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室性心动过速的解联和终止机制。

Mechanisms of unpinning and termination of ventricular tachycardia.

作者信息

Ripplinger Crystal M, Krinsky Valentin I, Nikolski Vladimir P, Efimov Igor R

机构信息

Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, Missouri, USA.

出版信息

Am J Physiol Heart Circ Physiol. 2006 Jul;291(1):H184-92. doi: 10.1152/ajpheart.01300.2005. Epub 2006 Feb 24.

Abstract

High-energy defibrillation shock is the only therapy for ventricular tachyarrhythmias. However, because of adverse side effects, lowering defibrillation energy is desirable. We investigated mechanisms of unpinning, destabilization, and termination of ventricular tachycardia (VT) by low-energy shocks in isolated rabbit right ventricular preparations (n = 22). Stable VT was initiated with burst pacing and was optically mapped. Monophasic "unpinning" shocks (10 ms) of different strengths were applied at various phases throughout the reentry cycle. In 8 of 22 preparations, antitachycardia pacing (ATP: 8-20 pulses, 50-105% of period, 0.8-10 mA) was also applied. Termination of reentry by ATP was achieved in only 5 of 8 preparations. Termination by unpinning occurred in all 22 preparations. Rayleigh's test showed a statistically significant unpinning phase window, during which reentry could be unpinned and subsequently terminated with E80 (magnitude at which 80% of reentries were unpinned) = 1.2 V/cm. All reentries were unpinned with field strengths < or = 2.4 V/cm. Unpinning was achieved by inducing virtual electrode polarization and secondary sources of excitation at the core of reentry. Optical mapping revealed the mechanisms of phase-dependent unpinning of reentry. These results suggest that a 20-fold reduction in energy could be achieved compared with conventional high-energy defibrillation and that the unpinning method may be more effective than ATP for terminating stable, pinned reentry in this experimental model.

摘要

高能量除颤电击是治疗室性快速心律失常的唯一方法。然而,由于存在不良副作用,降低除颤能量是可取的。我们在离体兔右心室标本(n = 22)中研究了低能量电击解除折返、使其失稳并终止室性心动过速(VT)的机制。通过短阵起搏诱发稳定的VT并进行光学标测。在整个折返周期的不同阶段施加不同强度的单相“解除折返”电击(10 ms)。在22个标本中的8个中,还施加了抗心动过速起搏(ATP:8 - 20个脉冲,周期的50 - 105%,0.8 - 10 mA)。ATP仅在8个标本中的5个中实现了折返终止。所有22个标本均通过解除折返实现了终止。瑞利检验显示存在统计学上显著的解除折返相位窗,在此期间折返可被解除,随后用E80(80%的折返被解除时的强度)= 1.2 V/cm终止。所有折返在电场强度≤2.4 V/cm时被解除。解除折返是通过在折返核心诱发虚拟电极极化和二次兴奋源实现的。光学标测揭示了折返相位依赖性解除折返的机制。这些结果表明,与传统高能量除颤相比,能量可降低20倍,并且在该实验模型中,解除折返方法可能比ATP更有效地终止稳定的、固定的折返。

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