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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, 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
Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA

View larger version (26K): [in a new window]   Figure 1 Pathophysiology of microvascular dysfunction after epicardial perfusion.

View larger version (28K): [in a new window]   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.

View larger version (24K): [in a new window]   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.

View larger version (53K): [in a new window]   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.