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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

Histopathology of chronic myocardial infarction at four weeks after myocardial infarction.A. Cardiomyocytes were the major structural elements in normal myocardium. B. Scar tissue was characterized by the discrete collagen fibers and loss of cellularity. Collagen fibers were stained blue using Masson’s trichrome staining (Arrowhead, Fig. 7B). C. Dilated remodeled vessels were frequently observed in the territory of the infarction (Arrowheads, Fig. 7C). D. Large thick-walled blood vessels were apparent at the peri-infarction zones (Arrowheads, Fig. 7D).
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pone.0121326.g007: Histopathology of chronic myocardial infarction at four weeks after myocardial infarction.A. Cardiomyocytes were the major structural elements in normal myocardium. B. Scar tissue was characterized by the discrete collagen fibers and loss of cellularity. Collagen fibers were stained blue using Masson’s trichrome staining (Arrowhead, Fig. 7B). C. Dilated remodeled vessels were frequently observed in the territory of the infarction (Arrowheads, Fig. 7C). D. Large thick-walled blood vessels were apparent at the peri-infarction zones (Arrowheads, Fig. 7D).

Mentions: The major structural elements were the intact cardiomyocytes and there existed relatively small extracellular space accessible to contrast media in normal myocardium (Fig. 7A). In chronic MI, the extracellular space enlargement was mostly attributed to the sparse collagen fibrous deposition (Arrowhead, Fig. 7B) and loss of cardiomyocytes. Residual dilated vessels were detected with infarction (Arrowheads, Fig. 7C), and large thick-walled blood vessels were manifest at the peri-infarction zone (Arrowheads, Fig. 7D). Regional MBF in infarction scar (0.91 ± 0.11 ml/min/g) approximately recovered to close-normal level (1.06 ± 0.08 ml/min/g). Significantly restored MBF was able to deliver contrast media into infarction scar through well-developed collateral vessels. The vascular permeability of scar tissue allowed only extracellular not intravascular contrast media to leak into the enlarged extracellular compartment, producing the differential delayed enhancement MR patterns between two kinds of media.


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)

Histopathology of chronic myocardial infarction at four weeks after myocardial infarction.A. Cardiomyocytes were the major structural elements in normal myocardium. B. Scar tissue was characterized by the discrete collagen fibers and loss of cellularity. Collagen fibers were stained blue using Masson’s trichrome staining (Arrowhead, Fig. 7B). C. Dilated remodeled vessels were frequently observed in the territory of the infarction (Arrowheads, Fig. 7C). D. Large thick-walled blood vessels were apparent at the peri-infarction zones (Arrowheads, Fig. 7D).
© Copyright Policy
Related In: Results  -  Collection

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

pone.0121326.g007: Histopathology of chronic myocardial infarction at four weeks after myocardial infarction.A. Cardiomyocytes were the major structural elements in normal myocardium. B. Scar tissue was characterized by the discrete collagen fibers and loss of cellularity. Collagen fibers were stained blue using Masson’s trichrome staining (Arrowhead, Fig. 7B). C. Dilated remodeled vessels were frequently observed in the territory of the infarction (Arrowheads, Fig. 7C). D. Large thick-walled blood vessels were apparent at the peri-infarction zones (Arrowheads, Fig. 7D).
Mentions: The major structural elements were the intact cardiomyocytes and there existed relatively small extracellular space accessible to contrast media in normal myocardium (Fig. 7A). In chronic MI, the extracellular space enlargement was mostly attributed to the sparse collagen fibrous deposition (Arrowhead, Fig. 7B) and loss of cardiomyocytes. Residual dilated vessels were detected with infarction (Arrowheads, Fig. 7C), and large thick-walled blood vessels were manifest at the peri-infarction zone (Arrowheads, Fig. 7D). Regional MBF in infarction scar (0.91 ± 0.11 ml/min/g) approximately recovered to close-normal level (1.06 ± 0.08 ml/min/g). Significantly restored MBF was able to deliver contrast media into infarction scar through well-developed collateral vessels. The vascular permeability of scar tissue allowed only extracellular not intravascular contrast media to leak into the enlarged extracellular compartment, producing the differential delayed enhancement MR patterns between two kinds of media.

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