Abstract
Volatile anaesthetics exert protective effects on the heart against perioperative ischaemic injury. However, there is growing evidence that these cardioprotective properties are reduced in case of type 2 diabetes mellitus. A strong predictor of postoperative cardiac function is myocardial substrate metabolism. In the type 2 diabetic heart, substrate metabolism is shifted from glucose utilisation to fatty acid oxidation, resulting in metabolic inflexibility and cardiac dysfunction. The ischaemic heart also loses its metabolic flexibility and can switch to glucose or fatty acid oxidation as its preferential state, which may deteriorate cardiac function even further in case of type 2 diabetes mellitus.Recent experimental studies suggest that the cardioprotective properties of volatile anaesthetics partly rely on changing myocardial substrate metabolism. Interventions that target at restoration of metabolic derangements, like lifestyle and pharmacological interventions, may therefore be an interesting candidate to reduce perioperative complications. This review will focus on the current knowledge regarding myocardial substrate metabolism during volatile anaesthesia in the obese and type 2 diabetic heart during perioperative ischaemia.
Highlights
Perioperative cardiac complications occur in 2-5% of all non-cardiac surgical procedures, which globally affect 5–12 million patients each year [1]
Whereas the metabolic undisturbed heart usually responds to injury by increasing myocardial glucose metabolism [22,24], this adaptive response is inhibited by insulin resistance, which is a characteristic of obesity and type 2 diabetes mellitus (T2DM)
It has been shown that sevoflurane and isoflurane open mitochondrial ATPactivated potassium channels [61,62], activates reactive oxygen species [62] and thereby alters mitochondrial metabolism [63]. These results suggest a role for myocardial substrate metabolism in the cardioprotective effects of volatile anaesthesia during ischaemia and reperfusion injury in animals, evidence is limited
Summary
Perioperative cardiac complications occur in 2-5% of all non-cardiac surgical procedures, which globally affect 5–12 million patients each year [1]. Whereas the metabolic undisturbed heart usually responds to injury by increasing myocardial glucose metabolism [22,24], this adaptive response is inhibited by insulin resistance, which is a characteristic of obesity and T2DM This inhibition results in increased myocardial fatty acid metabolism [31,32], increased oxygen consumption, decreased cardiac efficiency [31] and altered myocardial perfusion [33]. It has been shown that sevoflurane and isoflurane open mitochondrial ATPactivated potassium (mito KATP) channels [61,62], activates reactive oxygen species [62] and thereby alters mitochondrial metabolism [63] Together, these results suggest a role for myocardial substrate metabolism in the cardioprotective effects of volatile anaesthesia during ischaemia and reperfusion injury in animals, evidence is limited.
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