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Current Concepts in the Prevention of Perioperative Myocardial Injury.

Transl Perioper Pain Med

August 2020

Department of Anesthesiology and Pain Medicine, University of California Davis Health, Sacramento, California, USA.

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.

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Mitochondrial transplantation (MT) is a promising therapeutic strategy that involves introducing healthy mitochondria into damaged tissues to restore cellular function. This approach has shown promise in treating cardiac diseases, such as ischemia-reperfusion injury, myocardial infarction, and heart failure, where mitochondrial dysfunction plays a crucial role. Transplanting healthy mitochondria into affected cardiac tissue has resulted in improved cardiac function, reduced infract size, and enhanced cell survival in preclinical studies.

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Background: Myocardial injury after noncardiac surgery (MINS) is associated with an increased incidence of cardiac morbidity and mortality. Little is known about how these patients are managed.

Methods: We performed a single-centre retrospective chart review of patients referred to a postoperative clinic with the diagnosis of MINS.

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Background: Myocardial ischemia/reperfusion (I/R) injury significantly impacts the recovery of ischemic heart disease patients. Non-coding RNAs, including miRNAs, have been increasingly recognized for their roles in regulating cardiomyocyte responses to hypoxia/reoxygenation (H/R) injury. miR-181c-5p, in particular, has been implicated in inflammatory and apoptotic processes, suggesting its potential involvement in exacerbating cellular damage.

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Background: Endothelial function (EndFx) is a core component of cardiovascular (CV) health and cardioprotection following acute myocardial infarction (AMI) treated with primary percutaneous coronary intervention (PCI).

Hypothesis: AMI patients experience endothelial dysfunction (EndDys), associated with traditional CV risk factors and sleep patterns. EndFx may also predict short and mid-term outcomes.

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