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  • Title: MR imaging of spatial extent of microvascular injury in reperfused ischemically injured rat myocardium: value of blood pool ultrasmall superparamagnetic particles of iron oxide.
    Author: Krombach GA, Wendland MF, Higgins CB, Saeed M.
    Journal: Radiology; 2002 Nov; 225(2):479-86. PubMed ID: 12409583.
    Abstract:
    PURPOSE: To (a) assess the value of a blood pool magnetic resonance (MR) imaging contrast agent (Clariscan) for characterizing microvascular injury in ischemically injured rat myocardium and (b) compare the extent of microvascular injury at Clariscan-enhanced MR imaging with infarction and areas at risk seen with histochemical staining. MATERIALS AND METHODS: Twenty rats underwent 45 minutes of coronary artery occlusion and 3 hours of reperfusion. Sequential T1-weighted spin-echo MR images were acquired in 10 rats to assess leakage of Clariscan into myocardium over time. Ten other rats underwent the same duration of occlusion and reperfusion (3 hours) so that the extent of microvascular injury in the entire heart could be measured and correlated with infarction and area at risk at necropsy. The Student t test and Bland-Altman method were used for data analysis. RESULTS: Clariscan improved visualization of regions with transmural and nontransmural microvascular injury. Accumulation of Clariscan was best reflected by the mean ratios of signal intensity in injured myocardium to that in normal myocardium measured before (0.98 +/- 0.01 [standard error of the mean]) and after (1.34 +/- 0.04) injection. At 15 minutes after injection, the size of the enhanced region remained constant over the course of observation. The mean size of the hyperenhanced region (44% of the left ventricle +/- 2) was significantly (P <.001) larger than the mean size of true infarction at necropsy (29% +/- 3) but smaller than the mean size of the area at risk (50% +/- 2). CONCLUSION: Clariscan has potential for estimating the spatial extent of microvascular injury in ischemically injured myocardium and may be useful as a marker of microvascular injury after thrombolytic therapy.
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