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Updated: May 30, 2025

Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System
Published on: June 11, 2020
Current Concepts in the Prevention of Perioperative Myocardial Injury
Christian Bohringer1, Duc Le1, Hong Liu1
1Department of Anesthesiology and Pain Medicine, University of California Davis Health, Sacramento, California, USA.
Abstract:
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.
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