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This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/H1799    most recent 00590.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Leshnower, B. G. Articles by Gorman, R. C. Search for Related Content PubMed PubMed Citation Articles by Leshnower, B. G. Articles by Gorman, R. C.

Progression of myocardial injury during coronary occlusion in the collateral-deficient heart: a non-wavefront phenomenon

Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Submitted 19 May 2007 ; accepted in final form 14 July 2007

It is widely accepted that, during acute coronary occlusion, ischemic cell death progresses from the subendocardium to the subepicardium in a wavefront fashion. This concept, which implies that the subendocardium is the most susceptible myocardial region to ischemic injury, was established using a canine model with an extensive system of subepicardial coronary collaterals. In humans, particularly in those with coronary artery disease, there is a wide range in the distribution and functional capacity of the collateral circulation, which may affect the pattern of infarct evolution. Using an ovine model with a limited system of preformed subendocardial coronary collaterals, we characterized the effect of increasing lengths of ischemia on regional blood flow and infarct size in three regions of the ventricular wall: subendocardium, midmyocardium, and subepicardium. Our results demonstrate that the myocardium and microvasculature in these three regions are equally susceptible to injury after 45 min of ischemia. When ischemic time is increased to 1 h, infarct size in the midmyocardium (90 ± 2%) is greater than in the subendocardium (76 ± 4%, P = 0.004) and subepicardium (84 ± 3%, P = 0.13). Microvascular dysfunction as assessed as a percentage of baseline flow is also greater in the midmyocardium (14 ± 5%) compared with the subendocardium (20 ± 3%, P = 0.23) and subepicardium (51 ± 9%, P = 0.007). These findings suggest that, in subjects with a limited system of coronary collateral circulation, the midmyocardium is the most susceptible myocardial region to ischemia and the subendocardium is the most resistant. Myocardial viability during coronary occlusion appears to be primarily determined by the distribution and functional capacity of the collateral circulation.

myocardial infarction; reperfusion; microcirculation

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