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The ability of surgical interventions to minimize myocardial loss after myocardial infarction has advanced dramatically over the past two decades. Acute myocardial infarction still afflicts approximately 1.5 million individuals each year in the United States,1 and 30% of these patients die before reaching the hospital, whereas 5% die during hospital admission.1 Prompt medical attention, including transport to the hospital, diagnosis, and treatment of the myocardial infarction, is critical to patient survival. Since 1989, the death rate from acute myocardial infarctions has declined 24%, while the actual number of deaths declined only 7%.2 Over the last 40 years, especially during the 1980s, new pharmacologic agents, interventional cardiology procedures, and coronary artery bypass surgical techniques have advanced and have led to a decrease in the overall morbidity and mortality associated with acute myocardial infarction. Despite this overall improvement, mechanical and electrical complications such as cardiogenic shock, rupture of the ventricular septum or free wall, acute mitral regurgitation, pericarditis, tamponade, and arrhythmias challenge the medical community caring for patients presenting with acute myocardial infarction on a daily basis.3 Of these complications, cardiogenic shock complicating acute myocardial infarctions has the most significant impact on in-hospital mortality and long-term survival. The loss of more than 40% of functioning left ventricular mass and its accompanying systemic inflammatory response are major causes of cardiogenic shock and are determined by the degree of preinfarction ventricular dysfunction, the size of the infarcted vessel, and pathologic level of inflammatory mediators.4,5 Restoration of blood flow to the threatened myocardium offers the best chance of survival following acute coronary occlusion, but the means and timing of revascularization continue to be a highly debated and studied topic. Thrombolytics, percutaneous transluminal coronary angioplasty (PTCA), intracoronary stenting, and coronary artery bypass (CABG) surgery have decreased the mortality associated with acute myocardial infarctions. Advances in myocardial preservation and mechanical support lead the surgical armamentarium in the treatment of acute myocardial infarctions.

Myocardial ischemia resulting from coronary occlusion for as little as 60 seconds causes ischemic zone changes from a state of active systolic shortening to one of passive systolic lengthening.6 Occlusions for less than 20 minutes usually cause reversible cellular damage and depressed function with subsequent myocardial stunning. Furthermore, reperfusion of the infarct leads to variable amounts of salvageable myocardium. After 40 minutes of ischemia followed by reperfusion, 60 to 70% of the ultimate infarct is salvageable, but this decreases dramatically to 10% after 3 hours of ischemia.7,8 Animal model evidence has also demonstrated that 6 hours of regional ischemia produces extensive transmural necrosis.9 The exact timing in humans is even more difficult to analyze because of collateral flow, which is a major determinant of myocardial necrosis in the area at risk in humans.8 The collateral blood supply is extremely variable, especially in patients with long-standing coronary disease. However, collateral flow is jeopardized with arrhythmias, hypotension, or the rise of left ventricular end-diastolic pressure above tissue capillary ...

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