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Ann Thorac Surg 2002;74:101
© 2002 The Society of Thoracic Surgeons

Invited commentary

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The first 20% of the full text of this article appears below.

Each year in the United States over a half million individuals die of acute myocardial infarction. Epidemiology studies based on autopsies indicate that 8% to 24% of these deaths are a result of myocardial free wall rupture [1, 2]. In the current era, it seems implausible that this high incidence still exists. Causative factors such as hypertension, heart rate, preload, afterload, and inotropic state are routinely addressed in the coronary care unit. Early reperfusion by balloon dilatation or fibrinolytics has been demonstrated to preserve myocardial function, a factor undoubtably related to limitation of infarct size and depth [3]. Early studies with fibrinolytics did suggest a decreased incidence of rupture when they were employed within the first 5 . . . [Full Text of this Article]

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