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Marvin I. Dunn, MD; Roger J. Dreiling, MD
Arch Intern Med. 1985;145(8):1381-1383. doi:10.1001/archinte.1985.00360080051003.
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Each year in the United States, more than 1 million people suffer from acute myocardial infarction (AMI), resulting in over 350,000 deaths. The coronary care unit, which was developed in the early 1960s, provided an environment for improved recognition and management of the electrical complications of AMI. Hence, myocardial failure, which is directly related to the extent of damaged myocardium, is now the principle cause of in-hospital death in AMI. Unfortunately, inotropic agents, preload and afterload-reducing drugs, and circulatory-assist devices have made little impact on mortality due to myocardial failure.

Shortly after the development of the coronary care unit, interventions limiting infarct size were undertaken to reduce morbidity and mortality from AMI. Most of these interventions were aimed at reducing myocardial oxygen demand, but the quantity of myocardium salvaged appeared to be limited. When Maseri and associates1 demonstrated that coronary artery spasm was an important pathophysiologic factor in myocardial


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