(Circulation. 2002;105:2577.)
© 2002 American Heart Association, Inc.
From the Cardiovascular Division (M.A.P.), Brigham and Womens Hospital, Boston, Mass; and the University of Glasgow (J.J.V.M.), Glasgow, Scotland.
Correspondence to Marc A. Pfeffer, MD, PhD, Cardiovascular Division, Brigham and Womens Hospital, 75 Francis St, Boston, MA 02115. E-mail mpfeffer@rics.bwh.harvard.edu
Key Words: Editorials myocardial infarction coronary disease trials heart failure
Myocardial infarction (MI) connotes an appropriate sense of urgency to both healthcare workers and the lay community. The heightened risk of death in the period immediately after the acute coronary event makes MI a medical emergency in which response times are measured in minutes. Clinical signs, symptoms, and electrocardiographic evaluations currently are supplemented by highly specific cardiac markers that detect even minor amounts of myocardial necrosis: the pathonomia of MI. Indeed, major components of the roots of the subspecialty of cardiology can be traced to the concentration of resources and expertise derived from the establishment of coronary care units and studies of MI.
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In many respects, the millions of patients worldwide admitted to coronary care units for suspected acute MI are the fortunate ones, because out-of-hospital sudden death is an all too common heralding event. Those presenting to a hospital have the benefit of 40 solid years of cumulative medical advances. The ability to externally defibrillate what were previously fatal arrhythmias provided tangible immediate proof of the value of coronary care units. Moreover, the development of specialty nursing and the ability of nurses to deliver external defibrillation without awaiting physician directives have saved untold number of lives.
Another major quantum improvement in acute infarct care came from the use of basic physiological principles of understanding and improving the balance between myocardial oxygen supply and demand.1 In our view, the demonstration by Braunwald and colleagues that the extent of the loss of myocardium after coronary occlusion could be
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