Abstract
ObjectivesBecause the distribution volume and mechanism of extracellular and intravascular MR contrast media differ considerably, the enhancement pattern of chronic myocardial infarction with extracellular or intravascular media might also be different. This study aims to investigate the differences in MR enhancement patterns of chronic myocardial infarction between extracellular and intravascular contrast media.Materials and MethodsTwenty pigs with myocardial infarction underwent cine MRI, first pass perfusion MRI and delayed enhancement MRI with extracellular or intravascular media at four weeks after coronary occlusion. Myocardial blood flow (MBF) was determined with microsphere measurement. The infarction histopathological changes were evaluated by hematoxylin and eosin staining and Masson's trichrome method.ResultsCine MRI revealed the reduced wall thickening in chronic infarction compared with normal myocardium. Moreover, significant wall thinning in chronic infarction was observed in cine MRI. Peak first-pass signal intensity didn’t significantly differ between chronic infarction and normal myocardium no matter what kinds of contrast media. At the following delayed enhancement phase, extracellular media-enhanced signal intensity was significantly higher in chronic infarction than in normal myocardium. Conversely, intravascular media-enhanced signal intensity was almost equivalent among chronic infarction and normal myocardium. At four weeks after infarction, MBF in chronic infarction approached to that in normal myocardium. Large thick-walled vessels were detected at peri-infarction zones. The cardiomyocytes were replaced by scar tissue consisting of dilated blood vessels and discrete fibers of collagen.ConclusionsChronic infarction was characterized by the significantly reduced wall thickening and the definite wall thinning. First-pass myocardial perfusion defect was not detected in chronic infarction with two media due to the significantly recovered MBF and well-developed collateral vessels. Infarction remodeling enlarged the extracellular compartment, which was available for extracellular media but not accessible to intravascular media. Extracellular media identified chronic infarction as the hyper-enhancement; nonetheless, intravascular media didn’t provide delayed enhancement.
Highlights
Comprehensive MRI allows for a simultaneous state-of-the-art analysis of wall thickness and thickening, myocardial perfusion and the location and size of infarction [1]
Cine MRI revealed the reduced wall thickening in chronic infarction compared with normal myocardium
At the following delayed enhancement phase, extracellular media-enhanced signal intensity was significantly higher in chronic infarction than in normal myocardium
Summary
Comprehensive MRI allows for a simultaneous state-of-the-art analysis of wall thickness and thickening, myocardial perfusion and the location and size of infarction [1]. End-diastolic wall thickness and resting wall motion grade can predict recovery of regional dysfunction after revascularization [5]. Ischemic myocardial necrosis is the main reason for the reduced wall thickening post-infarction. MRI scar of patients was defined as diastolic wall thickness 2.5 standard deviation below corresponding normal values or systolic wall thickening less than or equal to 1 mm [4]. MRI study of rat myocardial infarction (MI) has demonstrated that wall thinning occurs and evolves since 4 weeks post-infarction [6]. This study investigated the regional wall thickening and wall thinning at 4 weeks post-infarction in a pig animal model
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