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      Cardiovascular Magnetic Resonance and Sport Cardiology: a Growing Role in Clinical Dilemmas

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          Abstract

          Exercise training induces morphological and functional cardiovascular adaptation known as the “athlete’s heart” with changes including dilatation, hypertrophy, and increased stroke volume. These changes may overlap with pathological appearances. Distinguishing athletic cardiac remodelling from cardiomyopathy is important and is a frequent medical dilemma. Cardiac magnetic resonance (CMR) has a role in clinical care as it can refine discrimination of health from a disease where ECG and echocardiography alone have left or generated uncertainty. CMR can more precisely assess cardiac structure and function as well as characterise the myocardium detecting key changes including myocardial scar and diffuse fibrosis. In this review, we will review the role of CMR in sports cardiology.

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          Clinical recommendations for cardiovascular magnetic resonance mapping of T1, T2, T2* and extracellular volume: A consensus statement by the Society for Cardiovascular Magnetic Resonance (SCMR) endorsed by the European Association for Cardiovascular Imaging (EACVI)

          Daniel R Messroghli, James Moon, Vanessa M. Ferreira … (2017)
          Parametric mapping techniques provide a non-invasive tool for quantifying tissue alterations in myocardial disease in those eligible for cardiovascular magnetic resonance (CMR). Parametric mapping with CMR now permits the routine spatial visualization and quantification of changes in myocardial composition based on changes in T1, T2, and T2*(star) relaxation times and extracellular volume (ECV). These changes include specific disease pathways related to mainly intracellular disturbances of the cardiomyocyte (e.g., iron overload, or glycosphingolipid accumulation in Anderson-Fabry disease); extracellular disturbances in the myocardial interstitium (e.g., myocardial fibrosis or cardiac amyloidosis from accumulation of collagen or amyloid proteins, respectively); or both (myocardial edema with increased intracellular and/or extracellular water). Parametric mapping promises improvements in patient care through advances in quantitative diagnostics, inter- and intra-patient comparability, and relatedly improvements in treatment. There is a multitude of technical approaches and potential applications. This document provides a summary of the existing evidence for the clinical value of parametric mapping in the heart as of mid 2017, and gives recommendations for practical use in different clinical scenarios for scientists, clinicians, and CMR manufacturers.
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            Classification of the cardiomyopathies: a position statement from the European Society Of Cardiology Working Group on Myocardial and Pericardial Diseases.

            Perry Elliott, Bert Andersson, Eloisa Arbustini … (2008)
            In biology, classification systems are used to promote understanding and systematic discussion through the use of logical groups and hierarchies. In clinical medicine, similar principles are used to standardise the nomenclature of disease. For more than three decades, heart muscle diseases have been classified into primary or idiopathic myocardial diseases (cardiomyopathies) and secondary disorders that have similar morphological appearances, but which are caused by an identifiable pathology such as coronary artery disease or myocardial infiltration (specific heart muscle diseases). In this document, The European Society of Cardiology Working Group on Myocardial and Pericardial Diseases presents an update of the existing classification scheme. The aim is to help clinicians look beyond generic diagnostic labels in order to reach more specific diagnoses.
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              Association of fibrosis with mortality and sudden cardiac death in patients with nonischemic dilated cardiomyopathy.

