Lowered cardiac sympathetic nerve performance in response to exercise in Parkinson's disease
Identifieur interne : 000E24 ( Main/Corpus ); précédent : 000E23; suivant : 000E25Lowered cardiac sympathetic nerve performance in response to exercise in Parkinson's disease
Auteurs : Tomohiko Nakamura ; Masaaki Hirayama ; Fumitada Yamashita ; Kei Uchida ; Tetsuo Hama ; Hirohisa Watanabe ; Gen SobueSource :
- Movement Disorders [ 0885-3185 ] ; 2010-07-15.
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Abstract
We examined whether cardiac sympathetic denervation influences the cardiovascular response to exercise in Parkinson's disease (PD). Sixteen patients with PD were divided into two groups, according to their cardiac uptake of 123I‐metaiodobenzylguanidine (denervated group, 10 patients with heart to mediastinum (H/M) ratio < 1.7; innervated group, six patients with H/M ratio > 1.7) and compared changes in blood pressure (BP), heart rate (HR), and cardiac contractility with 13 control subjects during ergometric exercise stress. Velocity index (VI), an indicator of cardiac contractility, was measured using impedance cardiography and recorded every minute. Exercise began at a power output of 20 W for the first 2 min and increased 10 W every 2 min to a maximal intensity of 60 W. All control subjects accomplished the procedure while six patients with PD could not continue after the first minute of 50 W loading. There were no significant differences in BP or HR change between the three groups. However, a significant reduction in VI was observed from the first minute of the 30 W workload in the denervated group compared to the control group. This lowered response continued till 50 W loading and was significantly different to the innervated group at 50 W loading. No significant VI changes were observed between the control and innervated groups throughout the exercise test. Patients with PD with reduced MIBG uptake had a lowered cardiac contractility than innervated subjects during exercise, suggesting that this response represents theimpaired exercise capacity of patients with PD with cardiac sympathetic denervation. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23127
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Uchida</name><affiliation><mods:affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hama, Tetsuo" sort="Hama, Tetsuo" uniqKey="Hama T" first="Tetsuo" last="Hama">Tetsuo Hama</name><affiliation><mods:affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</mods:affiliation></affiliation></author><author><name sortKey="Watanabe, Hirohisa" sort="Watanabe, Hirohisa" uniqKey="Watanabe H" first="Hirohisa" last="Watanabe">Hirohisa Watanabe</name><affiliation><mods:affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</mods:affiliation></affiliation></author><author><name sortKey="Sobue, Gen" sort="Sobue, Gen" uniqKey="Sobue G" first="Gen" last="Sobue">Gen Sobue</name><affiliation><mods:affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-07-15">2010-07-15</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1183">1183</biblScope><biblScope unit="page" to="1189">1189</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">CD1424095BEC67D0BADC8331EAFFCB109F910FAE</idno><idno type="DOI">10.1002/mds.23127</idno><idno type="ArticleID">MDS23127</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>MIBG</term><term>Parkinson's disease</term><term>cardiac contractility</term><term>cardiac sympathetic denervation</term><term>exercise test</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We examined whether cardiac sympathetic denervation influences the cardiovascular response to exercise in Parkinson's disease (PD). Sixteen patients with PD were divided into two groups, according to their cardiac uptake of 123I‐metaiodobenzylguanidine (denervated group, 10 patients with heart to mediastinum (H/M) ratio < 1.7; innervated group, six patients with H/M ratio > 1.7) and compared changes in blood pressure (BP), heart rate (HR), and cardiac contractility with 13 control subjects during ergometric exercise stress. Velocity index (VI), an indicator of cardiac contractility, was measured using impedance cardiography and recorded every minute. Exercise began at a power output of 20 W for the first 2 min and increased 10 W every 2 min to a maximal intensity of 60 W. All control subjects accomplished the procedure while six patients with PD could not continue after the first minute of 50 W loading. There were no significant differences in BP or HR change between the three groups. However, a significant reduction in VI was observed from the first minute of the 30 W workload in the denervated group compared to the control group. This lowered response continued till 50 W loading and was significantly different to the innervated group at 50 W loading. No significant VI changes were observed between the control and innervated groups throughout the exercise test. Patients with PD with reduced MIBG uptake had a lowered cardiac contractility than innervated subjects during exercise, suggesting that this response represents theimpaired exercise capacity of patients with PD with cardiac sympathetic denervation. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Tomohiko Nakamura MD</name><affiliations><json:string>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</json:string></affiliations></json:item><json:item><name>Masaaki Hirayama MD</name><affiliations><json:string>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</json:string></affiliations></json:item><json:item><name>Fumitada Yamashita MD</name><affiliations><json:string>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</json:string></affiliations></json:item><json:item><name>Kei Uchida MD</name><affiliations><json:string>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</json:string></affiliations></json:item><json:item><name>Tetsuo Hama MD</name><affiliations><json:string>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</json:string></affiliations></json:item><json:item><name>Hirohisa Watanabe MD</name><affiliations><json:string>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</json:string></affiliations></json:item><json:item><name>Gen