Analysis of the Factors Influencing the Cardiac Phenotype in Friedreich's Ataxia
Identifieur interne : 000C03 ( PascalFrancis/Checkpoint ); précédent : 000C02; suivant : 000C04Analysis of the Factors Influencing the Cardiac Phenotype in Friedreich's Ataxia
Auteurs : Bheeshma Rajagopalan [Royaume-Uni] ; Jane M. Francis [Royaume-Uni] ; Fraser Cooke [Royaume-Uni] ; L. V. Prasad Korlipara [Royaume-Uni] ; Andrew M. Blamire [Royaume-Uni] ; Anthony H. V. Schapira [Royaume-Uni] ; Jason Madan [Royaume-Uni] ; Stefan Neubauer [Royaume-Uni] ; J. Mark Cooper [Royaume-Uni]Source :
- Movement disorders [ 0885-3185 ] ; 2010.
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Abstract
Friedreich's ataxia (FRDA) has been associated with both cardiac hypertrophy and to a lesser degree dilated cardiomyopathy. We have conducted a cross sectional magnetic resonance imaging (MRI) study of 25 patients with clinically and genetically confirmed FRDA and 24 healthy controls to analyse how disease parameters influence cardiac features in FRDA. MR cine imaging in the long and short axis planes was performed alongside clinical assessments. LV mass was most pronounced in FRDA patients with a larger genetic mutation (GAA1 repeats >600), earlier age of onset (<16years) and a shorter disease duration (<15 years). LV mass decreased with longer disease duration (>15 years), and independent of GAA1 repeat size and age of onset, suggesting cardiac thinning occurred with prolonged disease. Heart function was lower in patients with larger GAA1 repeat number and longer disease duration. Consequently, cardiac hypertrophy was more marked in FRDA patients with a larger GAA1 repeat number and younger age of onset, while prolonged disease duration was associated with lower LV mass and decreased heart function. It is important not only to understand the biochemical basis for these cardiac changes but also allow for these changes when assessing the effect of treatment of FRDA patients.
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Mark" last="Cooper">J. Mark Cooper</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Clinical Neurosciences, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">10-0288338</idno><date when="2010">2010</date><idno type="stanalyst">PASCAL 10-0288338 INIST</idno><idno type="RBID">Pascal:10-0288338</idno><idno type="wicri:Area/PascalFrancis/Corpus">000B16</idno><idno type="wicri:Area/PascalFrancis/Curation">002203</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000C03</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Analysis of the Factors Influencing the Cardiac Phenotype in Friedreich's Ataxia</title><author><name sortKey="Rajagopalan, Bheeshma" sort="Rajagopalan, Bheeshma" uniqKey="Rajagopalan B" first="Bheeshma" last="Rajagopalan">Bheeshma Rajagopalan</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Nuffield Department of Medicine, Department of Biochemistry, University of Oxford</s1><s2>Oxford</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Oxford</settlement><region type="country">Angleterre</region><region type="comté" nuts="2">Oxfordshire</region></placeName><orgName type="university">Université d'Oxford</orgName></affiliation></author><author><name sortKey="Francis, Jane M" sort="Francis, Jane M" uniqKey="Francis J" first="Jane M." last="Francis">Jane M. Francis</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>University of Oxford Centre for Clinical Magnetic Resonance Research</s1><s2>Oxford</s2><s3>GBR</s3><sZ>2 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Oxford</settlement><region type="country">Angleterre</region><region type="comté" nuts="2">Oxfordshire</region></placeName></affiliation></author><author><name sortKey="Cooke, Fraser" sort="Cooke, Fraser" uniqKey="Cooke F" first="Fraser" last="Cooke">Fraser Cooke</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Nuffield Department of Medicine, Department of Biochemistry, University of Oxford</s1><s2>Oxford</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Oxford</settlement><region type="country">Angleterre</region><region type="comté" nuts="2">Oxfordshire</region></placeName><orgName type="university">Université d'Oxford</orgName></affiliation></author><author><name sortKey="Prasad Korlipara, L V" sort="Prasad Korlipara, L V" uniqKey="Prasad Korlipara L" first="L. V." last="Prasad Korlipara">L. V. Prasad Korlipara</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Clinical Neurosciences, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Blamire, Andrew M" sort="Blamire, Andrew M" uniqKey="Blamire A" first="Andrew M." last="Blamire">Andrew M. Blamire</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Nuffield Department of Medicine, Department of Biochemistry, University of Oxford</s1><s2>Oxford</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Oxford</settlement><region type="country">Angleterre</region><region type="comté" nuts="2">Oxfordshire</region></placeName><orgName type="university">Université d'Oxford</orgName></affiliation></author><author><name sortKey="Schapira, Anthony H V" sort="Schapira, Anthony H V" uniqKey="Schapira A" first="Anthony H. V." last="Schapira">Anthony