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J Am Coll Cardiol, 2001; 37:9-18
© 2001 by the American College of Cardiology Foundation
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Shifting the open-artery hypothesis downstream: the quest for optimal reperfusion

Matthew T. Roe, MD*, E. Magnus Ohman, MD, FACC*, Arthur C. P. Maas, MD*, Robert H. Christenson, PhD{dagger}, Kenneth W. Mahaffey, MD*, Christopher B. Granger, MD, FACC*, Robert A. Harrington, MD, FACC*, Robert M. Califf, MD, FACC* and Mitchell W. Krucoff, MD, FACC*

* Duke Clinical Research Institute, Durham, North Carolina, USA
{dagger} Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA



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Figure 1 Pathophysiology of microvascular dysfunction after epicardial perfusion.

 


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Figure 2 Stages of successful reperfusion depicted with angiographic techniques. As epicardial patency is re-established, tissue perfusion is restored if microvascular damage is not present. Adapted from Davies and Ormerod (6), with permission.

 


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Figure 3 Temporal pattern of creatine kinase (CK) release after fibrinolysis for successful (Thrombolysis In Myocardial Infarction [TIMI] flow grade 3) and unsuccessful (TIMI flow grade 0) reperfusion. Reproduced from Zabel et al. (44), with permission.

 


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Figure 4 Temporal pattern of ST segment resolution after fibrinolysis, with continuous 12-lead ST segment monitoring. Cyclic patency of the infarct-related artery (IRA) is depicted by intermittent ST segment re-elevation.

 




 
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