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Robert Roberts, MD

JAMA. 1979;242(2):183-185.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

SINCE the advent of the coronary care unit (CCU) in 1962, the in-hospital mortality of patients with acute myocardial infarction has been notably reduced, predominantly because of better management of ventricular arrhythmias. Despite adequate antiarrhythmic therapy, there remains a 15% to 25% acute mortality that is related primarily to pump failure, a major determinant of which is the extent of myocardial damage (infarct size).

Postmortem studies have shown that patients dying of cardiogenic shock exhibit 40% or more destruction of the myocardium. Clearly, therapeutic efforts in the modern CCU must be directed toward reducing the extent of myocardial damage associated with myocardial infarction. Pioneering studies by Braunwald and others¹ suggested that the development of myocardial damage is a dynamic event that can be favorably altered, notably by decreasing the imbalance between myocardial oxygen supply and demand. This provided the impetus for an area of research, namely, protection of ischemic myocardium, . . . [Full Text PDF of this Article]

Author Affiliations
From the Cardiovascular Division, Washington University School of Medicine, St Louis.

Footnotes
This article is one of a series sponsored by the American Heart Association, edited by C. Richard Conti, MD.

Reprint requests to Cardiac Care Unit, Washington University School of Medicine, 660 S Euclid Ave, St Louis, MO 63110 (Dr Roberts).

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