H. V. Schapira</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Clinical Neurosciences, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Madan, Jason" sort="Madan, Jason" uniqKey="Madan J" first="Jason" last="Madan">Jason Madan</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Health Economics and Decision Science, ScHARR, University of Sheffield</s1><s2>Sheffield</s2><s3>GBR</s3><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country><wicri:noRegion>Sheffield</wicri:noRegion></affiliation></author><author><name sortKey="Neubauer, Stefan" sort="Neubauer, Stefan" uniqKey="Neubauer S" first="Stefan" last="Neubauer">Stefan Neubauer</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>University of Oxford Centre for Clinical Magnetic Resonance Research</s1><s2>Oxford</s2><s3>GBR</s3><sZ>2 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Oxford</settlement><region type="country">Angleterre</region><region type="comté" nuts="2">Oxfordshire</region></placeName></affiliation></author><author><name sortKey="Cooper, J Mark" sort="Cooper, J Mark" uniqKey="Cooper J" first="J. Mark" last="Cooper">J. Mark Cooper</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Clinical Neurosciences, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Ataxia</term><term>Cardiomyopathy</term><term>Factor analysis</term><term>Friedreich ataxia</term><term>Nervous system diseases</term><term>Nuclear magnetic resonance imaging</term><term>Phenotype</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Hérédodégénérescence spinocérébelleuse de Friedreich</term><term>Cardiomyopathie</term><term>Ataxie</term><term>Pathologie du système nerveux</term><term>Analyse factorielle</term><term>Phénotype</term><term>Imagerie RMN</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Friedreich's ataxia (FRDA) has been associated with both cardiac hypertrophy and to a lesser degree dilated cardiomyopathy. We have conducted a cross sectional magnetic resonance imaging (MRI) study of 25 patients with clinically and genetically confirmed FRDA and 24 healthy controls to analyse how disease parameters influence cardiac features in FRDA. MR cine imaging in the long and short axis planes was performed alongside clinical assessments. LV mass was most pronounced in FRDA patients with a larger genetic mutation (GAA1 repeats >600), earlier age of onset (<16years) and a shorter disease duration (<15 years). LV mass decreased with longer disease duration (>15 years), and independent of GAA1 repeat size and age of onset, suggesting cardiac thinning occurred with prolonged disease. Heart function was lower in patients with larger GAA1 repeat number and longer disease duration. Consequently, cardiac hypertrophy was more marked in FRDA patients with a larger GAA1 repeat number and younger age of onset, while prolonged disease duration was associated with lower LV mass and decreased heart function. It is important not only to understand the biochemical basis for these cardiac changes but also allow for these changes when assessing the effect of treatment of FRDA patients.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>25</s2></fA05><fA06><s2>7</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Analysis of the Factors Influencing the Cardiac Phenotype in Friedreich's Ataxia</s1></fA08><fA11 i1="01" i2="1"><s1>RAJAGOPALAN (Bheeshma)</s1></fA11><fA11 i1="02" i2="1"><s1>FRANCIS (Jane M.)</s1></fA11><fA11 i1="03" i2="1"><s1>COOKE (Fraser)</s1></fA11><fA11 i1="04" i2="1"><s1>PRASAD KORLIPARA (L. V.)</s1></fA11><fA11 i1="05" i2="1"><s1>BLAMIRE (Andrew M.)</s1></fA11><fA11 i1="06" i2="1"><s1>SCHAPIRA (Anthony H. V.)</s1></fA11><fA11 i1="07" i2="1"><s1>MADAN (Jason)</s1></fA11><fA11 i1="08" i2="1"><s1>NEUBAUER (Stefan)</s1></fA11><fA11 i1="09" i2="1"><s1>COOPER (J. Mark)</s1></fA11><fA14 i1="01"><s1>Nuffield Department of Medicine, Department of Biochemistry, University of Oxford</s1><s2>Oxford</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>University of Oxford Centre for Clinical Magnetic Resonance Research</s1><s2>Oxford</s2><s3>GBR</s3><sZ>2 aut.</sZ><sZ>8 aut.</sZ></fA14><fA14 i1="03"><s1>Clinical Neurosciences, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="04"><s1>Health Economics and Decision Science, ScHARR, University of Sheffield</s1><s2>Sheffield</s2><s3>GBR</s3><sZ>7 aut.</sZ></fA14><fA20><s1>846-852</s1></fA20><fA21><s1>2010</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000193040220050</s5></fA43><fA44><s0>0000</s0><s1>© 2010 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>36 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>10-0288338</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Friedreich's ataxia (FRDA) has been associated with both cardiac hypertrophy and to a lesser degree dilated cardiomyopathy. We have conducted a cross sectional magnetic resonance imaging (MRI) study of 25 patients with clinically and genetically confirmed FRDA and 24 healthy controls to analyse how disease parameters influence cardiac features in FRDA. MR cine imaging in the long and short axis planes was performed alongside clinical assessments. LV mass was most pronounced in FRDA patients with a