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INTRODUCTION

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Acute myocardial infarction (MI) affects approximately 1.5 million individuals each year in the United States.1 Of these patients, 30% die before reaching the hospital and another 5% die during their hospital admission.1 Since 1998, the death rate from cardiovascular disease has declined 30.6%; however, cardiovascular disease remains the leading cause of death in the United States.2 Prompt medical attention including transport to the hospital, diagnosis, and treatment of the MI is critical to patient survival. Over the past 40 years, many developments have led to a decrease in the overall morbidity and mortality associated with acute MI. These developments include new pharmacologic agents, advancement in interventional cardiology procedures, modifications of coronary artery bypass surgical techniques, and the development of treatment algorithms and guidelines. Despite these advances, mechanical and electrical complications such as cardiogenic shock, rupture of the ventricular septum or free wall, acute mitral regurgitation, pericarditis, tamponade, and arrhythmias continue to challenge the medical community caring for patients presenting with acute MI on a daily basis.3 Of these complications, cardiogenic shock complicating acute MIs 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 the major causes of cardiogenic shock. Factors that impact the development of cardiogenic shock include the degree of pre-infarct ventricular dysfunction, the size of the infarcted vessel, and pathologic level of inflammatory mediators.4,5 Revascularization of threatened myocardium offers the best chance of survival following acute coronary occlusion, but the technique and timing of revascularization continue to evolve. The available therapies that can decrease the mortality associated with acute MIs include thrombolytics, percutaneous coronary intervention (PCI), and coronary artery bypass graft (CABG) surgery.

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PATHOGENESIS OF ACUTE OCCLUSION

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Myocardial ischemia resulting from coronary occlusion causes ischemic zone changes from a state of active systolic shortening to one of passive systolic lengthening within 60 seconds of onset of ischemia.6 Occlusions for less than 20 minutes usually cause reversible cellular damage and depressed function with subsequent myocardial stunning. Furthermore, reperfusion of the infarct results in 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 to approximately 10% after 3 hours of ischemia.7,8 Evidence from animal model has also demonstrated that 6 hours of regional ischemia produces extensive transmural necrosis.9 The exact timing in humans is 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. In addition, collateral flow is jeopardized with arrhythmias, hypotension, or the rise of left ventricular end-diastolic pressure above tissue capillary pressure.7 Thus, loss of collateral flow to the infarct area may lead to the ...

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