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      Semiautomatic detection of myocardial contours in order to investigate normal values of the left ventricular trabeculated mass using MRI : Quantification of Trabeculated LV Mass

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          A review of segmentation methods in short axis cardiac MR images.

          For the last 15 years, Magnetic Resonance Imaging (MRI) has become a reference examination for cardiac morphology, function and perfusion in humans. Yet, due to the characteristics of cardiac MR images and to the great variability of the images among patients, the problem of heart cavities segmentation in MRI is still open. This paper is a review of fully and semi-automated methods performing segmentation in short axis images using a cardiac cine MRI sequence. Medical background and specific segmentation difficulties associated to these images are presented. For this particularly complex segmentation task, prior knowledge is required. We thus propose an original categorization for cardiac segmentation methods, with a special emphasis on what level of external information is required (weak or strong) and how it is used to constrain segmentation. After reviewing method principles and analyzing segmentation results, we conclude with a discussion and future trends in this field regarding methodological and medical issues. Copyright © 2010 Elsevier B.V. All rights reserved.
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            Measurement of trabeculated left ventricular mass using cardiac magnetic resonance imaging in the diagnosis of left ventricular non-compaction.

            To describe a method for measuring trabeculated left ventricular (LV) mass using cardiac magnetic resonance imaging and to assess its value in the diagnosis of left ventricular non-compaction (LVNC). Between January 2003 and 2008, we prospectively included 16 patients with LVNC. During the mean period, we included 16 patients with dilated cardiomyopathy (DCM), 16 patients with hypertrophic cardiomyopathy (HCM), and 16 control subjects. Left ventricular volumes, LV ejection fraction, and trabeculated LV mass were measured in the four different populations. The percentage of trabeculated LV mass was almost three times higher in the patients with LVNC (32 +/- 10%), compared with those with DCM (11 +/- 4%, P < 0.0001), HCM (12 +/- 4%, P < 0.0001), and controls (12 +/- 5%, P < 0.0001). A value of trabeculated LV mass above 20% of the global mass of the LV predicted the diagnosis of LVNC with a sensitivity of 93.7% [95% confidence interval (CI), 71.6-98.8%] and a specificity of 93.7% (95% CI, 83.1-97.8%; kappa = 0.84). The method described is reproducible and provides an assessment of the global amount of LV trabeculation. A trabeculated LV mass above 20% of the global LV mass is highly sensitive and specific for the diagnosis of LVNC.
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              Mutations in sarcomere protein genes in left ventricular noncompaction.

              Left ventricular noncompaction constitutes a primary cardiomyopathy characterized by a severely thickened, 2-layered myocardium, numerous prominent trabeculations, and deep intertrabecular recesses. The genetic basis of this cardiomyopathy is still largely unresolved. We speculated that mutations in sarcomere protein genes known to cause hypertrophic cardiomyopathy and dilated cardiomyopathy may be associated with left ventricular noncompaction. Mutational analysis in a cohort of 63 unrelated adult probands with left ventricular noncompaction and no other congenital heart anomalies was performed by denaturing high-performance liquid chromatography analysis and direct DNA sequencing of 6 genes encoding sarcomere proteins. Heterozygous mutations were identified in 11 of 63 samples in genes encoding beta-myosin heavy chain (MYH7), alpha-cardiac actin (ACTC), and cardiac troponin T (TNNT2). Nine distinct mutations, 7 of them in MYH7, 1 in ACTC, and 1 in TNNT2, were found. Clinical evaluations demonstrated familial disease in 6 of 11 probands with sarcomere gene mutations. MYH7 mutations segregated with the disease in 4 autosomal dominant LVNC kindreds. Six of the MYH7 mutations were novel, and 1 encodes a splice-site mutation, a relatively unique finding for MYH7 mutations. Modified residues in beta-myosin heavy chain were located mainly within the ATP binding site. We conclude that left ventricular noncompaction is within the diverse spectrum of cardiac morphologies triggered by sarcomere protein gene defects. Our findings support the hypothesis that there is a shared molecular etiology of different cardiomyopathic phenotypes.
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                Author and article information

                Journal
                Journal of Magnetic Resonance Imaging
                J. Magn. Reson. Imaging
                Wiley
                10531807
                June 2016
                June 2016
                December 09 2015
                : 43
                : 6
                : 1398-1406
                Affiliations
                [1 ]Le2i, UMR 6306, CNRS, Arts et Métiers; Université de Bourgogne Franche-Comté; Dijon France
                [2 ]Service de radiologie; CHU; Grenoble France
                [3 ]Aix-Marseille Université; CNRS; CRMBM UMR 7339 Marseille France
                [4 ]Aix-Marseille Université, CNRS, IBDM UMR 7288; Marseille France
                [5 ]Département de Cardiologie, Hôpital de La Timone, AP-HM; Aix-Marseille Université; Marseille France
                [6 ]Service de Médecine Nucléaire; CHU; Grenoble France
                [7 ]Département de Radiologie, Aix Marseille Université; Hôpital Universitaire La Timone; Marseille France
                [8 ]Service d'IRM; CHU; Dijon France
                Article
                10.1002/jmri.25113
                8f9d188d-5162-48f1-8898-952941c741cd
                © 2015

                http://doi.wiley.com/10.1002/tdm_license_1.1

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