial mapping and can only be abolished by radiofrequency (RF) applications in the epicardial space.
对于左心室心动过速(VT)且心内膜消融失败的患者,可考虑心外膜基质。
对7例右束支传导阻滞形态的药物难治性VT患者进行研究,采用三维(3-D)电解剖心内膜和心外膜标测来识别致心律失常基质。
在3例重复性单形性VT患者中,心动过速期间的心内膜和心外膜标测显示为局灶性模式,在2例患者的心外膜流出道外侧,最早激动在QRS波群起始前20和28毫秒,在1例患者二尖瓣后外侧环附近最早激动在QRS波群起始前24毫秒;在2例持续性VT患者中,心动过速期间的心内膜标测显示为局灶性模式且有广泛突破,心外膜标测显示1例患者为大折返性VT,峡部位于左前壁,另1例位于左后下壁。在其余2例患者中,在窦性心律期间进行心内膜和心外膜标测。仅在心外膜左后下壁识别出一个有碎裂电位、延迟电位以及低振幅的区域。心动过速期间,仅在心外膜记录到舒张期电位,且与同一区域窦性心律时的延迟电位一致。心外膜局部或线性灌注射频消融灶终止了VT,并使所有7例患者均不能诱发VT。在中位随访16个月期间,2例患者在未使用抗心律失常药物的情况下VT复发。1例复发VT患者再次成功消融,另1例患者接受口服胺碘酮治疗。
心外膜左局灶性和大折返性VT在心内膜标测时可能表现为局灶起源,且只能通过在心外膜空间进行射频(RF)应用来消除。