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Quantification and time course of microvascular obstruction by contrast-enhanced echocardiography and magnetic resonance imaging following acute myocardial infarction and reperfusion

Katherine C. Wu, MD^*, Raymond J. Kim, MD, David A. Bluemke, MD, PhD, Carlos E. Rochitte, MD^*, Elias A. Zerhouni, MD, Lewis C. Becker, MD^* and Joao A. C. Lima, MD, FACC^*

^* Division of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Division of Cardiology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois, USA
Division of Diagnostic Imaging, Department of Radiology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

View larger version (55K): [in a new window]   Figure 1 Corresponding CE and MR images. The CE defect matches in spatial extent the MRI hypoenhanced region. Both the CE defect and MRI hypoenhanced region are in the same location as the MRI hyperenhanced area, but are smaller.

View larger version (21K): [in a new window]   Figure 2 Regional blood flow. The asterisk denotes the significant difference in flows between MO and infarcted (microvasculature intact) regions at the same timepoint. Microvascular obstruction and infarcted regions had similar baseline flows. At occlusion, flow to MO regions was lower than to regions that become infarcted but whose microvasculatures remain intact (p = 0.0002). With reperfusion, blood flow in both regions returns to baseline. At day 2, MO regions have lower blood flow than infarcted areas (p < 0.0001). At day 9, MO regions continue to have flow that is lower than infarcted areas (p < 0.0001). Within each region, flow rates at days 2 and 9 are similar (p = NS).

View larger version (17K): [in a new window]   Figure 3 Correlation between MO by noninvasive techniques versus radioactive microspheres.

View larger version (87K): [in a new window]   Figure 4 The CE images from separate animals (A and B) are compared to matched MR images and postmortem thioflavin-S stained slices. The CE defects correspond in location to MO defined by MRI hypoenhancement and thioflavin-negative regions.

View larger version (15K): [in a new window]   Figure 5 Correlation between MO by noninvasive techniques versus thioflavin-S.

View larger version (78K): [in a new window]   Figure 6 The CE and MR images from the same animal at 2 and 9 days after reperfusion. The CE defects correspond spatially to the regions of MRI hypoenhancement; both do not significantly change over time. The region of MRI hyperenhancement (infarct size) is larger than MO and also does not change over time.