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Assessment of Myocardial Fibrosis in Mice Using a T2*-Weighted 3D Radial Magnetic Resonance Imaging Sequence.

van Nierop BJ, Bax NA, Nelissen JL, Arslan F, Motaal AG, de Graaf L, Zwanenburg JJ, Luijten PR, Nicolay K, Strijkers GJ - PLoS ONE (2015)

Bottom Line: Detection of short T2* species resulting from fibrotic tissue may provide an attractive non-contrast-enhanced alternative to directly visualize the presence of both replacement and interstitial fibrosis.Infarct T2*slow decreased significantly, while a moderate decrease was observed in remote tissue in post-MI hearts and in TAC hearts.However, in vivo contrast on subtraction images was rather poor, hampering a straightforward visual assessment of the spatial distribution of the fibrotic tissue.

View Article: PubMed Central - PubMed

Affiliation: Biomedical NMR, Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands.

ABSTRACT

Background: Myocardial fibrosis is a common hallmark of many diseases of the heart. Late gadolinium enhanced MRI is a powerful tool to image replacement fibrosis after myocardial infarction (MI). Interstitial fibrosis can be assessed indirectly from an extracellular volume fraction measurement using contrast-enhanced T1 mapping. Detection of short T2* species resulting from fibrotic tissue may provide an attractive non-contrast-enhanced alternative to directly visualize the presence of both replacement and interstitial fibrosis.

Objective: To goal of this paper was to explore the use of a T2*-weighted radial sequence for the visualization of fibrosis in mouse heart.

Methods: C57BL/6 mice were studied with MI (n = 20, replacement fibrosis), transverse aortic constriction (TAC) (n = 18, diffuse fibrosis), and as control (n = 10). 3D center-out radial T2*-weighted images with varying TE were acquired in vivo and ex vivo (TE = 21 μs-4 ms). Ex vivo T2*-weighted signal decay with TE was analyzed using a 3-component model. Subtraction of short- and long-TE images was used to highlight fibrotic tissue with short T2*. The presence of fibrosis was validated using histology and correlated to MRI findings.

Results: Detailed ex vivo T2*-weighted signal analysis revealed a fast (T2*fast), slow (T2*slow) and lipid (T2*lipid) pool. T2*fast remained essentially constant. Infarct T2*slow decreased significantly, while a moderate decrease was observed in remote tissue in post-MI hearts and in TAC hearts. T2*slow correlated with the presence of diffuse fibrosis in TAC hearts (r = 0.82, P = 0.01). Ex vivo and in vivo subtraction images depicted a positive contrast in the infarct co-localizing with the scar. Infarct volumes from histology and subtraction images linearly correlated (r = 0.94, P<0.001). Region-of-interest analysis in the in vivo post-MI and TAC hearts revealed significant T2* shortening due to fibrosis, in agreement with the ex vivo results. However, in vivo contrast on subtraction images was rather poor, hampering a straightforward visual assessment of the spatial distribution of the fibrotic tissue.

No MeSH data available.


Related in: MedlinePlus

Ex vivo and in vivo signal intensity time curves.Representative ROI-based T2*-weighted signal intensity curves as a function of echo time (TE) for ex vivo (top row) and in vivo (bottom row) measurements in control hearts, remote tissue and infarct area of the post-MI hearts and the TAC hearts, together with the corresponding model fit (gray line, top row) and lines to guide the eye (bottom row). Signal intensities were normalized to the signal intensity at TE = 21 μs.
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pone.0129899.g001: Ex vivo and in vivo signal intensity time curves.Representative ROI-based T2*-weighted signal intensity curves as a function of echo time (TE) for ex vivo (top row) and in vivo (bottom row) measurements in control hearts, remote tissue and infarct area of the post-MI hearts and the TAC hearts, together with the corresponding model fit (gray line, top row) and lines to guide the eye (bottom row). Signal intensities were normalized to the signal intensity at TE = 21 μs.

Mentions: Upon inspection of the raw signal decay curves (Fig 1) it became clear that the frequency of the oscillation was approximately the same for the healthy, infarct and TAC hearts. This makes sense, since the origin of this oscillation are lipids with a fixed off-resonance frequency with respect to water. Moreover, the number of visible oscillation periods was approximately 3 in all cases, which suggested that we could fix the damping term (T2*lipid) of the oscillations in Eq 1 to a common value to prevent over-parameterization of the data. Therefore, based on initial model fits the water-lipid chemical shift difference was fixed to ω/2π = 1.3 kHz and T2*lipid at 820 μs.


