Bohringer Christian, Le Duc, Liu Hong
Department of Anesthesiology and Pain Medicine, University of California Davis Health, Sacramento, California, USA.
Transl Perioper Pain Med. 2020;7(4):279-287. doi: 10.31480/2330-4871/127. Epub 2020 Aug 4.
Perioperative myocardial injury is frequently caused by tachycardia from excessive sympathetic nervous system activity resulting from the surgical stimulation (type 2) rather than by rupture of atherosclerotic plaques with superimposed thrombosis (type 1). The elevated sympathetic nervous system activity results in tachycardia that induces demand ischemia within the myocardium and damages the heart muscle. A rise in troponin has been shown to be a reliable predictor of adverse cardiovascular events when measured in a population at risk. This holds true even when the troponin rise is isolated and other markers for myocardial damage like prolonged ischemic type chest pain, new electrocardiogram changes or evidence of new myocardial damage on echocardiography and other cardiac imaging studies are absent. Treatments that prevent tachycardia by successfully controlling elevated sympathetic tone, like dexmedetomidine and thoracic epidural blockade with local anesthetic reduce troponin release and have been shown to prevent myocardial damage. Intravenous lidocaine and magnesium can also prevent tachycardia. Beta blockers reduce myocardial injury, but are associated with an increase in hypotension and ischemic stroke. Any method of attenuating sympathetic nervous system activity, may however, require treatment with intravenous fluids and vasopressors to prevent hypotension. Rupture of atherosclerotic plaques with superimposed coronary thrombosis is a far less common cause of myocardial infarction in the perioperative period than elevated sympathetic tone. This explains why prophylactic statins in previously statin-naïve patients do not reduce major adverse cardiovascular event rates. Antiplatelet agents are also ineffective in reducing adverse cardiovascular events in the perioperative period. Clinicians, therefore, need to focus their attention on heart rate control and the attenuation of the stress response to surgery, rather than on atherosclerotic plaque stability and antiplatelet drugs in order to successfully prevent perioperative myocardial injury.
围手术期心肌损伤通常是由手术刺激导致交感神经系统活动过度引起的心动过速（2型）所致，而非动脉粥样硬化斑块破裂伴血栓形成（1型）。交感神经系统活动增强导致心动过速，进而诱发心肌内需求性缺血并损害心肌。在有风险的人群中测量时，肌钙蛋白升高已被证明是不良心血管事件的可靠预测指标。即使肌钙蛋白升高是孤立的，且没有其他心肌损伤标志物，如长时间缺血型胸痛、新的心电图变化或超声心动图及其他心脏成像研究显示的新的心肌损伤证据，情况也是如此。通过成功控制交感神经张力升高来预防心动过速的治疗方法，如右美托咪定和局部麻醉药胸段硬膜外阻滞，可减少肌钙蛋白释放，并已被证明可预防心肌损伤。静脉注射利多卡因和镁也可预防心动过速。β受体阻滞剂可减轻心肌损伤，但与低血压和缺血性中风的增加有关。然而，任何减弱交感神经系统活动的方法可能都需要静脉输液和血管升压药治疗以预防低血压。与交感神经张力升高相比，动脉粥样硬化斑块破裂伴冠状动脉血栓形成在围手术期心肌梗死中是远为少见的原因。这就解释了为什么在以前未服用过他汀类药物的患者中预防性使用他汀类药物并不能降低主要不良心血管事件发生率。抗血小板药物在围手术期减少不良心血管事件方面也无效。因此，临床医生需要将注意力集中在心率控制和减轻手术应激反应上，而不是动脉粥样硬化斑块稳定性和抗血小板药物上，以便成功预防围手术期心肌损伤。
