Anesth Pain Med.  2018 Jan;13(1):1-9. 10.17085/apm.2018.13.1.1.

Anesthetic-induced myocardial protection in cardiac surgery: relevant mechanisms and clinical translation

Affiliations
  • 1Department of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, Seoul, Korea. aneshim@yuhs.ac
  • 2Anesthesia and Pain Research Institute, Yonsei University College of Medicine, Seoul, Korea.

Abstract

Cardiac surgery is still associated with complications such as adverse perioperative cardiovascular events. Over the past two decades, many studies have shown that volatile anesthetics and opioids provide myocardial protection against ischemia-reperfusion injury in a similar manner as ischemic conditioning. First (1-2 hours) and second (24-72 hours) windows of protection are provided, the underlying mechanisms for which involve activation of G-protein-coupled receptors, protein kinases, and the opening of adenosine triphosphate-sensitive potassium channels. These processes ultimately result in inhibition of the mitochondrial permeability transition pore. Post-conditioning can also be effective when treatment is applied in the proximity of reperfusion. Although propofol lacks these conditioning effects, it acts as a strong antioxidant and protects the myocardium by attenuating oxidative stress related to reperfusion injury. Clinical evidence favors the use of volatile anesthetics over propofol in terms of reduced cardiac enzyme release, length of hospital stay, and mortality. However, the existing evidence level is insufficient to draw a definite conclusion regarding the mortality benefit of one anesthetic over the others. In addition, many common clinical conditions, such as advanced age, hyperglycemia/diabetes, and hypertrophy, have been shown to mitigate the protective efficacy of the anesthetics, although this effect also lacks clinical validation. Propofol may also abolish the protective effects of volatile anesthetics and opioids by scavenging reactive oxygen species, an essential trigger for pre-conditioning. The following review addresses these issues from a clinical perspective.

Keyword

Analgesics; opioid; Anesthetics; inhalation; Myocardial ischemia; Propofol; Reperfusion injury

MeSH Terms

Adenosine
Analgesics
Analgesics, Opioid
Anesthetics
Hypertrophy
Inhalation
Length of Stay
Mortality
Myocardial Ischemia
Myocardium
Oxidative Stress
Permeability
Potassium Channels
Propofol
Protein Kinases
Reactive Oxygen Species
Receptors, G-Protein-Coupled
Reperfusion
Reperfusion Injury
Thoracic Surgery*
Adenosine
Analgesics
Analgesics, Opioid
Anesthetics
Potassium Channels
Propofol
Protein Kinases
Reactive Oxygen Species
Receptors, G-Protein-Coupled

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