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      Quantification correction for free-breathing myocardial T mapping in mice using a recursively derived description of a T * relaxation pathway

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          Abstract

          Background

          Fast and accurate T mapping in myocardium is still a major challenge, particularly in small animal models. The complex sequence design owing to electrocardiogram and respiratory gating leads to quantification errors in in vivo experiments, due to variations of the T relaxation pathway. In this study, we present an improved quantification method for T using a newly derived formalism of a T * relaxation pathway.

          Methods

          The new signal equation was derived by solving a recursion problem for spin-lock prepared fast gradient echo readouts. Based on Bloch simulations, we compared quantification errors using the common monoexponential model and our corrected model. The method was validated in phantom experiments and tested in vivo for myocardial T mapping in mice. Here, the impact of the breath dependent spin recovery time T rec on the quantification results was examined in detail.

          Results

          Simulations indicate that a correction is necessary, since systematically underestimated values are measured under in vivo conditions. In the phantom study, the mean quantification error could be reduced from − 7.4% to − 0.97%. In vivo, a correlation of uncorrected T with the respiratory cycle was observed. Using the newly derived correction method, this correlation was significantly reduced from r = 0.708 (p < 0.001) to r = 0.204 and the standard deviation of left ventricular T values in different animals was reduced by at least 39%.

          Conclusion

          The suggested quantification formalism enables fast and precise myocardial T quantification for small animals during free breathing and can improve the comparability of study results. Our new technique offers a reasonable tool for assessing myocardial diseases, since pathologies that cause a change in heart or breathing rates do not lead to systematic misinterpretations. Besides, the derived signal equation can be used for sequence optimization or for subsequent correction of prior study results.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12968-022-00864-2.

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          Most cited references53

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          Heart Disease and Stroke Statistics—2021 Update: A Report From the American Heart Association

          The American Heart Association, in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, diet, and weight) and health factors (cholesterol, blood pressure, and glucose control) that contribute to cardiovascular health. The Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, congenital heart disease, rhythm disorders, subclinical atherosclerosis, coronary heart disease, heart failure, valvular disease, venous disease, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs). The American Heart Association, through its Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States to provide the most current information available in the annual Statistical Update. The 2021 Statistical Update is the product of a full year’s worth of effort by dedicated volunteer clinicians and scientists, committed government professionals, and American Heart Association staff members. This year’s edition includes data on the monitoring and benefits of cardiovascular health in the population, an enhanced focus on social determinants of health, adverse pregnancy outcomes, vascular contributions to brain health, the global burden of cardiovascular disease, and further evidence-based approaches to changing behaviors related to cardiovascular disease. Each of the 27 chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics. The Statistical Update represents a critical resource for the lay public, policy makers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.
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            Demographic and epidemiologic drivers of global cardiovascular mortality.

            Global deaths from cardiovascular disease are increasing as a result of population growth, the aging of populations, and epidemiologic changes in disease. Disentangling the effects of these three drivers on trends in mortality is important for planning the future of the health care system and benchmarking progress toward the reduction of cardiovascular disease.
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              Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration

              Ischemic cell death during a myocardial infarction leads to a multiphase reparative response in which the damaged tissue is replaced with a fibrotic scar produced by fibroblasts and myofibroblasts. This also induces geometrical, biomechanical, and biochemical changes in the uninjured ventricular wall eliciting a reactive remodeling process that includes interstitial and perivascular fibrosis. Although the initial reparative fibrosis is crucial for preventing rupture of the ventricular wall, an exaggerated fibrotic response and reactive fibrosis outside the injured area are detrimental as they lead to progressive impairment of cardiac function and eventually to heart failure. In this review, we summarize current knowledge of the mechanisms of both reparative and reactive cardiac fibrosis in response to myocardial infarction, discuss the potential of inducing cardiac regeneration through direct reprogramming of fibroblasts and myofibroblasts into cardiomyocytes, and review the currently available and potential future therapeutic strategies to inhibit cardiac fibrosis. Graphical abstract Reparative response following a myocardial infarction. Hypoxia-induced cardiomyocyte death leads to the activation of myofibroblasts and a reparative fibrotic response in the injured area. Right top In adult mammals, the fibrotic scar formed at the infarcted area is permanent and promotes reactive fibrosis in the uninjured myocardium. Right bottom In teleost fish and newts and in embryonic and neonatal mammals, the initial formation of a fibrotic scar is followed by regeneration of the cardiac muscle tissue. Induction of post-infarction cardiac regeneration in adult mammals is currently the target of intensive research and drug discovery attempts
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                Author and article information

                Contributors
                nordbeck_p@ukw.de
                Journal
                J Cardiovasc Magn Reson
                J Cardiovasc Magn Reson
                Journal of Cardiovascular Magnetic Resonance
                BioMed Central (London )
                1097-6647
                1532-429X
                9 May 2022
                9 May 2022
                2022
                : 24
                : 30
                Affiliations
                [1 ]GRID grid.411760.5, ISNI 0000 0001 1378 7891, Department of Internal Medicine I, , University Hospital Würzburg, ; Würzburg, Germany
                [2 ]GRID grid.8379.5, ISNI 0000 0001 1958 8658, Experimental Physics 5, , University of Würzburg, ; Würzburg, Germany
                [3 ]GRID grid.411760.5, ISNI 0000 0001 1378 7891, Comprehensive Heart Failure Center (CHFC), , University Hospital Würzburg, ; Würzburg, Germany
                [4 ]GRID grid.411760.5, ISNI 0000 0001 1378 7891, Department of Nuclear Medicine, , University Hospital Würzburg, ; Würzburg, Germany
                Article
                864
                10.1186/s12968-022-00864-2
                9082875
                35534901
                363f781c-fd4c-4394-a878-81a8bd1077e8
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 1 December 2021
                : 7 April 2022
                Funding
                Funded by: Federal Ministry for Education and Research of the Federal Republic of Germany
                Award ID: BMBF 01EO1504
                Award ID: MO.6
                Award Recipient :
                Funded by: Universitätsklinikum Würzburg (8913)
                Categories
                Technical Notes
                Custom metadata
                © The Author(s) 2022

                Cardiovascular Medicine
                t1rho,t1ρ,spin-lock,mapping,quantitative mri,correction,cardiac,radial
                Cardiovascular Medicine
                t1rho, t1ρ, spin-lock, mapping, quantitative mri, correction, cardiac, radial

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