EXPERIMENTAL STUDIES
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
Manuscript received January 20, 1998;
revised manuscript received July 8, 1998,
accepted July 29, 1998.
Address for correspondence: Dr. Joao A.C. Lima, The Johns Hopkins Hospital, Division of Cardiology, Blalock 569, 600 North Wolfe Street, Baltimore, Maryland 21287 jlima{at}welchlink.welch.jhu.edu
Objectives. We aimed to validate contrast-enhanced echocardiography (CE) in the quantification of microvascular obstruction (MO) against magnetic resonance imaging (MRI) and the histopathologic standards of radioactive microspheres and thioflavin-S staining. We also determined the time course of MO at days 2 and 9 after infarction and reperfusion.
Background. Postinfarction MO occurs because prolonged ischemia produces microvessel occlusion at the infarct core, preventing adequate reperfusion. Microvascular obstruction expands up to 48 h after reperfusion; the time course beyond 2 days is unknown. Though used to study MO, CE has not been compared with MRI and thioflavin-S, which yield precise visual maps of MO.
Methods. Ten closed-chest dogs underwent 90-min coronary artery occlusion and reperfusion. Both CE and MRI were performed at 2 and 9 days after reperfusion. The MO regions by both methods were quantified as percent left ventricular (% LV) mass. Radioactive microspheres were injected for blood flow determination. Postmortem, the myocardium was stained with thioflavin-S and 2,3,5-triphenyltetrazolium chloride.
Results. Expressed as % total LV, MO by MRI matched in size MO by microspheres using a flow threshold of <40% remote (4.96 ± 3.52% vs. 5.32 ± 3.98%, p = NS). For matched LV cross sections, MO by CE matched in size MO by microspheres using a flow threshold of <60% remote (13.27 ± 4.31% vs. 13.5 ± 4.94%, p = NS). Both noninvasive techniques correlated well with microspheres (MRI vs. CE, r = 0.87 vs. 0.74; p = NS). Microvascular obstruction by CE corresponded spatially to MRI-hypoenhanced regions and thioflavin-negative regions. For matched LV slices at 9 days after reperfusion, MO measured 12.94 ± 4.51% by CE, 7.11 ± 3.68% by MRI and 9.18 ± 4.32% by thioflavin-S. Compared to thioflavin-S, both noninvasive techniques correlated well (CE vs. MRI, r = 0.79 vs. 0.91; p = NS). Microvascular obstruction size was unchanged at 2 and 9 days (CE: 13.23 ± 4.11% vs. 12.69 ± 4.97%; MRI: 5.53 ± 4.94% vs. 4.68 ± 3.44%; p = NS for both).
Conclusions. Both CE and MRI can quantify MO. Both correlate well with the histopathologic standards. While MRI can detect regions of MO with blood flow <40% of remote, the threshold for MO by CE is <60% remote. The extent of MO is unchanged at 2 and 9 days after reperfusion.
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Abbreviations and Acronyms
| | CE | = contrast-enhanced echocardiography | | LAD | = left anterior descending artery | | LV | = left ventricular | | MI | = myocardial infarction | | MO | = microvascular obstruction | | MRI | = magnetic resonance imaging | | TTC | = 2,3,5-triphenyltetrazolium chloride |
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