Mechanical alternans in human idiopathic dilated cardiomyopathy is caused with impaired force–frequency relationship and enhanced poststimulation potentiation
Mechanical alternans (MA) is frequently observed in patients with heart failure, and is a predictor of cardiac events. However, there have been controversies regarding the conditions and mechanisms of MA. To clarify heart rate-dependent contractile properties related to MA, we performed incremental...
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| Veröffentlicht in: | Heart and vessels 2013-05, Vol.28 (3), p.336-344 |
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| creator | Kashimura, Takeshi Kodama, Makoto Tanaka, Komei Sonoda, Keiko Watanabe, Satoru Ohno, Yukako Tomita, Makoto Obata, Hiroaki Mitsuma, Wataru Ito, Masahiro Hirono, Satoru Hanawa, Haruo Aizawa, Yoshifusa |
| description | Mechanical alternans (MA) is frequently observed in patients with heart failure, and is a predictor of cardiac events. However, there have been controversies regarding the conditions and mechanisms of MA. To clarify heart rate-dependent contractile properties related to MA, we performed incremental right atrial pacing in 17 idiopathic dilated cardiomyopathy (DCM) patients and in six control patients. The maximal increase in left ventricular d
P
/d
t
during pacing-induced tachycardia was assessed as the force gain in the force–frequency relationship (FG-FFR), and the maximal increase in left ventricular d
P
/d
t
of the first post-pacing beats was examined as the force gain in poststimulation potentiation (FG-PSP). As a result, MA was induced in 9 DCM patients (DCM MA(+)) but not in the other 8 DCM patients (DCM MA(−)), and not in any of the control patients. DCM MA(+) had significantly lower FG-FFR (34.7 ± 40.9 vs 159.4 ± 103.9 mmHg/s,
P
= 0.0091) and higher FG-PSP (500.0 ± 96.8 vs 321.9 ± 94.9 mmHg/s,
P
= 0.0017), and accordingly a wider gap between FG-PSP and FG-FFR (465.3 ± 119.4 vs 162.5 ± 123.6 mmHg/s,
P
= 0.0001) than DCM MA(−) patients. These characteristics of DCM MA(+) showed clear contrasts to those of the control patients. In conclusion, MA is caused with an impaired force–frequency relationship despite significant poststimulation potentiation, suggesting that MA reflects ineffective utilization of the potentiated intrinsic force during tachycardia. |
| doi_str_mv | 10.1007/s00380-012-0251-8 |
| format | Article |
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P
/d
t
during pacing-induced tachycardia was assessed as the force gain in the force–frequency relationship (FG-FFR), and the maximal increase in left ventricular d
P
/d
t
of the first post-pacing beats was examined as the force gain in poststimulation potentiation (FG-PSP). As a result, MA was induced in 9 DCM patients (DCM MA(+)) but not in the other 8 DCM patients (DCM MA(−)), and not in any of the control patients. DCM MA(+) had significantly lower FG-FFR (34.7 ± 40.9 vs 159.4 ± 103.9 mmHg/s,
P
= 0.0091) and higher FG-PSP (500.0 ± 96.8 vs 321.9 ± 94.9 mmHg/s,
P
= 0.0017), and accordingly a wider gap between FG-PSP and FG-FFR (465.3 ± 119.4 vs 162.5 ± 123.6 mmHg/s,
P
= 0.0001) than DCM MA(−) patients. These characteristics of DCM MA(+) showed clear contrasts to those of the control patients. In conclusion, MA is caused with an impaired force–frequency relationship despite significant poststimulation potentiation, suggesting that MA reflects ineffective utilization of the potentiated intrinsic force during tachycardia.