Sweeney Michael O, Ruetz Linda L, Belk Paul, Mullen Thomas J, Johnson James W, Sheldon Todd
Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Am Coll Cardiol. 2007 Aug 14;50(7):614-22. doi: 10.1016/j.jacc.2007.02.077. Epub 2007 Jul 30.
The purpose of this study was to characterize interactions between normal pacing system operation and the initiating sequence of ventricular tachycardia (VT)/ventricular fibrillation (VF).
Abrupt changes in ventricular cycle lengths (short-long-short, S-L-S) might initiate VT/VF. The S-L-S sequences might be passively permitted or actively facilitated by bradycardia pacing.
Initiating sequences of 1,356 VT/VF episodes in the PainFree Rx II (n = 634) and EnTrust Trial (n = 421) were analyzed with stored electrograms and by pacing mode (DDD/R, VVI/R, and Managed Ventricular Pacing [MVP]). Interactions between pacing and VT/VF initiation were classified as: non-pacing associated, pacing associated, pacing permitted, and pacing facilitated.
Non-pacing associated (no pacing, no S-L-S) and pacing associated (ventricular pacing without S-L-S) onset accounted for 44.0% and 29.8% of all VT/VF, respectively. Pacing permitted (S-L-S sequences without ventricular pacing) episodes accounted for 6.4% (DDD/R), 20.0% (MVP), and 25.6% (VVI/R) of 1,356 VT/VF episodes. Pacing facilitated onset (S-L-S sequences actively facilitated by ventricular pacing including the terminal beat after a pause) accounted for 8.2% (MVP), 9.4% (VVI/R), and 14.8% (DDD/R) of 1,356 VT/VF episodes. Pacing facilitated S-L-S VT/VF occurred in 2.6% (MVP), 3.3% (VVI/R), and 5.2% (DDD/R) of patients with episodes and was the sole initiating sequence in approximately 1% of patients. Pause durations during pacing facilitated S-L-S differed between modes (DDD/R 793 +/- 172 ms vs. MVP 865 +/- 278 ms vs. VVI/R 1180 +/- 414 ms, p = 0.002). The majority of these episodes were monomorphic VT.
Ventricular tachycardia/VF in some implantable cardioverter-defibrillator patients might be initiated by S-L-S sequences that are actively facilitated by bradycardia pacing operation and might constitute an important mechanism of ventricular proarrhythmia.
本研究旨在描述正常起搏系统运作与室性心动过速(VT)/心室颤动(VF)起始序列之间的相互作用。
心室周期长度的突然变化(短-长-短,S-L-S)可能引发VT/VF。S-L-S序列可能被心动过缓起搏被动允许或主动促进。
利用存储的心电图并按起搏模式(DDD/R、VVI/R和心室管理起搏[MVP])分析了PainFree Rx II试验(n = 634)和EnTrust试验(n = 421)中1356次VT/VF发作的起始序列。起搏与VT/VF起始之间的相互作用分为:非起搏相关、起搏相关、起搏允许和起搏促进。
非起搏相关(无起搏,无S-L-S)和起搏相关(无S-L-S心室起搏)起始分别占所有VT/VF的44.0%和29.8%。起搏允许(无心室起搏的S-L-S序列)发作在1356次VT/VF发作中分别占6.4%(DDD/R)、20.0%(MVP)和25.6%(VVI/R)。起搏促进起始(由心室起搏主动促进的S-L-S序列,包括停顿后的终末搏动)在1356次VT/VF发作中分别占8.2%(MVP)、9.4%(VVI/R)和14.8%(DDD/R)。起搏促进的S-L-S VT/VF在发作患者中分别占2.6%(MVP)、3.3%(VVI/R)和5.2%(DDD/R),并且在约1%的患者中是唯一的起始序列。起搏促进S-L-S期间的停顿持续时间在不同模式之间有所不同(DDD/R 793±172毫秒 vs. MVP 865±278毫秒 vs. VVI/R 1180±414毫秒,p = 0.002)。这些发作大多数为单形性VT。
一些植入式心脏复律除颤器患者中的室性心动过速/VF可能由心动过缓起搏操作主动促进的S-L-S序列引发,并可能构成心室性心律失常的重要机制。