Anaesthesia and Myocardial Ischaemia/Reperfusion Injury
Anaesthesia and Myocardial Ischaemia/Reperfusion Injury
Anaesthetists are confronted on a daily basis with patients with coronary artery disease, myocardial ischaemia, or both during the perioperative period. Therefore, prevention and ultimately adequate therapy of perioperative myocardial ischaemia and its consequences are the major challenges in current anaesthetic practice. This review will focus on the translation of the laboratory evidence of anaesthetic-induced cardioprotection into daily clinical practice.
Prevention and adequate treatment of perioperative myocardial ischaemia and its consequences are the frequent challenges of current anaesthetic practice. The main goal in the therapy of myocardial ischaemia is to restore perfusion to the ischaemic tissue. However, reperfusion itself can induce additional cellular damage that can exceed that caused by the ischaemic injury, even resulting in death. This phenomenon is called lethal reperfusion injury. Rosenkranz and colleagues defined lethal reperfusion injury as an irreversible deterioration of the myocardium, which can be reduced by modifications of the conditions of reperfusion. However, not only modifications of reperfusion conditions but also the application of interventions before the occurrence of myocardial ischaemia may help to reduce the extent of ischaemic damage and subsequent reperfusion injury. Interestingly, the use of certain anaesthetic drugs seems to represent one such intervention.
There are three time frames in which protection against ischaemia – reperfusion injury can be induced: before ischaemia occurs, during ischaemia, and after the ischaemia at the onset of reperfusion. The first report that sublethal ischaemia before otherwise lethal ischaemia induces strong cardioprotection was published in 1986 by Murry and colleagues. This preconditioning typically consists of two distinct phases: the early phase which starts immediately after the ischaemic stimulus and protects the myocardium for 2 – 3 h, followed by a late protection period occurring after 12 – 24 h and lasting for 2 – 3 days. The latter is called the late preconditioning phase. It has since been shown that the application of short ischaemic episodes interspersed by short periods of reperfusion after the longer period of myocardial ischaemia was also associated with a protective effect on the extent of myocardial damage and post-ischaemic dysfunction. This phenomenon was called post-conditioning.
Evidence has now accumulated that anaesthetics and some narcotics may be cardioprotective. While experimental findings are increasingly being applied to clinical practice, continuing efforts are directed towards the unravelling of the underlying mechanisms. The understanding of the underlying signal transduction cascade is of special importance because there is conflicting clinical evidence concerning the relative contributions of early or late pre- and post-conditioning to clinical cardioprotection provided by anaesthetic agents. Several factors may be responsible for this conflicting evidence such as the differences in the extent and degree of myocardial ischaemia between different studies, possible interference by the use of other drugs, and the presence of co-existing disease such as diabetes. This review will focus on the translation of laboratory evidence of anaesthetic-induced cardioprotection into daily clinical practice.
Abstract and Introduction
Abstract
Anaesthetists are confronted on a daily basis with patients with coronary artery disease, myocardial ischaemia, or both during the perioperative period. Therefore, prevention and ultimately adequate therapy of perioperative myocardial ischaemia and its consequences are the major challenges in current anaesthetic practice. This review will focus on the translation of the laboratory evidence of anaesthetic-induced cardioprotection into daily clinical practice.
Introduction
Prevention and adequate treatment of perioperative myocardial ischaemia and its consequences are the frequent challenges of current anaesthetic practice. The main goal in the therapy of myocardial ischaemia is to restore perfusion to the ischaemic tissue. However, reperfusion itself can induce additional cellular damage that can exceed that caused by the ischaemic injury, even resulting in death. This phenomenon is called lethal reperfusion injury. Rosenkranz and colleagues defined lethal reperfusion injury as an irreversible deterioration of the myocardium, which can be reduced by modifications of the conditions of reperfusion. However, not only modifications of reperfusion conditions but also the application of interventions before the occurrence of myocardial ischaemia may help to reduce the extent of ischaemic damage and subsequent reperfusion injury. Interestingly, the use of certain anaesthetic drugs seems to represent one such intervention.
There are three time frames in which protection against ischaemia – reperfusion injury can be induced: before ischaemia occurs, during ischaemia, and after the ischaemia at the onset of reperfusion. The first report that sublethal ischaemia before otherwise lethal ischaemia induces strong cardioprotection was published in 1986 by Murry and colleagues. This preconditioning typically consists of two distinct phases: the early phase which starts immediately after the ischaemic stimulus and protects the myocardium for 2 – 3 h, followed by a late protection period occurring after 12 – 24 h and lasting for 2 – 3 days. The latter is called the late preconditioning phase. It has since been shown that the application of short ischaemic episodes interspersed by short periods of reperfusion after the longer period of myocardial ischaemia was also associated with a protective effect on the extent of myocardial damage and post-ischaemic dysfunction. This phenomenon was called post-conditioning.
Evidence has now accumulated that anaesthetics and some narcotics may be cardioprotective. While experimental findings are increasingly being applied to clinical practice, continuing efforts are directed towards the unravelling of the underlying mechanisms. The understanding of the underlying signal transduction cascade is of special importance because there is conflicting clinical evidence concerning the relative contributions of early or late pre- and post-conditioning to clinical cardioprotection provided by anaesthetic agents. Several factors may be responsible for this conflicting evidence such as the differences in the extent and degree of myocardial ischaemia between different studies, possible interference by the use of other drugs, and the presence of co-existing disease such as diabetes. This review will focus on the translation of laboratory evidence of anaesthetic-induced cardioprotection into daily clinical practice.
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