</description><identifier>ISSN: 0910-8327</identifier><identifier>EISSN: 1615-2573</identifier><identifier>DOI: 10.1007/s00380-012-0251-8</identifier><identifier>PMID: 22573070</identifier><identifier>CODEN: HEVEEO</identifier><language>eng</language><publisher>Japan: Springer Japan</publisher><subject>Adult ; Biomedical Engineering and Bioengineering ; Calcium ; Cardiac arrhythmia ; Cardiac Catheterization ; Cardiac Pacing, Artificial ; Cardiac Surgery ; Cardiology ; Cardiomyocytes ; Cardiomyopathy, Dilated - diagnosis ; Cardiomyopathy, Dilated - physiopathology ; Cardiovascular disease ; Case-Control Studies ; Electrocardiography ; Electrophysiologic Techniques, Cardiac ; Female ; Heart Rate ; Humans ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Myocardial Contraction ; Original Article ; Tachycardia, Ventricular - diagnosis ; Tachycardia, Ventricular - physiopathology ; Time Factors ; Vascular Surgery ; Ventricular Function, Left ; Ventricular Function, Right ; Ventricular Pressure</subject><ispartof>Heart and vessels, 2013-05, Vol.28 (3), p.336-344</ispartof><rights>Springer 2012</rights><rights>Springer Japan 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-6367d5fdfe4c1b3fc82cb5d43c561a0b01c16676405825fc55708e4083a4f02f3</citedby><cites>FETCH-LOGICAL-c396t-6367d5fdfe4c1b3fc82cb5d43c561a0b01c16676405825fc55708e4083a4f02f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00380-012-0251-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00380-012-0251-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22573070$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kashimura, Takeshi</creatorcontrib><creatorcontrib>Kodama, Makoto</creatorcontrib><creatorcontrib>Tanaka, Komei</creatorcontrib><creatorcontrib>Sonoda, Keiko</creatorcontrib><creatorcontrib>Watanabe, Satoru</creatorcontrib><creatorcontrib>Ohno, Yukako</creatorcontrib><creatorcontrib>Tomita, Makoto</creatorcontrib><creatorcontrib>Obata, Hiroaki</creatorcontrib><creatorcontrib>Mitsuma, Wataru</creatorcontrib><creatorcontrib>Ito, Masahiro</creatorcontrib><creatorcontrib>Hirono, Satoru</creatorcontrib><creatorcontrib>Hanawa, Haruo</creatorcontrib><creatorcontrib>Aizawa, Yoshifusa</creatorcontrib><title>Mechanical alternans in human idiopathic dilated cardiomyopathy is caused with impaired force–frequency relationship and enhanced poststimulation potentiation</title><title>Heart and vessels</title><addtitle>Heart Vessels</addtitle><addtitle>Heart Vessels</addtitle><description>Mechanical alternans (MA) is frequently observed in patients with heart failure, and is a predictor of cardiac events. However, there have been controversies regarding the conditions and mechanisms of MA. To clarify heart rate-dependent contractile properties related to MA, we performed incremental right atrial pacing in 17 idiopathic dilated cardiomyopathy (DCM) patients and in six control patients. The maximal increase in left ventricular d
P
/d
t
during pacing-induced tachycardia was assessed as the force gain in the force–frequency relationship (FG-FFR), and the maximal increase in left ventricular d
P
/d
t
of the first post-pacing beats was examined as the force gain in poststimulation potentiation (FG-PSP). As a result, MA was induced in 9 DCM patients (DCM MA(+)) but not in the other 8 DCM patients (DCM MA(−)), and not in any of the control patients. DCM MA(+) had significantly lower FG-FFR (34.7 ± 40.9 vs 159.4 ± 103.9 mmHg/s,
P
= 0.0091) and higher FG-PSP (500.0 ± 96.8 vs 321.9 ± 94.9 mmHg/s,
P
= 0.0017), and accordingly a wider gap between FG-PSP and FG-FFR (465.3 ± 119.4 vs 162.5 ± 123.6 mmHg/s,
P
= 0.0001) than DCM MA(−) patients. These characteristics of DCM MA(+) showed clear contrasts to those of the control patients. In conclusion, MA is caused with an impaired force–frequency relationship despite significant poststimulation potentiation, suggesting that MA reflects ineffective utilization of the potentiated intrinsic force during tachycardia.