Department of Surgery, University of Minnesota, Minneapolis, Minn 55417, USA.
J Thorac Cardiovasc Surg. 2011 Jan;141(1):261-8. doi: 10.1016/j.jtcvs.2010.08.061.
Clinical studies indicate incomplete functional recovery of hibernating myocardium after coronary artery bypass grafting. We hypothesized that persistent contractile abnormalities after coronary artery bypass grafting are associated with decreased mitochondrial proteins involving electron transport chain that might limit maximal oxygen consumption.
Seven pigs with hibernating myocardium underwent off-pump revascularization with left internal thoracic artery to mid left anterior descending artery. At 4 weeks, left internal thoracic artery anastomosis was patent by multidetector computed tomography. Regional function (transthoracic echocardiography) and blood flow (microspheres) were assessed at rest and during high-dose dobutamine (40 μg/[kg · min]). Expression of electron transport chain proteins was analyzed with isobaric tags for relative and absolute quantification.
After revascularization, multidetector computed tomography confirmed severe left anterior descending stenosis and patent left internal thoracic artery graft. Regional function and blood flow normalized at rest; however, function in left anterior descending distribution remained depressed relative to remote regions, and myocardial blood flow in that region did not increase normally when challenged with high-work state. Concomitant with reduced maximal blood flow response in left anterior descending region was more than 40% reduction in electron transport chain proteins essential to adenosine triphosphate production.
Despite successful revascularization of hibernating myocardium, regional function and blood flow remained depressed during catecholamine stress. Electron transport chain proteins known to be downregulated during adaptive process within hibernating myocardium did not normalize after revascularization. These data demonstrate a potential bioenergetic cause of persistent dysfunction and heart failure within successfully revascularized hibernating myocardium.
临床研究表明，冬眠心肌在冠状动脉旁路移植术后不能完全恢复功能。我们假设，冠状动脉旁路移植术后持续的收缩功能异常与涉及电子传递链的线粒体蛋白减少有关，这可能限制了最大耗氧量。
7 只患有冬眠心肌的猪接受非体外循环血运重建，使用左内乳动脉到中前降支。4 周时，多排螺旋 CT 显示左内乳动脉吻合口通畅。在静息和大剂量多巴酚丁胺（40μg/[kg·min]）时评估左内乳动脉吻合口通畅情况。通过等压标签相对和绝对定量分析电子传递链蛋白的表达。
血运重建后，多排螺旋 CT 证实前降支严重狭窄，左内乳动脉桥通畅。静息时局部功能和血流恢复正常；然而，前降支分布区的功能仍低于远隔区域，当该区域处于高工作状态时，心肌血流不能正常增加。与前降支区域最大血流反应减少超过 40%相关的是，对三磷酸腺苷生成至关重要的电子传递链蛋白减少了 40%以上。
尽管冬眠心肌的血运重建成功，但在儿茶酚胺应激时，局部功能和血流仍保持降低。在冬眠心肌的适应性过程中已知下调的电子传递链蛋白在血运重建后并未恢复正常。这些数据表明，在成功血运重建的冬眠心肌中，持续功能障碍和心力衰竭存在潜在的生物能量学原因。
