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J Am Coll Cardiol, 1998; 32:1756-1764
© 1998 by the American College of Cardiology Foundation
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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{dagger}, David A. Bluemke, MD, PhD{ddagger}, Carlos E. Rochitte, MD*, Elias A. Zerhouni, MD{ddagger}, 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
{dagger} Division of Cardiology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois, USA
{ddagger} 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.

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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