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In the setting of heart surgery, myocardial protection refers to strategies and methodologies used in the operating room to attenuate or prevent perioperative infarction and/or postischemic ventricular dysfunction. This is in contrast to the instance in which a patient presents with an acute myocardial infarction (MI). Here the objective is to reduce infarct size at reperfusion. The underlying pathophysiology in both settings, however, relates to the etiology and consequences of ischemia-reperfusion injury. After surgery the injury manifests by low cardiac output, hypotension, and a need for postoperative inotropic support. The damage may be reversible or irreversible and is differentiated by the presence of electrocardiographic abnormalities, elevations in the levels of specific plasma enzymes or proteins such as creatine kinase and troponin I or T, and/or the presence of regional or global echocardiographic wall motion abnormalities. Depending on the criteria, the incidence of postoperative MI after CABG surgery ranges between 3% and 18%. The incidence of severe ventricular dysfunction, heart failure, and death, despite advances in surgical techniques, ranges between 2 and 15%; the higher mortality rates are associated with high-risk patients with minimal cardiac reserve.


These complications have an enormous impact on both families and society. From an economic standpoint alone, revascularization procedures are costly. In 2004 cardiovascular disease was responsible for more than 1 million hospital stays; it was the most expensive condition treated, with a total cost of more than $44 billion. More than half of the hospitalizations for coronary atherosclerosis were for patients who received percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) surgery.1 With respect to CABG surgery alone, the initial hospital cost is approximately $10 billion annually; the complications after CABG consume an additional $2 billion in U.S. health care resources each year.2–5 A reduction in perioperative complications associated with heart surgery could have a significant impact on resource utilization and overall operative costs. Because one cause of morbidity and mortality after heart surgery is ischemia-reperfusion injury, the purpose of this chapter is to review its underlying mechanisms, review the history of myocardial protection, update the reader regarding the current protective techniques, and discuss new strategies under investigation.


The etiologies of perioperative myocardial necrosis and postischemic myocardial dysfunction after cardiac surgery are multifactorial. Myocardial necrosis and associated cardiac biomarkers may arise as a result of ischemia caused by intrinsic coronary disease not amenable to revascularization, anesthetic factors, atrial cannulation, aortic cross-clamping, suturing of heart muscle, plaque and platelet embolism, and graft spasm or thrombosis. Despite the considerable progress made to date, high-risk heart surgery patients including those with unstable angina, poor ventricular function, diabetes, repeat CABG, and advanced age continue to experience postoperative complications such as low cardiac output, perioperative myocardial infarction, and heart failure requiring prolonged intensive care. In many of these patients these complications are caused by ischemia-reperfusion injury and inadequate myocardial protection. Thus there is a compelling unmet need to develop new methods to protect the heart during surgery.


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