Myocardial preservation during ischemia and reperfusion

Abstract

Protection of the myocardium during cardiac surgery is necessary because of two distinctly different forms of injury: ischemia during cross-clamping of the aorta and secondary destructive phenomena during reperfusion. The primary injury of ischemia is caused by a combination of inadequate or no delivery of substrate and inadequate or no flow, which prevents the removal of toxic intermediary and end products of anaerobic metabolism. The secondary injury, that due to myocardial reperfusion after prolonged ischemia, has been shown in experimental models to accentuate ischemic injury, hasten cell death, and thus may extend infarct size. Protection of the myocardium from the primary ischemic injury with chemical cardioplegia was first introduced by Melrose et al.’ in 1955. Since then extensive animal studies2e5 have provided not only a foundation for understanding the physiologic and metabolic derangements in myocardium during ischemia but also the basis for formulating the various cardioplegic solutions for clinical use. Roe et a1.6 were among the first to describe a large clinical experience with single-dose, crystalloid, hypothermic potassium cardioplegia, which yielded very low morbidity and mortality. Tylers et a1.,7 Conti et al.,s and Adams et al9 reported similar results when multidose cardioplegia was used. The use of oxygenated blood as a vehicle for cardioplegic arrest was advocated by Follette et al.l” in 1978. The superiority of sanguineous cardioplegia was then demonstrated in several clinical studies”-l3 both in terms of longer cross-clamping time and lower perioperative