Department of Surgery, Columbia University, New York, NY.
J Thorac Cardiovasc Surg. 2013 Dec;146(6):1494-500. doi: 10.1016/j.jtcvs.2013.06.056. Epub 2013 Sep 26.
The Biventricular Pacing After Cardiac Surgery trial investigates hemodynamics of temporary pacing in selected patients at risk of left ventricular dysfunction. This trial demonstrates improved hemodynamics during optimized biventricular pacing compared with atrial pacing at the same heart rate 1 and 2 hours after bypass and reduced vasoactive-inotropic score over the first 4 hours after bypass. However, this advantage of biventricular versus atrial pacing disappears 12 to 24 hours later. We hypothesized that changes in intrinsic heart rate can explain variable effects of atrial pacing in this setting.
Heart rate, mean arterial pressure, cardiac output, and medications depressing heart rate were analyzed in patients randomized to continuous biventricular pacing (n = 16) or standard of care (n = 18).
During 30-second testing periods without pacing, intrinsic heart rate was lower in the paced group 12 to 24 hours after bypass (76.5 ± 17.5 vs 91.7 ± 13.0 beats per minute; P = .040) but not 1 or 2 hours after bypass. Cardiac output (4.4 ± 1.2 vs 3.6 ± 1.9 L/min; P = .054) and stroke volume (53 ± 2 vs 42 ± 2 mL; P = .051) increased overnight in the paced group. Vasoactive medication doses were not different between groups, whereas dexmedetomidine administration was prolonged over postoperative hours 12 to 24 in the paced group (793 ± 528 vs 478 ± 295 minutes; P = .013).
These observations suggest that hemodynamic benefits of biventricular pacing 12 to 24 hours after cardiopulmonary bypass lead to withdrawal of sympathetic drive and decreased intrinsic heart rate. Depression of intrinsic rate increases the apparent benefit of atrial pacing in the chronically paced group but not in the control group. Additional study is needed to define clinical benefits of these effects.
心脏手术后双心室起搏试验研究了在左心室功能障碍风险患者中，选择的临时起搏的血液动力学。与心房起搏相比，该试验显示在体外循环后 1 至 2 小时以及体外循环后 4 小时内减少血管活性正性肌力评分，优化双心室起搏时可改善血液动力学。然而，双心室起搏与心房起搏相比的优势在 12 至 24 小时后消失。我们假设，在这种情况下，内在心率的变化可以解释心房起搏的可变作用。
分析随机接受持续双心室起搏（n=16）或标准护理（n=18）的患者的心率、平均动脉压、心输出量和抑制心率的药物。
在没有起搏的 30 秒测试期间，体外循环后 12 至 24 小时，起搏组的内在心率较低（76.5±17.5 与 91.7±13.0 次/分钟；P=0.040），但在体外循环后 1 或 2 小时则没有。起搏组的心脏输出量（4.4±1.2 与 3.6±1.9 L/min；P=0.054）和每搏量（53±2 与 42±2 mL；P=0.051）在夜间增加。两组之间血管活性药物剂量没有差异，而在起搏组，右美托咪定的给药时间在术后 12 至 24 小时延长（793±528 与 478±295 分钟；P=0.013）。
这些观察结果表明，体外循环后 12 至 24 小时双心室起搏的血液动力学益处导致交感神经驱动和内在心率降低。内在率的降低增加了慢性起搏组中心房起搏的明显益处，但在对照组中则没有。需要进一步研究来确定这些影响的临床益处。
