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

• Published in: Journal of the American College of Cardiology Vol. 32; no. 6; pp. 1756 - 1764
• Main Authors: Wu, Katherine C, Kim, Raymond J, Bluemke, David A, Rochitte, Carlos E, Zerhouni, Elias A, Becker, Lewis C, Lima, Joao A.C
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 15.11.1998; Elsevier Science
• Subjects: Animals; Biological and medical sciences; Cardiology. Vascular system; Coloring Agents; Contrast Media; Coronary Circulation - physiology; Coronary heart disease; Dogs; Echocardiography; Fluorescent Dyes; Heart; Magnetic Resonance Imaging; Medical sciences; Microcirculation - physiology; Microspheres; Myocardial Infarction - diagnostic imaging; Myocardial Infarction - physiopathology; Myocardial Reperfusion Injury - diagnostic imaging; Tetrazolium Salts; Thiazoles; Time Factors; CE; MO; TTC; MRI; LV; MI; LAD; Prognosis; Infarct; Cardiovascular disease; Myocardial disease; Arterial disease; Vascular disease; Microcirculation; Complication; Dog; Contrast media; Sonography; Fissipedia; Carnivora; Echocardiography; Acute; Coronary heart disease; Nuclear magnetic resonance imaging; Artery; Vertebrata; Mammalia; Animal; Myocardium; Medical imagery; Hemodynamics; Obliteration
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(98)00429-X

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.