Assessment of Myocardial Fibrosis in Mice Using a T2*-Weighted 3D Radial Magnetic Resonance Imaging Sequence.

van Nierop BJ, Bax NA, Nelissen JL, Arslan F, Motaal AG, de Graaf L, Zwanenburg JJ, Luijten PR, Nicolay K, Strijkers GJ - PLoS ONE (2015)

Ex vivo and in vivo signal intensity time curves.Representative ROI-based T2*-weighted signal intensity curves as a function of echo time (TE) for ex vivo (top row) and in vivo (bottom row) measurements in control hearts, remote tissue and infarct area of the post-MI hearts and the TAC hearts, together with the corresponding model fit (gray line, top row) and lines to guide the eye (bottom row). Signal intensities were normalized to the signal intensity at TE = 21 μs.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4482648&req=5

pone.0129899.g001: Ex vivo and in vivo signal intensity time curves.Representative ROI-based T2*-weighted signal intensity curves as a function of echo time (TE) for ex vivo (top row) and in vivo (bottom row) measurements in control hearts, remote tissue and infarct area of the post-MI hearts and the TAC hearts, together with the corresponding model fit (gray line, top row) and lines to guide the eye (bottom row). Signal intensities were normalized to the signal intensity at TE = 21 μs.
Mentions: Upon inspection of the raw signal decay curves (Fig 1) it became clear that the frequency of the oscillation was approximately the same for the healthy, infarct and TAC hearts. This makes sense, since the origin of this oscillation are lipids with a fixed off-resonance frequency with respect to water. Moreover, the number of visible oscillation periods was approximately 3 in all cases, which suggested that we could fix the damping term (T2*lipid) of the oscillations in Eq 1 to a common value to prevent over-parameterization of the data. Therefore, based on initial model fits the water-lipid chemical shift difference was fixed to ω/2π = 1.3 kHz and T2*lipid at 820 μs.

Bottom Line: Detection of short T2* species resulting from fibrotic tissue may provide an attractive non-contrast-enhanced alternative to directly visualize the presence of both replacement and interstitial fibrosis.Infarct T2*slow decreased significantly, while a moderate decrease was observed in remote tissue in post-MI hearts and in TAC hearts.However, in vivo contrast on subtraction images was rather poor, hampering a straightforward visual assessment of the spatial distribution of the fibrotic tissue.

View Article: PubMed Central - PubMed

Affiliation: Biomedical NMR, Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands.

ABSTRACT

Background: Myocardial fibrosis is a common hallmark of many diseases of the heart. Late gadolinium enhanced MRI is a powerful tool to image replacement fibrosis after myocardial infarction (MI). Interstitial fibrosis can be assessed indirectly from an extracellular volume fraction measurement using contrast-enhanced T1 mapping. Detection of short T2* species resulting from fibrotic tissue may provide an attractive non-contrast-enhanced alternative to directly visualize the presence of both replacement and interstitial fibrosis.

Objective: To goal of this paper was to explore the use of a T2*-weighted radial sequence for the visualization of fibrosis in mouse heart.

Methods: C57BL/6 mice were studied with MI (n = 20, replacement fibrosis), transverse aortic constriction (TAC) (n = 18, diffuse fibrosis), and as control (n = 10). 3D center-out radial T2*-weighted images with varying TE were acquired in vivo and ex vivo (TE = 21 μs-4 ms). Ex vivo T2*-weighted signal decay with TE was analyzed using a 3-component model. Subtraction of short- and long-TE images was used to highlight fibrotic tissue with short T2*. The presence of fibrosis was validated using histology and correlated to MRI findings.

Results: Detailed ex vivo T2*-weighted signal analysis revealed a fast (T2*fast), slow (T2*slow) and lipid (T2*lipid) pool. T2*fast remained essentially constant. Infarct T2*slow decreased significantly, while a moderate decrease was observed in remote tissue in post-MI hearts and in TAC hearts. T2*slow correlated with the presence of diffuse fibrosis in TAC hearts (r = 0.82, P = 0.01). Ex vivo and in vivo subtraction images depicted a positive contrast in the infarct co-localizing with the scar. Infarct volumes from histology and subtraction images linearly correlated (r = 0.94, P<0.001). Region-of-interest analysis in the in vivo post-MI and TAC hearts revealed significant T2* shortening due to fibrosis, in agreement with the ex vivo results. However, in vivo contrast on subtraction images was rather poor, hampering a straightforward visual assessment of the spatial distribution of the fibrotic tissue.

No MeSH data available.


Related in: MedlinePlus