              Ankur Gulati, Andrew Jabbour, Tevfik Ismail … (2013)
              Risk stratification of patients with nonischemic dilated cardiomyopathy is primarily based on left ventricular ejection fraction (LVEF). Superior prognostic factors may improve patient selection for implantable cardioverter-defibrillators (ICDs) and other management decisions. To determine whether myocardial fibrosis (detected by late gadolinium enhancement cardiovascular magnetic resonance [LGE-CMR] imaging) is an independent and incremental predictor of mortality and sudden cardiac death (SCD) in dilated cardiomyopathy. Prospective, longitudinal study of 472 patients with dilated cardiomyopathy referred to a UK center for CMR imaging between November 2000 and December 2008 after presence and extent of midwall replacement fibrosis were determined. Patients were followed up through December 2011. Primary end point was all-cause mortality. Secondary end points included cardiovascular mortality or cardiac transplantation; an arrhythmic composite of SCD or aborted SCD (appropriate ICD shock, nonfatal ventricular fibrillation, or sustained ventricular tachycardia); and a composite of HF death, HF hospitalization, or cardiac transplantation. Among the 142 patients with midwall fibrosis, there were 38 deaths (26.8%) vs 35 deaths (10.6%) among the 330 patients without fibrosis (hazard ratio [HR], 2.96 [95% CI, 1.87-4.69]; absolute risk difference, 16.2% [95% CI, 8.2%-24.2%]; P < .001) during a median follow-up of 5.3 years (2557 patient-years of follow-up). The arrhythmic composite was reached by 42 patients with fibrosis (29.6%) and 23 patients without fibrosis (7.0%) (HR, 5.24 [95% CI, 3.15-8.72]; absolute risk difference, 22.6% [95% CI, 14.6%-30.6%]; P < .001). After adjustment for LVEF and other conventional prognostic factors, both the presence of fibrosis (HR, 2.43 [95% CI, 1.50-3.92]; P < .001) and the extent (HR, 1.11 [95% CI, 1.06-1.16]; P < .001) were independently and incrementally associated with all-cause mortality. Fibrosis was also independently associated with cardiovascular mortality or cardiac transplantation (by fibrosis presence: HR, 3.22 [95% CI, 1.95-5.31], P < .001; and by fibrosis extent: HR, 1.15 [95% CI, 1.10-1.20], P < .001), SCD or aborted SCD (by fibrosis presence: HR, 4.61 [95% CI, 2.75-7.74], P < .001; and by fibrosis extent: HR, 1.10 [95% CI, 1.05-1.16], P < .001), and the HF composite (by fibrosis presence: HR, 1.62 [95% CI, 1.00-2.61], P = .049; and by fibrosis extent: HR, 1.08 [95% CI, 1.04-1.13], P < .001). Addition of fibrosis to LVEF significantly improved risk reclassification for all-cause mortality and the SCD composite (net reclassification improvement: 0.26 [95% CI, 0.11-0.41]; P = .001 and 0.29 [95% CI, 0.11-0.48]; P = .002, respectively). Assessment of midwall fibrosis with LGE-CMR imaging provided independent prognostic information beyond LVEF in patients with nonischemic dilated cardiomyopathy. The role of LGE-CMR in the risk stratification of dilated cardiomyopathy requires further investigation.
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                Author and article information

                Contributors
                James C. Moon:
                ORCID: http://orcid.org/0000-0001-8071-1491
                j.moon@ucl.ac.uk
                Journal
                Journal ID (nlm-ta): J Cardiovasc Transl Res
                Journal ID (iso-abbrev): J Cardiovasc Transl Res
                Title: Journal of Cardiovascular Translational Research
                Publisher: Springer US (New York )
                ISSN (Print): 1937-5387
                ISSN (Electronic): 1937-5395
                Publication date (Electronic): 20 May 2020
                Publication date PMC-release: 20 May 2020
                Publication date (Print): 2020
                Volume: 13
                Issue: 3
                Pages: 296-305
                Affiliations
                [1 ]GRID grid.7841.a, Department of Cardiovascular, Respiratory, Nephrology, Anesthesiology and Geriatric Sciences, , Sapienza University of Rome, ; Viale del Policlinico 155, 00161 Rome, Italy
                [2 ]GRID grid.7563.7, ISNI 0000 0001 2174 1754, Department of Medicine and Surgery, , University of Milano-Bicocca, ; Milan, Italy
                [3 ]GRID grid.414603.4, Department of Cardiovascular, Neural and Metabolic Sciences, S.Luca Hospital, Istituto Auxologico Italiano, , IRCCS, ; Milan, Italy
                [4 ]GRID grid.83440.3b, ISNI 0000000121901201, Institute of Cardiovascular Science, , University College London, ; Gower Street, London, UK
                [5 ]GRID grid.416353.6, ISNI 0000 0000 9244 0345, Barts Heart Centre, Advanced Cardiac Imaging and The Inherited Cardiovascular Diseases Unit, , St Bartholomew’s Hospital, ; West Smithfield, London, EC1A 7BE UK
                Author notes

                Associate Editor Domingo A. Pascual-Figal oversaw the review of this article

                Author information
                http://orcid.org/0000-0001-8071-1491
                Article
                Publisher ID: 10022
                DOI: 10.1007/s12265-020-10022-7
                PMC ID: 7360536
                PubMed ID: 32436168
                SO-VID: 06fd3820-7586-4a0d-b6fb-528687b780a9
                Copyright © © The Author(s) 2020
                License:

                Open Access This 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/.

                History
                Date received : 27 April 2020
                Date accepted : 5 May 2020
                Funding
                Funded by: University College London (UCL)
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2020

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: athlete’s heart,cmr,sport cardiology
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: athlete’s heart, cmr, sport cardiology

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