Cardiomyopathy in Friedreich's ataxia-assessment by cardiac MRI.
Identifieur interne : 002929 ( PubMed/Checkpoint ); précédent : 002928; suivant : 002930Cardiomyopathy in Friedreich's ataxia-assessment by cardiac MRI.
Auteurs : Chris Meyer [Allemagne] ; Gebhard Schmid ; Sabine Görlitz ; Monika Ernst ; Christian Wilkens ; Inga Wilhelms ; Peter H. Kraus ; Peter Bauer ; Jürgen Tomiuk ; Horst Przuntek ; Andreas Mügge ; Ludger SchölsSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Adolescent, Adult, Cardiomyopathies (etiology), Cardiomyopathies (genetics), Cardiomyopathies (pathology), Case-Control Studies, Echocardiography, Female, Friedreich Ataxia (complications), Friedreich Ataxia (genetics), Heart Septum (pathology), Heart Ventricles (pathology), Humans, Longitudinal Studies, Magnetic Resonance Imaging, Middle Aged, Myocardium (pathology), Trinucleotide Repeats (genetics).
- MESH :
- complications : Friedreich Ataxia.
- etiology : Cardiomyopathies.
- genetics : Cardiomyopathies, Friedreich Ataxia, Trinucleotide Repeats.
- pathology : Cardiomyopathies, Heart Septum, Heart Ventricles, Myocardium.
- Adolescent, Adult, Case-Control Studies, Echocardiography, Female, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Middle Aged.
Abstract
Cardiomyopathy is an important and frequently life limiting manifestation of Friedreich's ataxia (FA), the most prevalent form of autosomal recessive ataxia. Left ventricular mass is used as primary outcome measure in recent intervention studies but systematic analyses of FA cardiomyopathy are sparse. To assess cardiac hypertrophy by cardiac magnetic resonance imaging (MRI) in vivo, we assessed 41 adult patients with genetically confirmed FA and 33 age- and sex-matched healthy controls by cardiac MRI and echocardiogarphy. Septal hypertrophy and left ventricular mass index were determined by two independent raters. MRI revealed hypertrophy of the interventricular septum in 40% and increased left ventricular mass index in 29% of patients. Interobserver variability was less than 5% for both measures. GAA repeat length had only minor influence on interventricular septum thickness. Left ventricular mass index decreased with age. Severity of ataxia did not correlate with cardiac disease. In echocardiography wall diameter was assessable only in 31 of 41 FA patients with 32% of patients presenting septal hypertrophy and 6% increased left ventricular mass index. We conclude that cardiac hypertrophy is present only in a minority of adult FA patients. If despite this limitation intervention studies use left ventricular mass as outcome measure, MRI is recommended as the most accurate assessment of cardiac anatomy in vivo.
DOI: 10.1002/mds.21590
PubMed: 17546670
Affiliations:
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pubmed:17546670Le document en format XML
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<term>Cardiomyopathies (pathology)</term>
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<term>Echocardiography</term>
<term>Female</term>
<term>Friedreich Ataxia (complications)</term>
<term>Friedreich Ataxia (genetics)</term>
<term>Heart Septum (pathology)</term>
<term>Heart Ventricles (pathology)</term>
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<term>Case-Control Studies</term>
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<front><div type="abstract" xml:lang="en">Cardiomyopathy is an important and frequently life limiting manifestation of Friedreich's ataxia (FA), the most prevalent form of autosomal recessive ataxia. Left ventricular mass is used as primary outcome measure in recent intervention studies but systematic analyses of FA cardiomyopathy are sparse. To assess cardiac hypertrophy by cardiac magnetic resonance imaging (MRI) in vivo, we assessed 41 adult patients with genetically confirmed FA and 33 age- and sex-matched healthy controls by cardiac MRI and echocardiogarphy. Septal hypertrophy and left ventricular mass index were determined by two independent raters. MRI revealed hypertrophy of the interventricular septum in 40% and increased left ventricular mass index in 29% of patients. Interobserver variability was less than 5% for both measures. GAA repeat length had only minor influence on interventricular septum thickness. Left ventricular mass index decreased with age. Severity of ataxia did not correlate with cardiac disease. In echocardiography wall diameter was assessable only in 31 of 41 FA patients with 32% of patients presenting septal hypertrophy and 6% increased left ventricular mass index. We conclude that cardiac hypertrophy is present only in a minority of adult FA patients. If despite this limitation intervention studies use left ventricular mass as outcome measure, MRI is recommended as the most accurate assessment of cardiac anatomy in vivo.</div>
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<Abstract><AbstractText>Cardiomyopathy is an important and frequently life limiting manifestation of Friedreich's ataxia (FA), the most prevalent form of autosomal recessive ataxia. Left ventricular mass is used as primary outcome measure in recent intervention studies but systematic analyses of FA cardiomyopathy are sparse. To assess cardiac hypertrophy by cardiac magnetic resonance imaging (MRI) in vivo, we assessed 41 adult patients with genetically confirmed FA and 33 age- and sex-matched healthy controls by cardiac MRI and echocardiogarphy. Septal hypertrophy and left ventricular mass index were determined by two independent raters. MRI revealed hypertrophy of the interventricular septum in 40% and increased left ventricular mass index in 29% of patients. Interobserver variability was less than 5% for both measures. GAA repeat length had only minor influence on interventricular septum thickness. Left ventricular mass index decreased with age. Severity of ataxia did not correlate with cardiac disease. In echocardiography wall diameter was assessable only in 31 of 41 FA patients with 32% of patients presenting septal hypertrophy and 6% increased left ventricular mass index. We conclude that cardiac hypertrophy is present only in a minority of adult FA patients. If despite this limitation intervention studies use left ventricular mass as outcome measure, MRI is recommended as the most accurate assessment of cardiac anatomy in vivo.</AbstractText>
<CopyrightInformation>Copyright (c) 2007 Movement Disorder Society.</CopyrightInformation>
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