Patel H J, Lankford E B, Polidori D J, Pilla J J, Plappert T, St John Sutton M S, Acker M A
Division of Cardiothoracic Surgery, University of Pennsylvania School of Medicine, Philadelphia, USA.
J Thorac Cardiovasc Surg. 1997 Aug;114(2):169-78. doi: 10.1016/s0022-5223(97)70141-7.
Dynamic cardiomyoplasty is an alternative therapy for end-stage heart failure. We investigated the mechanisms, both acute and chronic, by which a synchronously stimulated conditioned muscle wrap affects left ventricular function in a chronic canine model of dilated cardiomyopathy.
Nineteen dogs underwent rapid ventricular pacing at a rate of 215 beats/min for 4 weeks to create a model of heart failure. Eight dogs were then randomly selected to undergo cardiomyoplasty, and all dogs received 6 additional weeks of rapid ventricular pacing. The cardiomyoplasty group also received a graded muscle conditioning protocol of synchronized burst stimulation to transform the muscle wrap. All dogs were studied with pressure-volume analysis and echocardiography at baseline and after 4 and 10 weeks of rapid ventricular pacing. Data in the cardiomyoplasty group were analyzed with the stimulator off, with it augmenting every beat (1:1), and with it augmenting only every other beat (1:2).
Stimulator "of" data at 10 weeks of rapid pacing demonstrated chronic effects by enhanced ventricular function (end-systolic elastance = 1.80 after myoplasty vs 1.17 for controls, p = 0.005) and a stabilization of volumes and composite end-systolic and end-diastolic pressure-volume relations in the cardiomyoplasty group when compared with controls. Myoplasty stimulation increased apparent contractility (preload recruitable stroke work = 31.3 for stimulator "of" vs 40.6 for stimulator 1:2 assisted beats [p < 0.05] and vs 45.4 for stimulator 1:1 [p < 0.05]).
Benefits from dynamic cardiomyoplasty are by at least two mechanisms: (1) the girdling effects of a conditioned muscle wrap, which halts the chronic remodeling of heart failure, and (2) active systolic assistance, which augments the apparent contractility of the failing heart.
动力性心肌成形术是终末期心力衰竭的一种替代治疗方法。我们研究了在慢性扩张型心肌病犬模型中,同步刺激的条件性肌肉包裹影响左心室功能的急性和慢性机制。
19只犬以215次/分钟的速率进行快速心室起搏4周以建立心力衰竭模型。然后随机选择8只犬进行心肌成形术,所有犬再接受6周的快速心室起搏。心肌成形术组还接受了同步爆发刺激的分级肌肉调节方案以转化肌肉包裹。在基线以及快速心室起搏4周和10周后,对所有犬进行压力-容积分析和超声心动图检查。对心肌成形术组的数据在刺激器关闭、每搏增强(1:1)以及仅每隔一搏增强(1:2)的情况下进行分析。
快速起搏10周时刺激器“关闭”的数据显示,与对照组相比,心肌成形术组通过增强心室功能(心肌成形术后收缩末期弹性 = 1.80,对照组为1.17,p = 0.005)以及稳定容积和复合收缩末期及舒张末期压力-容积关系,表现出慢性效应。心肌成形术刺激增加了表观收缩性(刺激器“关闭”时的前负荷可募集搏功 = 31.3,刺激器1:2辅助搏动时为40.6 [p < 0.05],刺激器1:1时为45.4 [p < 0.05])。
动力性心肌成形术的益处至少通过两种机制实现:(1)条件性肌肉包裹的束带效应,可阻止心力衰竭的慢性重塑;(2)主动收缩辅助,可增强衰竭心脏的表观收缩性。