Sobue MD</name><affiliations><json:string>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MIBG</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>exercise test</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cardiac contractility</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cardiac sympathetic denervation</value></json:item></subject><articleId><json:string>MDS23127</json:string></articleId><language><json:string>eng</json:string></language><abstract>We examined whether cardiac sympathetic denervation influences the cardiovascular response to exercise in Parkinson's disease (PD). Sixteen patients with PD were divided into two groups, according to their cardiac uptake of 123I‐metaiodobenzylguanidine (denervated group, 10 patients with heart to mediastinum (H/M) ratio > 1.7; innervated group, six patients with H/M ratio > 1.7) and compared changes in blood pressure (BP), heart rate (HR), and cardiac contractility with 13 control subjects during ergometric exercise stress. Velocity index (VI), an indicator of cardiac contractility, was measured using impedance cardiography and recorded every minute. Exercise began at a power output of 20 W for the first 2 min and increased 10 W every 2 min to a maximal intensity of 60 W. All control subjects accomplished the procedure while six patients with PD could not continue after the first minute of 50 W loading. There were no significant differences in BP or HR change between the three groups. However, a significant reduction in VI was observed from the first minute of the 30 W workload in the denervated group compared to the control group. This lowered response continued till 50 W loading and was significantly different to the innervated group at 50 W loading. No significant VI changes were observed between the control and innervated groups throughout the exercise test. Patients with PD with reduced MIBG uptake had a lowered cardiac contractility than innervated subjects during exercise, suggesting that this response represents theimpaired exercise capacity of patients with PD with cardiac sympathetic denervation. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>7.022</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1666</abstractCharCount><pdfWordCount>4022</pdfWordCount><pdfCharCount>25015</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>255</abstractWordCount></qualityIndicators><title>Lowered cardiac sympathetic nerve performance in response to exercise in Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>25</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>7</total><last>1189</last><first>1183</first></pages><issn><json:string>0885-3185</json:string></issn><issue>9</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.23127</json:string></doi><id>CD1424095BEC67D0BADC8331EAFFCB109F910FAE</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/CD1424095BEC67D0BADC8331EAFFCB109F910FAE/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/CD1424095BEC67D0BADC8331EAFFCB109F910FAE/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/CD1424095BEC67D0BADC8331EAFFCB109F910FAE/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Lowered cardiac sympathetic nerve performance in response to exercise in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Lowered cardiac sympathetic nerve performance in response to exercise in Parkinson's disease</title><author><persName><forename type="first">Tomohiko</forename><surname>Nakamura</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation></author><author><persName><forename type="first">Masaaki</forename><surname>Hirayama</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation></author><author><persName><forename type="first">Fumitada</forename><surname>Yamashita</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation></author><author><persName><forename type="first">Kei</forename><surname>Uchida</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation></author><author><persName><forename type="first">Tetsuo</forename><surname>Hama</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation></author><author><persName><forename type="first">Hirohisa</forename><surname>Watanabe</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation></author><author><persName><forename type="first">Gen</forename><surname>Sobue</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai‐cho, Showa‐ku, Nagoya 466‐8550, Japan</p></note><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-07-15"></date><biblScope unit="volume">25</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1183">1183</biblScope><biblScope unit="page" to="1189">1189</biblScope></imprint></monogr><idno type="istex">CD1424095BEC67D0BADC8331EAFFCB109F910FAE</idno><idno type="DOI">10.1002/mds.23127</idno><idno type="ArticleID">MDS23127</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We examined whether cardiac sympathetic denervation influences the cardiovascular response to exercise in Parkinson's disease (PD). Sixteen patients with PD were divided into two groups, according to their cardiac uptake of 123I‐metaiodobenzylguanidine (denervated group, 10 patients with heart to mediastinum (H/M) ratio < 1.7; innervated group, six patients with H/M ratio > 1.7) and compared changes in blood pressure (BP), heart rate (HR), and cardiac contractility with 13 control subjects during ergometric exercise stress. Velocity index (VI), an indicator of cardiac contractility, was measured using impedance cardiography and recorded every minute. Exercise began at a power output of 20 W for the first 2 min and increased 10 W every 2 min to a maximal intensity of 60 W. All control subjects accomplished the procedure while six patients with PD could not continue after the first minute of 50 W loading. There were no significant differences in BP or HR change between the three groups. However, a significant reduction in VI was observed from the first minute of the 30 W workload in the denervated group compared to the control group. This lowered response continued till 50 W loading and was significantly different to the innervated group at 50 W loading. No significant VI changes were observed between the control and innervated groups throughout the exercise test. Patients with PD with reduced MIBG uptake had a lowered cardiac contractility than innervated subjects during exercise, suggesting that this response represents theimpaired exercise capacity of patients with PD with cardiac sympathetic denervation. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>MIBG</term></item><item><term>exercise test</term></item><item><term>cardiac contractility</term></item><item><term>cardiac sympathetic denervation</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2009-06-19">Received</change><change when="2009-03-03">Registration</change><change when="2010-07-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CD1424095BEC67D0BADC8331EAFFCB109F910FAE/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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Sixteen patients with PD were divided into two groups, according to their cardiac uptake of <sup>123</sup>I‐metaiodobenzylguanidine (denervated group, 10 patients with heart to mediastinum (H/M) ratio < 1.7; innervated group, six patients with H/M ratio > 1.7) and compared changes in blood pressure (BP), heart rate (HR), and cardiac contractility with 13 control subjects during ergometric exercise stress. Velocity index (VI), an indicator of cardiac contractility, was measured using impedance cardiography and recorded every minute. Exercise began at a power output of 20 W for the first 2 min and increased 10 W every 2 min to a maximal intensity of 60 W. All control subjects accomplished the procedure while six patients with PD could not continue after the first minute of 50 W loading. There were no significant differences in BP or HR change between the three groups. However, a significant reduction in VI was observed from the first minute of the 30 W workload in the denervated group compared to the control group. This lowered response continued till 50 W loading and was significantly different to the innervated group at 50 W loading. No significant VI changes were observed between the control and innervated groups throughout the exercise test. Patients with PD with reduced MIBG uptake had a lowered cardiac contractility than innervated subjects during exercise, suggesting that this response represents theimpaired exercise capacity of patients with PD with cardiac sympathetic denervation. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Lowered cardiac sympathetic nerve performance in response to exercise in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Cardiac Responses to Exercise in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Lowered cardiac sympathetic nerve performance in response to exercise in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Tomohiko</namePart><namePart type="family">Nakamura</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masaaki</namePart><namePart type="family">Hirayama</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Fumitada</namePart><namePart type="family">Yamashita</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kei</namePart><namePart type="family">Uchida</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tetsuo</namePart><namePart type="family">Hama</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hirohisa</namePart><namePart type="family">Watanabe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gen</namePart><namePart type="family">Sobue</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Nagoya University Graduate School of Medicine, Showa‐ku, Nagoya, Japan</affiliation><description>Correspondence: Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai‐cho, Showa‐ku, Nagoya 466‐8550, Japan</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-07-15</dateIssued><dateCaptured encoding="w3cdtf">2009-06-19</dateCaptured><dateValid encoding="w3cdtf">2009-03-03</dateValid><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">38</extent><extent unit="words">4466</extent></physicalDescription><abstract lang="en">We examined whether cardiac sympathetic denervation influences the cardiovascular response to exercise in Parkinson's disease (PD). Sixteen patients with PD were divided into two groups, according to their cardiac uptake of 123I‐metaiodobenzylguanidine (denervated group, 10 patients with heart to mediastinum (H/M) ratio < 1.7; innervated group, six patients with H/M ratio > 1.7) and compared changes in blood pressure (BP), heart rate (HR), and cardiac contractility with 13 control subjects during ergometric exercise stress. Velocity index (VI), an indicator of cardiac contractility, was measured using impedance cardiography and recorded every minute. Exercise began at a power output of 20 W for the first 2 min and increased 10 W every 2 min to a maximal intensity of 60 W. All control subjects accomplished the procedure while six patients with PD could not continue after the first minute of 50 W loading. There were no significant differences in BP or HR change between the three groups. However, a significant reduction in VI was observed from the first minute of the 30 W workload in the denervated group compared to the control group. This lowered response continued till 50 W loading and was significantly different to the innervated group at 50 W loading. No significant VI changes were observed between the control and innervated groups throughout the exercise test. Patients with PD with reduced MIBG uptake had a lowered cardiac contractility than innervated subjects during exercise, suggesting that this response represents theimpaired exercise capacity of patients with PD with cardiac sympathetic denervation. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>MIBG</topic><topic>exercise test</topic><topic>cardiac contractility</topic><topic>cardiac sympathetic denervation</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1183</start><end>1189</end><total>7</total></extent></part></relatedItem><identifier type="istex">CD1424095BEC67D0BADC8331EAFFCB109F910FAE</identifier><identifier type="DOI">10.1002/mds.23127</identifier><identifier type="ArticleID">MDS23127</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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