</description><subject>Adult</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Calcium</subject><subject>Cardiac arrhythmia</subject><subject>Cardiac Catheterization</subject><subject>Cardiac Pacing, Artificial</subject><subject>Cardiac Surgery</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy, Dilated - diagnosis</subject><subject>Cardiomyopathy, Dilated - physiopathology</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Electrocardiography</subject><subject>Electrophysiologic Techniques, Cardiac</subject><subject>Female</subject><subject>Heart Rate</subject><subject>Humans</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Myocardial Contraction</subject><subject>Original Article</subject><subject>Tachycardia, Ventricular - diagnosis</subject><subject>Tachycardia, Ventricular - physiopathology</subject><subject>Time Factors</subject><subject>Vascular Surgery</subject><subject>Ventricular Function, Left</subject><subject>Ventricular Function, Right</subject><subject>Ventricular Pressure</subject><issn>0910-8327</issn><issn>1615-2573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kc1u1TAQhS0EopeWB2CDLLFhExjb8U-WqOKnUhEburZ8HZu4SpxgO0J313fgBXg2nqS-TUEIqSvrzHxzZuSD0AsCbwiAfJsBmIIGCG2ActKoR2hHBOEN5ZI9RjvoCDSKUXmCnuV8DUB4R7qn6IQeAZCwQ78-OzuYGKwZsRmLS9HEjEPEwzqZiEMf5sWUIVjch9EU12NrUi1Oh7v6AYdcK2uujR-hDDhMiwmpKj8n637f_PTJfV9dtAecXDUIc8xDWLCJPXaxbraVXeZccgnTugFVFxdLuBNn6Ik3Y3bP799TdPXh_dfzT83ll48X5-8uG8s6URrBhOy5771rLdkzbxW1e963zHJBDOyBWCKEFC1wRbm3nEtQrgXFTOuBenaKXm--S5rrwbnoKWTrxtFEN69ZE8ZZp7hoSUVf_Ydez2v9uHGjqJCS0kqRjbJpzjk5r5cUJpMOmoA-xqe3-HSNTx_j06rOvLx3XveT6_9O_MmrAnQDcm3Fby79s_pB11sI_aoR</recordid><startdate>20130501</startdate><enddate>20130501</enddate><creator>Kashimura, Takeshi</creator><creator>Kodama, Makoto</creator><creator>Tanaka, Komei</creator><creator>Sonoda, Keiko</creator><creator>Watanabe, Satoru</creator><creator>Ohno, Yukako</creator><creator>Tomita, Makoto</creator><creator>Obata, Hiroaki</creator><creator>Mitsuma, Wataru</creator><creator>Ito, Masahiro</creator><creator>Hirono, Satoru</creator><creator>Hanawa, Haruo</creator><creator>Aizawa, Yoshifusa</creator><general>Springer Japan</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20130501</creationdate><title>Mechanical alternans in human idiopathic dilated cardiomyopathy is caused with impaired force–frequency relationship and enhanced poststimulation potentiation</title><author>Kashimura, Takeshi ; Kodama, Makoto ; Tanaka, Komei ; Sonoda, Keiko ; Watanabe, Satoru ; Ohno, Yukako ; Tomita, Makoto ; Obata, Hiroaki ; Mitsuma, Wataru ; Ito, Masahiro ; Hirono, Satoru ; Hanawa, Haruo ; Aizawa, Yoshifusa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-6367d5fdfe4c1b3fc82cb5d43c561a0b01c16676405825fc55708e4083a4f02f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Biomedical Engineering and Bioengineering</topic><topic>Calcium</topic><topic>Cardiac arrhythmia</topic><topic>Cardiac Catheterization</topic><topic>Cardiac Pacing, Artificial</topic><topic>Cardiac Surgery</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy, Dilated - diagnosis</topic><topic>Cardiomyopathy, Dilated - physiopathology</topic><topic>Cardiovascular disease</topic><topic>Case-Control Studies</topic><topic>Electrocardiography</topic><topic>Electrophysiologic Techniques, Cardiac</topic><topic>Female</topic><topic>Heart Rate</topic><topic>Humans</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Myocardial Contraction</topic><topic>Original Article</topic><topic>Tachycardia, Ventricular - diagnosis</topic><topic>Tachycardia, Ventricular - physiopathology</topic><topic>Time Factors</topic><topic>Vascular Surgery</topic><topic>Ventricular Function, Left</topic><topic>Ventricular Function, Right</topic><topic>Ventricular Pressure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kashimura, Takeshi</creatorcontrib><creatorcontrib>Kodama, Makoto</creatorcontrib><creatorcontrib>Tanaka, Komei</creatorcontrib><creatorcontrib>Sonoda, Keiko</creatorcontrib><creatorcontrib>Watanabe, Satoru</creatorcontrib><creatorcontrib>Ohno, Yukako</creatorcontrib><creatorcontrib>Tomita, Makoto</creatorcontrib><creatorcontrib>Obata, Hiroaki</creatorcontrib><creatorcontrib>Mitsuma, Wataru</creatorcontrib><creatorcontrib>Ito, Masahiro</creatorcontrib><creatorcontrib>Hirono, Satoru</creatorcontrib><creatorcontrib>Hanawa, Haruo</creatorcontrib><creatorcontrib>Aizawa, Yoshifusa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Heart