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    Quantifying the area-at-risk of myocardial infarction in-vivo using arterial spin labeling cardiac magnetic resonance

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    Author
    Dongworth, RK; Campbell-Washburn, AE; Cabrera-Fuentes, HA; Bulluck, H; Roberts, T; Price, AN; Hernandez-Resendiz, S; Ordidge, RJ; Thomas, DL; Yellon, DM; ...
    Date
    2017-05-23
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Ordidge, Roger
    Affiliation
    Medicine and Radiology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Dongworth, R. K., Campbell-Washburn, A. E., Cabrera-Fuentes, H. A., Bulluck, H., Roberts, T., Price, A. N., Hernandez-Resendiz, S., Ordidge, R. J., Thomas, D. L., Yellon, D. M., Lythgoe, M. F. & Hausenloy, D. J. (2017). Quantifying the area-at-risk of myocardial infarction in-vivo using arterial spin labeling cardiac magnetic resonance. SCIENTIFIC REPORTS, 7 (1), https://doi.org/10.1038/s41598-017-02544-z.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259404
    DOI
    10.1038/s41598-017-02544-z
    Abstract
    T2-weighted cardiovascular magnetic resonance (T2-CMR) of myocardial edema can quantify the area-at-risk (AAR) following acute myocardial infarction (AMI), and has been used to assess myocardial salvage by new cardioprotective therapies. However, some of these therapies may reduce edema, leading to an underestimation of the AAR by T2-CMR. Here, we investigated arterial spin labeling (ASL) perfusion CMR as a novel approach to quantify the AAR following AMI. Adult B6sv129-mice were subjected to in vivo left coronary artery ligation for 30 minutes followed by 72 hours reperfusion. T2-mapping was used to quantify the edema-based AAR (% of left ventricle) following ischemic preconditioning (IPC) or cyclosporin-A (CsA) treatment. In control animals, the AAR by T2-mapping corresponded to that delineated by histology. As expected, both IPC and CsA reduced MI size. However, IPC, but not CsA, also reduced myocardial edema leading to an underestimation of the AAR by T2-mapping. In contrast, regions of reduced myocardial perfusion delineated by cardiac ASL were able to delineate the AAR when compared to both T2-mapping and histology in control animals, and were not affected by either IPC or CsA. Therefore, ASL perfusion CMR may be an alternative method for quantifying the AAR following AMI, which unlike T2-mapping, is not affected by IPC.

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