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Differential MR delayed enhancement patterns of chronic myocardial infarction between extracellular and intravascular contrast media.

Wang J, Xiang B, Lin HY, Liu H, Freed D, Arora RC, Tian G - PLoS ONE (2015)

Bottom Line: Cine MRI revealed the reduced wall thickening in chronic infarction compared with normal myocardium.Chronic 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Vascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Street, Wuhan, Hubei, China 430022; National Research Council of Canada, 435 Ellice Avenue, Winnipeg, Manitoba, Canada R3B 1Y6; Department of Physiology, Faculty of Medicine, University of Manitoba, 727 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 3P5.

ABSTRACT

Objectives: Because 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 methods: Twenty 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.

Results: Cine 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.

Conclusions: Chronic 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.

No MeSH data available.


Related in: MedlinePlus

The wall thickness in chronic infarction by cine MR images.A. Left ventricular short-axis Gd-DTPA delayed enhancement image. B. Corresponding left ventricular short-axis cine images obtained from end-diastole and end-systole. C. End-diastolic wall thickness in chronic infarction and normal myocardium. D. End-systolic wall thickness in chronic infarction and normal myocardium. The chronic anterior-lateral wall infarction was identified as the hyper-enhanced region in Gd-DTPA delayed enhanced image (Arrowhead, Fig. 2A). The anterio-lateral wall thinning was significant in end-diastolic and end-systolic cine images (Arrowheads, Fig. 2B). The end-diastolic and end-systolic wall thicknesses were significantly lower in chronic infarction than in normal myocardium (Fig. 2C and 2D).
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pone.0121326.g002: The wall thickness in chronic infarction by cine MR images.A. Left ventricular short-axis Gd-DTPA delayed enhancement image. B. Corresponding left ventricular short-axis cine images obtained from end-diastole and end-systole. C. End-diastolic wall thickness in chronic infarction and normal myocardium. D. End-systolic wall thickness in chronic infarction and normal myocardium. The chronic anterior-lateral wall infarction was identified as the hyper-enhanced region in Gd-DTPA delayed enhanced image (Arrowhead, Fig. 2A). The anterio-lateral wall thinning was significant in end-diastolic and end-systolic cine images (Arrowheads, Fig. 2B). The end-diastolic and end-systolic wall thicknesses were significantly lower in chronic infarction than in normal myocardium (Fig. 2C and 2D).

Mentions: The chronic anterio-lateral wall infarction was identified as the hyper-enhancement in Gd-DTPA delayed enhancement image (Arrowhead, Fig. 2A). The corresponding cine MR images from end-systole and end-diastole in LV short axis views were illustrated in Fig. 2B. The significant wall thinning was observed in anterio-lateral chronic MI (Arrowheads, Fig. 2B). The end-diastolic wall thickness was markedly lower in chronic MI (6.31 ± 0.17mm) than in normal myocardium (8.61 ± 0.49) (Fig. 2C). Likewise, the end-systolic wall thickness was dramatically smaller in chronic MI (7.47 ± 0.77) than in normal myocardium (12.8 ± 1.01) (Fig. 2D). These suggested that chronic MI developed a significant wall thinning at 4 weeks post-infarction (S2 Video).


Differential MR delayed enhancement patterns of chronic myocardial infarction between extracellular and intravascular contrast media.

Wang J, Xiang B, Lin HY, Liu H, Freed D, Arora RC, Tian G - PLoS ONE (2015)

The wall thickness in chronic infarction by cine MR images.A. Left ventricular short-axis Gd-DTPA delayed enhancement image. B. Corresponding left ventricular short-axis cine images obtained from end-diastole and end-systole. C. End-diastolic wall thickness in chronic infarction and normal myocardium. D. End-systolic wall thickness in chronic infarction and normal myocardium. The chronic anterior-lateral wall infarction was identified as the hyper-enhanced region in Gd-DTPA delayed enhanced image (Arrowhead, Fig. 2A). The anterio-lateral wall thinning was significant in end-diastolic and end-systolic cine images (Arrowheads, Fig. 2B). The end-diastolic and end-systolic wall thicknesses were significantly lower in chronic infarction than in normal myocardium (Fig. 2C and 2D).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4376775&req=5

pone.0121326.g002: The wall thickness in chronic infarction by cine MR images.A. Left ventricular short-axis Gd-DTPA delayed enhancement image. B. Corresponding left ventricular short-axis cine images obtained from end-diastole and end-systole. C. End-diastolic wall thickness in chronic infarction and normal myocardium. D. End-systolic wall thickness in chronic infarction and normal myocardium. The chronic anterior-lateral wall infarction was identified as the hyper-enhanced region in Gd-DTPA delayed enhanced image (Arrowhead, Fig. 2A). The anterio-lateral wall thinning was significant in end-diastolic and end-systolic cine images (Arrowheads, Fig. 2B). The end-diastolic and end-systolic wall thicknesses were significantly lower in chronic infarction than in normal myocardium (Fig. 2C and 2D).
Mentions: The chronic anterio-lateral wall infarction was identified as the hyper-enhancement in Gd-DTPA delayed enhancement image (Arrowhead, Fig. 2A). The corresponding cine MR images from end-systole and end-diastole in LV short axis views were illustrated in Fig. 2B. The significant wall thinning was observed in anterio-lateral chronic MI (Arrowheads, Fig. 2B). The end-diastolic wall thickness was markedly lower in chronic MI (6.31 ± 0.17mm) than in normal myocardium (8.61 ± 0.49) (Fig. 2C). Likewise, the end-systolic wall thickness was dramatically smaller in chronic MI (7.47 ± 0.77) than in normal myocardium (12.8 ± 1.01) (Fig. 2D). These suggested that chronic MI developed a significant wall thinning at 4 weeks post-infarction (S2 Video).

Bottom Line: Cine MRI revealed the reduced wall thickening in chronic infarction compared with normal myocardium.Chronic 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Vascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Street, Wuhan, Hubei, China 430022; National Research Council of Canada, 435 Ellice Avenue, Winnipeg, Manitoba, Canada R3B 1Y6; Department of Physiology, Faculty of Medicine, University of Manitoba, 727 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 3P5.

ABSTRACT

Objectives: Because 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 methods: Twenty 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.

Results: Cine 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.

Conclusions: Chronic 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.

No MeSH data available.


Related in: MedlinePlus