Sato S, Yamauchi S, Schuessler R B, Boineau J P, Matsunaga Y, Cox J L
Department of Surgery, Washington University School of Medicine, Barnes Hospital, St. Louis, Mo.
J Thorac Cardiovasc Surg. 1992 Aug;104(2):297-306.
The purpose of this study was to test the assumption that the cause for postoperative atrial flutter/fibrillation after cardiopulmonary bypass is inadequate atrial myocardial protection. Dogs were subjected to cardioplegic arrest for 60 minutes without augmented atrial hypothermia (seven dogs, control group) or augmented atrial hypothermia with topical atrial cooling (seven dogs, study group). Twenty-five electrodes (15 on the right atrium and 10 on the left atrium) were fixed on the atria to measure effective refractory period and conduction time. Data were taken before bypass, immediately after bypass, and 2 hours after bypass. During cardioplegic arrest the mean temperatures measured in the atria were significantly lower (p less than 0.001) in the study group (13.5 degrees +/- 7.0 degrees C) than in the control group (23.7 degrees +/- 3.2 degrees C). There was no significant change in the mean effective refractory period after bypass in the control or study groups or in the prevalence of inducibility of atrial flutter/fibrillation by extrastimulation (3/7 dogs in the control group and 2/7 in the study group). During right atrial pacing, total conduction times were significantly longer (p less than 0.025 at cycle lengths of 300 and 350 msec) in the control group (74 +/- 5 msec and 75 +/- 7 msec, respectively) than in the study group (65 +/- 9 msec and 64 +/- 8 msec, respectively) immediately after bypass. Two hours after bypass, however, there were no significant differences under the same conditions between the two groups. There were no significant differences in conduction during left atrial pacing after bypass. Comparing those atria that were inducible with those not inducible demonstrated a significantly increased dispersion of effective refractory period (90 +/- 23 msec versus 74 +/- 18 msec, p less than 0.05) and increased conduction time in the inducible group. We concluded that augmented atrial hypothermia during cardioplegic arrest had no effect on the inducibility of fibrillation, had no effect on repolarization, and had only a small effect on conduction, which resolved within 2 hours after bypass. However, the study demonstrates that when the atria are inducible the substrates are an increased dispersion of refractoriness and a prolongation of conduction time.
体外循环后发生术后心房扑动/颤动的原因是心房心肌保护不足。将犬分为两组，一组在无增强心房低温的情况下进行60分钟心脏停搏（7只犬，对照组），另一组采用局部心房冷却进行增强心房低温（7只犬，研究组）。在心房固定25个电极（右心房15个，左心房10个）以测量有效不应期和传导时间。在体外循环前、体外循环后即刻以及体外循环后2小时采集数据。在心脏停搏期间，研究组心房测得的平均温度（13.5℃±7.0℃）显著低于对照组（23.7℃±3.2℃）（p<0.001）。对照组或研究组体外循环后平均有效不应期以及额外刺激诱发心房扑动/颤动的发生率均无显著变化（对照组3/7只犬，研究组2/7只犬）。在右心房起搏期间，体外循环后即刻对照组的总传导时间显著长于研究组（在300和350毫秒的周期长度时，p<0.025）（分别为74±5毫秒和75±7毫秒）（研究组分别为65±9毫秒和64±8毫秒）。然而，体外循环后2小时，两组在相同条件下无显著差异。体外循环后左心房起搏期间的传导无显著差异。将可诱发心房扑动/颤动的心房与不可诱发的心房进行比较，发现可诱发组的有效不应期离散度显著增加（90±23毫秒对74±18毫秒，p<0.05）且传导时间延长。我们得出结论，心脏停搏期间增强心房低温对颤动的可诱发性无影响，对复极化无影响，对传导仅有轻微影响，且在体外循环后2小时内消失。然而，该研究表明，当心房可被诱发时，其基质是不应期离散度增加和传导时间延长。