larger genetic mutation (GAA1 repeats >600), earlier age of onset (<16years) and a shorter disease duration (<15 years). LV mass decreased with longer disease duration (>15 years), and independent of GAA1 repeat size and age of onset, suggesting cardiac thinning occurred with prolonged disease. Heart function was lower in patients with larger GAA1 repeat number and longer disease duration. Consequently, cardiac hypertrophy was more marked in FRDA patients with a larger GAA1 repeat number and younger age of onset, while prolonged disease duration was associated with lower LV mass and decreased heart function. It is important not only to understand the biochemical basis for these cardiac changes but also allow for these changes when assessing the effect of treatment of FRDA patients.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC02 i1="02" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Hérédodégénérescence spinocérébelleuse de Friedreich</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Friedreich ataxia</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Heredodegeneración espinocerebelosa Friedreich</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Cardiomyopathie</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Cardiomyopathy</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Cardiomiopatía</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Ataxie</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Ataxia</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Ataxia</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Analyse factorielle</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Factor analysis</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Análisis factorial</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Phénotype</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Phenotype</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Fenotipo</s0><s5>10</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Imagerie RMN</s0><s5>11</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Nuclear magnetic resonance imaging</s0><s5>11</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Imaginería RMN</s0><s5>11</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Maladie héréditaire</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Genetic disease</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Pathologie de la moelle épinière</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Spinal cord disease</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Médula espinal patología</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Pathologie de l'appareil circulatoire</s0><s5>43</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Cardiovascular disease</s0><s5>43</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Aparato circulatorio patología</s0><s5>43</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Cardiopathie</s0><s5>44</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Heart disease</s0><s5>44</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Cardiopatía</s0><s5>44</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Pathologie du myocarde</s0><s5>45</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Myocardial disease</s0><s5>45</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Miocardio patología</s0><s5>45</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Trouble neurologique</s0><s5>46</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Neurological disorder</s0><s5>46</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Trastorno neurológico</s0><s5>46</s5></fC07><fN21><s1>186</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li><li>Oxfordshire</li></region><settlement><li>Londres</li><li>Oxford</li></settlement><orgName><li>Université d'Oxford</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Rajagopalan, Bheeshma" sort="Rajagopalan, Bheeshma" uniqKey="Rajagopalan B" first="Bheeshma" last="Rajagopalan">Bheeshma Rajagopalan</name></region><name sortKey="Blamire, Andrew M" sort="Blamire, Andrew M" uniqKey="Blamire A" first="Andrew M." last="Blamire">Andrew M. Blamire</name><name sortKey="Cooke, Fraser" sort="Cooke, Fraser" uniqKey="Cooke F" first="Fraser" last="Cooke">Fraser Cooke</name><name sortKey="Cooper, J Mark" sort="Cooper, J Mark" uniqKey="Cooper J" first="J. Mark" last="Cooper">J. Mark Cooper</name><name sortKey="Francis, Jane M" sort="Francis, Jane M" uniqKey="Francis J" first="Jane M." last="Francis">Jane M. Francis</name><name sortKey="Madan, Jason" sort="Madan, Jason" uniqKey="Madan J" first="Jason" last="Madan">Jason Madan</name><name sortKey="Neubauer, Stefan" sort="Neubauer, Stefan" uniqKey="Neubauer S" first="Stefan" last="Neubauer">Stefan Neubauer</name><name sortKey="Prasad Korlipara, L V" sort="Prasad Korlipara, L V" uniqKey="Prasad Korlipara L" first="L. V." last="Prasad Korlipara">L. V. Prasad Korlipara</name><name sortKey="Schapira, Anthony H V" sort="Schapira, Anthony H V" uniqKey="Schapira A" first="Anthony H. V." last="Schapira">Anthony H. V. Schapira</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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