Byrd Israel A, Kay Matthew W, Pollard Andrew E
Cardiac Rhythm Management Laboratory, Department of Biomedical Engineering, University of Alabama at Birmingham, Alabama 35294, USA.
J Cardiovasc Electrophysiol. 2006 Oct;17(10):1129-39. doi: 10.1111/j.1540-8167.2006.00579.x.
Interactions between paced wavefronts and monomorphic ventricular tachycardia (VT) dictate antitachycardia pacing outcomes. We used optical mapping to assess those interactions during single and dual site pacing of rabbit ventricular epicardium.
Monomorphic VTs were initiated in six isolated rabbit hearts that were endocardially cryoablated to limit viable tissue to visible epicardium and establish apical tissue as the anatomic anchor. Preparations were optically mapped during single (n = 39) and dual (n = 43) site pacing at 50%-90% of VT cycle length (CL) with eight pulses per trial. Overall, we found six pulses that abruptly terminated VT. This occurred because the VT wavefront collided with the antidromic portion of the paced wavefront and the orthodromic portion of paced wavefront blocked in the VT's refractory region. When effective, dual site pacing that captured tissue at both leads simultaneously terminated the VT immediately, while single site pacing or dual site pacing that captured tissue at only one lead terminated the VT after resetting advanced the orthodromic wavefront. We found 12 pulses that induced polymorphic VT, with 11 of those pulses occurring during capture at only one lead. Expansion of the combined antidromic-VT wavefront around one or both ends of the arc of conduction block formed by the interaction of the orthodromic wavefront with the VT's refractory region initiated functional reentry. Six of these polymorphic VTs were nonsustained because the underlying wavefronts self-terminated. The wavefronts did persist for 4.2 +/- 3.5 cycles before self-terminating in these trials, and the post-pacing cycles presented a 146% increase in CL variability, compared with the variability prior to pacing. These temporal characteristics are similar to those of delayed termination in patients with ICDs.
The main difference between pulses that terminated abruptly and pulses that induced polymorphic VT was the effective separation of the antidromic and orthodromic portions of the paced wavefront from one another.
起搏波前与单形性室性心动过速(VT)之间的相互作用决定了抗心动过速起搏的结果。我们使用光学标测来评估兔心室心外膜单部位和双部位起搏期间的这些相互作用。
在6个离体兔心脏中诱发单形性VT,这些心脏经心内膜冷冻消融,将存活组织限制在可见的心外膜,并将心尖组织作为解剖锚定。在以VT周期长度(CL)的50%-90%进行单部位(n = 39)和双部位(n = 43)起搏期间,每次试验施加8个脉冲,对标本进行光学标测。总体而言,我们发现6个脉冲可突然终止VT。这是因为VT波前与起搏波前的逆向部分发生碰撞,且起搏波前的正向部分在VT的不应期区域被阻滞。当有效时,同时在两根导联捕获组织的双部位起搏可立即终止VT,而仅在一根导联捕获组织的单部位起搏或双部位起搏在重置后推进正向波前时终止VT。我们发现12个脉冲可诱发多形性VT,其中11个脉冲发生在仅一根导联捕获时。由正向波前与VT不应期区域相互作用形成的传导阻滞弧的一端或两端周围,逆向-VT复合波前的扩展引发了功能性折返。这些多形性VT中有6个是非持续性的,因为潜在的波前自行终止。在这些试验中,波前在自行终止前持续了4.2±3.5个周期,与起搏前相比,起搏后周期的CL变异性增加了146%。这些时间特征与植入式心律转复除颤器(ICD)患者延迟终止的特征相似。
突然终止的脉冲与诱发多形性VT的脉冲之间的主要区别在于起搏波前的逆向和正向部分彼此有效分离。