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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http://dx.doi.org/10.31480/2330-4871/127 | DOI Listing |
PLoS One
January 2025
Precision Laboratory of Vascular Medicine, Shanxi Cardiovascular Hospital Affiliated Shanxi Medical University, Taiyuan, PR China.
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J Vis Exp
January 2025
Department of Cardiac Surgery, the First Affiliated Hospital of Xinjiang Medical University;
The objective of this study was to investigate the cardioprotective effects of Munziq on abnormal body fluid myocardial ischemia-reperfusion injury (MIRI) and its underlying mechanism.Normal rats and rats with abnormal body fluid (ABF) were pre-treated with Munziq for 21 days. Following this, MIRI models were established.
View Article and Find Full Text PDFClin Res Cardiol
January 2025
Clinic for General and Interventional Cardiology/Angiology, Herz- und Diabeteszentrum NRW, Ruhr-Universität Bochum, Georgstraße 11, 32545, Bad Oeynhausen, Germany.
Background: Impaired renal function can increase cardiac troponin levels due to reduced elimination, potentially affecting its diagnostic utility. Limited data exist on high-sensitivity cardiac troponin I (hs-cTnI) kinetics after cardiac surgery relative to renal function. This study evaluates how impaired renal function influences hs-cTnI kinetics following cardiac surgery, distinguishing between patients with and without postoperative myocardial infarction (PMI).
View Article and Find Full Text PDFInt J Gynecol Cancer
January 2025
Division of Gynecologic Oncology, Obstetrics & Gynecology Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
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Cureus
December 2024
Physics and Engineering, London Regional Cancer Program, London, CAN.
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