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      Non-contrast-enhanced T 1 Mapping of Dilated Cardiomyopathy: Comparison between Native T 1 Values and Late Gadolinium Enhancement

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          Abstract

          Purpose:

          We sought to use non-contrast-enhanced T 1 mapping to determine the native T 1 values required to identify myocardial fibrosis in patients with dilated cardiomyopathy (DCM).

          Methods:

          A total of 25 patients with DCM and 15 healthy controls were enrolled. All subjects underwent T 1 mapping using modified look–locker inversion recovery, and the patients underwent late gadolinium-enhancement (LGE) imaging. Basal and mid-ventricular levels were divided into eight segments and the T 1 value was measured in each segment. The T 1 values of septal segments with LGE were compared with those of the septal segments without LGE, the minimum T 1 value of each patient, and the T 1 values of the normal septal myocardium.

          Results:

          Late gadolinium-enhancement was present in 12 septal segments (24.0%) from 10 patients (40.0%). T 1 values were significantly higher in septal segments with LGE than in those without (1373.7 vs. 1288.0 ms; P = 0.035) or in normal septal myocardium (1209.1 ms; P < 0.01). A receiver operating characteristic analysis revealed the appropriate cutoff value of 1349.4 ms for identifying LGE with a sensitivity of 75% and specificity of 92.1%. When the minimum T 1 value + 1.2 standard deviation (SD) was used as the threshold, the sensitivity was 75% and specificity was 89.5%.

          Conclusion:

          Non-contrast-enhanced T 1 mapping can be used for assessment of myocardial fibrosis associated with DCM by using the appropriate threshold.

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          Most cited references11

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          Association of fibrosis with mortality and sudden cardiac death in patients with nonischemic dilated cardiomyopathy.

          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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            Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies.

            Non-ischaemic cardiomyopathies (NICMs) are chronic, progressive myocardial diseases with distinct patterns of morphological, functional, and electrophysiological changes. In the setting of cardiomyopathy (CM), determining the exact aetiology is important because the aetiology is directly related to treatment and patient survival. Determining the exact aetiology, however, can be difficult using currently available imaging techniques, such as echocardiography, radionuclide imaging or X-ray coronary angiography, since overlap of features between CMs may be encountered. Cardiovascular magnetic resonance (CMR) imaging has recently emerged as a new non-invasive imaging modality capable of providing high-resolution images of the heart in any desired plane. Delayed contrast enhanced CMR (DE-CMR) can be used for non-invasive tissue characterization and may hold promise in differentiating ischaemic from NICMs, as the typical pattern of hyperenhancement can be classified as 'ischaemic-type' or 'non-ischaemic type' on the basis of pathophysiology of ischaemia. This article reviews the potential of DE-CMR to distinguish between ischaemic and NICM as well as to differentiate non-ischaemic aetiologies. Rather than simply describing various hyperenhancement patterns that may occur in different disease states, our goal will be (i) to provide an overall imaging approach for the diagnosis of CM and (ii) to demonstrate how this approach is based on the underlying relationships between contrast enhancement and myocardial pathophysiology.
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              The role of cardiovascular magnetic resonance imaging in heart failure.

              Noninvasive imaging plays a central role in the diagnosis of heart failure, assessment of prognosis, and monitoring of therapy. Cardiovascular magnetic resonance (CMR) offers a comprehensive assessment of heart failure patients and is now the gold standard imaging technique to assess myocardial anatomy, regional and global function, and viability. Furthermore, it allows assessment of perfusion and acute tissue injury (edema and necrosis), whereas in nonischemic heart failure, fibrosis, infiltration, and iron overload can be detected. The information derived from CMR often reveals the underlying etiology of heart failure, and its high measurement accuracy makes it an ideal technique for monitoring disease progression and the effects of treatment. Evidence on the prognostic value of CMR-derived parameters in heart failure is rapidly emerging. This review summarizes the advantages of CMR for patients with heart failure and its important role in key areas.
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                Author and article information

                Journal
                Magn Reson Med Sci
                Magn Reson Med Sci
                mrms
                Magnetic Resonance in Medical Sciences
                Japanese Society for Magnetic Resonance in Medicine
                1347-3182
                1880-2206
                2019
                07 March 2018
                : 18
                : 1
                : 12-18
                Affiliations
                [1 ]Department of Radiology, Nippon Medical School, Tokyo, Japan
                [2 ]Department of Radiology, Nihon University Hospital, 1-6 Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8309, Japan
                [3 ]Department of Cardiology, Nippon Medical School, Tokyo, Japan
                Author notes
                [* ]Corresponding author, Phone: +81-3-3293-1711, E-mail: yas-amano@ 123456nifty.com
                Article
                mrms-18-12
                10.2463/mrms.mp.2017-0136
                6326770
                29515087
                01f27d02-9372-49e0-b3ca-ab12aea3a634
                © 2018 Japanese Society for Magnetic Resonance in Medicine

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

                History
                : 30 July 2017
                : 07 February 2018
                Categories
                Major Paper

                dilated cardiomyopathy,late gadolinium enhancement,myocardial fibrosis,t1 mapping

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