ArticleThe international journal of cardiovascular imaging2012
Characterization of the failing murine heart in a desmin knock-out model using a clinical 3 T MRI scanner.
Article in The international journal of cardiovascular imaging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Desmin variants: Trigger for cardiac arrhythmias?Frontiers in cell and developmental biology · 2022Review
- Molecular insights into cardiomyopathies associated with desmin (DES) mutations.Biophysical reviews · 2018Review
- Cardiovascular imaging 2012 in the International Journal of Cardiovascular Imaging.The international journal of cardiovascular imaging · 2013Review
- Desminopathies: pathology and mechanisms.Acta neuropathologica · 2013Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purpose of this study was to establish an MRI protocol on a clinical scanner for assessment of left (LV) and right (RV) ventricular myocardial function of the murine heart, and to apply this protocol for the first in vivo assessment of myocardial function in a mouse model of cardiomyopathy (Desmin-/-). MRI was performed on a clinical 3 T whole body MRI system using a dedicated solenoid receive-only coil. Contiguous short axis slices were acquired covering the entire heart using a spoiled cine gradient echo sequence (TR 9-12 ms, TE 3-4 ms, α 25°, 1.0 × 0.23 × 0.23 mm³). Global LV- and RV-myocardial functional parameters such as end-diastolic ventricular volume, ejection fraction (EF), LV mass and cardiac output (CO) of Desmin-/- mice and age-matched controls were determined. Global myocardial functional data of healthy controls (n = 4) were in very good agreement with previously reported data. The transgenic mice (n = 8) revealed a significantly reduced LV- and RV-EF as well as CO. Body weight-normalized LV- and RV-end-diastolic volumes and LV mass were significantly increased. In addition desmin deficient mice exhibited segmental wall thinning and akinesia, suggesting myocardial necrosis. This study demonstrates that clinical 3 T MRI-systems may reliably be used for non-invasive assessment of LV- and RV-myocardial function in normal and in genetically engineered mice with cardiomyopathies. In addition, this proof of principle study presents first in vivo MRI data of the cardiac phenotype of desmin knock-out mice.
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