Prakash A, Saksena S, Hill M, Krol R B, Munsif A N, Giorgberidze I, Mathew P, Mehra R
Cardiac Arrhythmia and Pacemaker Service, Eastern Heart Institute, Passaic, New Jersey, USA.
J Am Coll Cardiol. 1997 Apr;29(5):1007-14. doi: 10.1016/s0735-1097(97)00043-0.
We tested the ability of dual-site right atrial pacing to prevent atrial fibrillation (AF) or atrial flutter induced by single-site atrial pacing and correlated its efficacy with clinical patient characteristics, atrial activation times and refractory periods.
Prevention of recurrent AF with long-term dual-site right atrial pacing has been demonstrated in our previous studies. However, the mechanism of antiarrhythmic benefit is unclear.
Using standard electrophysiologic methods, baseline electrocardiographic and electrophysiologic measurements (mean +/- SD) were obtained. Programmed atrial stimulation was performed for AF or atrial flutter induction. Atrial pacing was performed at two drive cycle lengths (600 and 400 ms) and followed by one to three atrial extrastimuli at one to four pacing sites in the right atrium. In patients with inducible AF or atrial flutter, reinduction was then attempted during a dual-site atrial pacing drive train. This was achieved by simultaneously pacing at the high right atrium and coronary sinus ostium at an identical rate to the baseline stimulation, with the atrial extrastimuli being delivered at the pacing site responsible for the initial AF episode initiation.
Twenty patients (10 men, 10 women, mean [+/- SD] age 64 +/- 16 years) with symptomatic AF (n = 10) or atrial flutter (n = 10) were studied. There was a significant abbreviation of the P wave duration to 103 +/- 17 ms with dual-site pacing compared with sinus rhythm (120 +/- 12 ms, p = 0.005) and high right atrial pacing (121 +/- 17 ms, p = 0.005). This was also associated with a characteristic change in P wave configuration with an inferior and leftward axis shift. The effective refractory period at the high right atrium remained unchanged with dual-site atrial pacing compared with single-site high right atrial pacing. Sixteen patients had inducible AF or atrial flutter and could be tested after dual-site atrial pacing. The induced atrial tachyarrhythmia was suppressed in nine patients (56%), who had either induced AF (n = 5) or atrial flutter (n = 4). The difference in the effective refractory period between the high right atrium and the coronary sinus ostium pacing sites was significantly greater (33 +/- 12 ms) in patients with suppression of atrial tachyarrhythmia with dual-site atrial pacing compared with patients without suppression (15 +/- 13 ms, p = 0.001). P wave abbreviation did not correlate with arrhythmia suppression. There was no correlation between suppression of inducible AF or atrial flutter and demographic or clinical patient characteristics.
Dual-site right atrial pacing from the high right atrium and coronary sinus ostium can suppress inducible AF or atrial flutter elicited after single-site high right atrial pacing in selected patients. Acute suppression is more likely in patients with greater dispersion of right atrial refractoriness between these two sites.
我们测试了双部位右心房起搏预防单部位心房起搏诱发心房颤动（AF）或心房扑动的能力，并将其疗效与临床患者特征、心房激动时间和不应期相关联。
我们之前的研究已证明长期双部位右心房起搏可预防复发性AF。然而，抗心律失常益处的机制尚不清楚。
采用标准电生理方法，获得基线心电图和电生理测量值（均值±标准差）。进行程控心房刺激以诱发AF或心房扑动。在两个驱动周期长度（600和400毫秒）下进行心房起搏，然后在右心房的一至四个起搏部位给予一至三次心房期外刺激。对于可诱发AF或心房扑动的患者，然后在双部位心房起搏驱动序列期间尝试再次诱发。这是通过以与基线刺激相同的速率同时在高位右心房和冠状窦口起搏来实现的，心房期外刺激在负责初始AF发作起始的起搏部位发放。
研究了20例有症状AF（n = 10）或心房扑动（n = 10）的患者（10名男性，10名女性，平均[±标准差]年龄64±16岁）。与窦性心律（120±12毫秒，p = 0.005）和高位右心房起搏（121±17毫秒，p = 0.005）相比，双部位起搏时P波持续时间显著缩短至103±17毫秒。这也与P波形态的特征性变化相关，伴有下壁和左向轴偏移。与单部位高位右心房起搏相比，双部位心房起搏时高位右心房的有效不应期保持不变。16例患者可诱发AF或心房扑动，在双部位心房起搏后可进行测试。9例患者（56%）的诱发房性快速心律失常得到抑制，这些患者既有诱发的AF（n = 5）也有诱发的心房扑动（n = 4）。与未得到抑制的患者（15±13毫秒，p = 0.001）相比，双部位心房起搏抑制房性快速心律失常的患者中，高位右心房和冠状窦口起搏部位之间的有效不应期差异显著更大（33±12毫秒）。P波缩短与心律失常抑制无关。可诱发AF或心房扑动的抑制与患者的人口统计学或临床特征之间无相关性。
从高位右心房和冠状窦口进行双部位右心房起搏可抑制部分患者单部位高位右心房起搏后诱发的AF或心房扑动。这两个部位之间右心房不应期离散度更大的患者更可能出现急性抑制。
