Copies: This document is available on the World Wide Web sites of the American College of Cardiology (www.acc.org), the American Heart Association (www. americanheart.org), and the European Society of Cardiology (www.escardio.org). Single and bulk reprints of both the online full-text guidelines and the published executive summary (published in the August 15, 2006, issues of Circulation and the Journal of the American College of Cardiology and the August 16, 2006, issue of the European Heart Journal) are available from Oxford University Press by contacting Special Sales

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Irreversible ischemic myocardial cell injury developes in an increasing number of cells as the duration of coronary occlusion is prolonged. The present study quantitates myocardial necrosis produced by 40 minutes, 3 hours, or 6 hours of temporary circumflex coronary occlusion (CO) followed by 2 to 4 days of reperfusion, or by 24 or 96 hours of permanent circumflex ligation in pentobarbital anesthetized open chest dogs. After 40 minutes of ischemia, myocyte necrosis was subendocardial but with increasing duration of coronary occlusion, irreversible injury progressed as a wavefront toward the subepicardium. Transmural necrosis was 38 +/- 4% after 40 min, 57 +/- 7% after 3 hours, 71 +/- 7% after 6 hours and 85 +/- 2% after 24 hours of ischemic injury. These results document the presence of a subepicardial zone of ischemic but viable myocardium which is available for pharmacologic or surgical salvage for at least three and perhaps six hours following circumflex occlusion in the dog.

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