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Total-mention mortal- ity due to coronary heart disease is 653,000 per year, making coronary heart disease the largest killer of Americans (males and females). AMI is fatal in one third of cases, with 250,000 deaths per year occur- ring before the patient reaches the hospital [1,2]. Complications of AMI include cardiogenic shock, ruptured ventricular septum, ruptured free wall with tamponade, papillary muscle dysfunction with mitral regurgitation, pericarditis, and arrhyth- mia. The death rate from AMI has fallen by nearly 30% since the 1990s, with in-hospital mortality from AMI falling from 11.2% to 9.4% from 1900 to 1999 [3]. Improvements in mortality and morbid- ity over the past decade have been attributed to innovations in pharmacologic treatment, interven- tional cardiology, as well as techniques in bypass surgery and circulatory support [4]. Surgery has played a key role in addressing emergent catastro- phes with resultant improvement in mortality and salvage of myocardium in the aftermath of AMI. Surgery has also been shown to reduce long-term morbidity from AMI as a result of emerging knowl- edge, new procedures, and technical advances. This article addresses the pathophysiology, the treat- ment options, and their rationale in the setting of life-threatening AMI and acute on chronic ischemia. Although biases may exist between cardi- ologists and surgeons, this review hopes to provide the reader with information that will shed light on the options that best suit the individual patient in a given set of circumstances. Pathophysiology of acute ischemia Pathophysiology Occlusion of an infarct-related artery (IRA) can lead to ischemia directly or reduce collateral flow to already ischemic or vascularly compromised areas. Consequences include arrhythmia, hypotension, and high left ventricular (LV) end diastolic pres- sure. As a result of no flow or low flow, myocardial damage can develop rapidly as cellular death evolves. In the first minute, contractile dysfunction within the ischemic zone results from sarcomere deterioration. Active systolic shortening progresses to passive lengthening. Within 20 minutes of IRA occlusion, cardiac myocytes have depressed func- tion and show the stigmata of myocardial stunning. As occlusion persists, damage becomes irreversible. After 40 minutes of ischemia, reperfusion is able to salvage only 60% to 70% of viable myocardium. This value falls to 10% at 3 hours of ischemia [5]. Animal models have shown a zone of widespread transmural necrosis at 6 hours of localized myocar- dial ischemia [6]. In humans, irreversible damage occurs at 4 to 6 hours of ischemia. Thus, success of myocardial salvage is a function of time. After excitation–contraction decoupling occurs acutely in the minutes following AMI, prolonged systolic and diastolic dysfunction occurs [7]. Cell death proceeds by way of apoptosis (programmed cell death) or oncosis (cell swelling), depending on available energy levels. Apoptosis, the main * Corresponding author. New York Presbyterian Hospital, Milstein Hospital Building, Room 7-435, 177 Fort Washington Avenue, New York, NY 10032. E-mail address: gc2124@columbia.edu(G.M. Comas). 1551-7136/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.hfc.2007.04.006 heartfailure.theclinics.com Heart Failure Clin 3 (2007) 181–210 . per year with the annual in- cidence of AMI at 865 ,000. Total-mention mortal- ity due to coronary heart disease is 65 3,000 per year, making coronary heart disease the largest killer of Americans. result of emerging knowl- edge, new procedures, and technical advances. This article addresses the pathophysiology, the treat- ment options, and their rationale in the setting of life-threatening. has played a key role in addressing emergent catastro- phes with resultant improvement in mortality and salvage of myocardium in the aftermath of AMI. Surgery has also been shown to reduce long-term morbidity