New strategies for intraoperative myocardial protection.
In the past, most strategies for intraoperative myocardial protection were developed in models using nondiseased adult hearts from various animal species. In the clinical setting, however, myocardial status in cardiac patients may be quite different and there is a need to adapt our current protective strategies to the actual pathophysiological status of the heart. In the immature heart as well as in the senescent heart, current protective techniques have been shown to be deficient and further research is required. New insights have been gained into the pathophysiological processes underlying chronic ischemic left ventricular dysfunction in the "hibernating" myocardium. It has been shown that viability in these hearts is associated with subcellular alterations related to dedifferentiation of the myocytes. This finding explains the delayed recovery in function of these hearts after revascularization and the need for intraoperative protective strategies focusing on the prevention of stunning in the nonhibernating segments. Tepid continuous retrograde blood cardioplegia is suggested as the optimal technique. Unraveling the mechanisms of preconditioning in the heart and understanding endogenous myocardial protection may provide clues for novel cardioprotective techniques. Adenosine itself may be used as an adjunct to cardioplegia, and treatment with adenosine regulating agents or nucleoside transport inhibitors shows promising results. Like adenosine, other hyperpolarizing agents (potassium-channel openers) are suggested for arrest of the heart instead of the depolarizing agents commonly used in cardioplegia. Finally, the role of Na(+)-H+ exchange in the development of ischemic and postischemic injury has become more clear. By the use of a new selective Na(+)-H+ exchange inhibitor, postischemic contracture can be dramatically reduced and contractility improved. This opens prospective approaches in emergency coronary bypass surgery for evolving myocardial infarction.
Flameng
W
W
Centrum voor Experimentele Heelkunde en Anaesthesiologie, Katholieke Universiteit Leuven, Belgium.
D000241:Adenosine / Q000627:therapeutic use; D000818:Animals; D006348:Cardiac Surgical Procedures; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced / Q000379:methods; D006801:Humans; D007430:Intraoperative Care; D009203:Myocardial Infarction / Q000503:physiopathology / Q000517:prevention & control; D017202:Myocardial Ischemia / Q000503:physiopathology / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*; D017682:Myocardial Stunning / Q000503:physiopathology / Q000517:prevention & control; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors; D014022:Tissue Survival; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000517:prevention & control
D017923:Sodium-Hydrogen Exchangers; D000241:Adenosine