and vessels</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kashimura, Takeshi</au><au>Kodama, Makoto</au><au>Tanaka, Komei</au><au>Sonoda, Keiko</au><au>Watanabe, Satoru</au><au>Ohno, Yukako</au><au>Tomita, Makoto</au><au>Obata, Hiroaki</au><au>Mitsuma, Wataru</au><au>Ito, Masahiro</au><au>Hirono, Satoru</au><au>Hanawa, Haruo</au><au>Aizawa, Yoshifusa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanical alternans in human idiopathic dilated cardiomyopathy is caused with impaired force–frequency relationship and enhanced poststimulation potentiation</atitle><jtitle>Heart and vessels</jtitle><stitle>Heart Vessels</stitle><addtitle>Heart Vessels</addtitle><date>2013-05-01</date><risdate>2013</risdate><volume>28</volume><issue>3</issue><spage>336</spage><epage>344</epage><pages>336-344</pages><issn>0910-8327</issn><eissn>1615-2573</eissn><coden>HEVEEO</coden><abstract>Mechanical alternans (MA) is frequently observed in patients with heart failure, and is a predictor of cardiac events. However, there have been controversies regarding the conditions and mechanisms of MA. To clarify heart rate-dependent contractile properties related to MA, we performed incremental right atrial pacing in 17 idiopathic dilated cardiomyopathy (DCM) patients and in six control patients. The maximal increase in left ventricular d
P
/d
t
during pacing-induced tachycardia was assessed as the force gain in the force–frequency relationship (FG-FFR), and the maximal increase in left ventricular d
P
/d
t
of the first post-pacing beats was examined as the force gain in poststimulation potentiation (FG-PSP). As a result, MA was induced in 9 DCM patients (DCM MA(+)) but not in the other 8 DCM patients (DCM MA(−)), and not in any of the control patients. DCM MA(+) had significantly lower FG-FFR (34.7 ± 40.9 vs 159.4 ± 103.9 mmHg/s,
P
= 0.0091) and higher FG-PSP (500.0 ± 96.8 vs 321.9 ± 94.9 mmHg/s,
P
= 0.0017), and accordingly a wider gap between FG-PSP and FG-FFR (465.3 ± 119.4 vs 162.5 ± 123.6 mmHg/s,
P
= 0.0001) than DCM MA(−) patients. These characteristics of DCM MA(+) showed clear contrasts to those of the control patients. In conclusion, MA is caused with an impaired force–frequency relationship despite significant poststimulation potentiation, suggesting that MA reflects ineffective utilization of the potentiated intrinsic force during tachycardia.</abstract><cop>Japan</cop><pub>Springer Japan</pub><pmid>22573070</pmid><doi>10.1007/s00380-012-0251-8</doi><tpages>9</tpages></addata></record> |
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| ispartof | Heart and vessels, 2013-05, Vol.28 (3), p.336-344 |
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| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Adult Biomedical Engineering and Bioengineering Calcium Cardiac arrhythmia Cardiac Catheterization Cardiac Pacing, Artificial Cardiac Surgery Cardiology Cardiomyocytes Cardiomyopathy, Dilated - diagnosis Cardiomyopathy, Dilated - physiopathology Cardiovascular disease Case-Control Studies Electrocardiography Electrophysiologic Techniques, Cardiac Female Heart Rate Humans Male Medicine Medicine & Public Health Middle Aged Myocardial Contraction Original Article Tachycardia, Ventricular - diagnosis Tachycardia, Ventricular - physiopathology Time Factors Vascular Surgery Ventricular Function, Left Ventricular Function, Right Ventricular Pressure |
| title | Mechanical alternans in human idiopathic dilated cardiomyopathy is caused with impaired force–frequency relationship and enhanced poststimulation potentiation |
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