Narrowing of the Left Ventricular Cavity Associated With Transient Ventricular Wall Thickening Reduces Stroke Volume in Patients With Acute Myocarditis
It has been reported that some patients with acute myocarditis have transient ventricular thickening associated with narrowing of the left ventricular cavity caused by interstitial edema. The present study investigated this phenomenon in 20 patients with acute myocarditis. Based on the sum of the in...
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| Veröffentlicht in: | Circulation Journal 2003, Vol.67(6), pp.490-494 |
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| creator | Morimoto, Shin-ichiro Kato, Shigeru Hiramitsu, Shinya Uemura, Akihisa Ohtsuki, Masatsugu Kato, Yasuchika Sugiura, Atsushi Miyagishima, Kenji Iwase, Masatsugu Ito, Teruo Hishida, Hitoshi |
| description | It has been reported that some patients with acute myocarditis have transient ventricular thickening associated with narrowing of the left ventricular cavity caused by interstitial edema. The present study investigated this phenomenon in 20 patients with acute myocarditis. Based on the sum of the interventricular septal wall thickness and left ventricular posterior wall thickness (IVST + PWT), measured by M-mode echocardiography, patients were divided into group A (IVST + PWT ≥25 mm, n=12) and group B (IVST + PWT |
| doi_str_mv | 10.1253/circj.67.490 |
| format | Article |
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The present study investigated this phenomenon in 20 patients with acute myocarditis. Based on the sum of the interventricular septal wall thickness and left ventricular posterior wall thickness (IVST + PWT), measured by M-mode echocardiography, patients were divided into group A (IVST + PWT ≥25 mm, n=12) and group B (IVST + PWT <25 mm, n=8). The IVST + PWT was 31.8 ±3.5 mm in group A and 21.9±2.7 mm in group B (p<0.0001). The left ventricular end-diastolic dimension (LVDd) was 42.3±6.0 mm in group A and 49.4±6.7 mm in group B (p<0.05). The stroke volume (SV) was 41.1±20.5 ml and 73.0±32.3 ml in groups A and B, respectively (p<0.05). The left ventricular ejection fraction (LVEF) was similar in group A (47.9±13.0%) and group B (56.9±9.0%). The SV correlated inversely with IVST + PWT (r=-0.62, p<0.01), and directly with both the LVDd (r=0.95, p<0.0001) and LVEF (r=0.64, p<0.01). The LVDd correlated inversely with IVST + PWT (r=-0.62, p<0.01). In conclusion, the reduction in SV that occurs during the acute phase of myocarditis is not only the result of systolic dysfunction, but also of the concentric left ventricular wall thickening associated with myocardial interstitial edema, which results in narrowing of the left ventricular cavity at end diastole. (Circ J 2003; 67: 490 - 494)]]></description><identifier>ISSN: 1346-9843</identifier><identifier>EISSN: 1347-4820</identifier><identifier>DOI: 10.1253/circj.67.490</identifier><identifier>PMID: 12808264</identifier><language>eng</language><publisher>Kyoto: The Japanese Circulation Society</publisher><subject>Acute Disease ; Adolescent ; Adult ; Aged ; Biological and medical sciences ; Cardiology. Vascular system ; Child ; Convalescence ; Diastole ; Echocardiography ; Edema ; Edema - etiology ; Female ; Heart ; Heart Septum - pathology ; Heart Ventricles - diagnostic imaging ; Heart Ventricles - pathology ; Humans ; Male ; Medical sciences ; Middle Aged ; Myocarditis ; Myocarditis - complications ; Myocarditis - diagnostic imaging ; Myocarditis - pathology ; Myocarditis - physiopathology ; Myocarditis. Cardiomyopathies ; Myocardium - pathology ; Retrospective Studies ; Stroke Volume ; Ultrasonography ; Ventricular Dysfunction, Left - diagnostic imaging ; Ventricular Dysfunction, Left - etiology ; Ventricular Dysfunction, Left - pathology ; Ventricular Dysfunction, Left - physiopathology ; Wall thickness</subject><ispartof>Circulation Journal, 2003, Vol.67(6), pp.490-494</ispartof><rights>2003 THE JAPANESE CIRCULATION SOCIETY</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-d58618f886f358f5726855fd566e7c525bd8ce4c6df94d94cee3f46433357a823</citedby><cites>FETCH-LOGICAL-c503t-d58618f886f358f5726855fd566e7c525bd8ce4c6df94d94cee3f46433357a823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14898042$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12808264$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morimoto, Shin-ichiro</creatorcontrib><creatorcontrib>Kato, Shigeru</creatorcontrib><creatorcontrib>Hiramitsu, Shinya</creatorcontrib><creatorcontrib>Uemura, Akihisa</creatorcontrib><creatorcontrib>Ohtsuki, Masatsugu</creatorcontrib><creatorcontrib>Kato, Yasuchika</creatorcontrib><creatorcontrib>Sugiura, Atsushi</creatorcontrib><creatorcontrib>Miyagishima, Kenji</creatorcontrib><creatorcontrib>Iwase, Masatsugu</creatorcontrib><creatorcontrib>Ito, Teruo</creatorcontrib><creatorcontrib>Hishida, Hitoshi</creatorcontrib><title>Narrowing of the Left Ventricular Cavity Associated With Transient Ventricular Wall Thickening Reduces Stroke Volume in Patients With Acute Myocarditis</title><title>Circulation Journal</title><addtitle>Circ J</addtitle><description><![CDATA[It has been reported that some patients with acute myocarditis have transient ventricular thickening associated with narrowing of the left ventricular cavity caused by interstitial edema. The present study investigated this phenomenon in 20 patients with acute myocarditis. Based on the sum of the interventricular septal wall thickness and left ventricular posterior wall thickness (IVST + PWT), measured by M-mode echocardiography, patients were divided into group A (IVST + PWT ≥25 mm, n=12) and group B (IVST + PWT <25 mm, n=8). The IVST + PWT was 31.8 ±3.5 mm in group A and 21.9±2.7 mm in group B (p<0.0001). The left ventricular end-diastolic dimension (LVDd) was 42.3±6.0 mm in group A and 49.4±6.7 mm in group B (p<0.05). The stroke volume (SV) was 41.1±20.5 ml and 73.0±32.3 ml in groups A and B, respectively (p<0.05). The left ventricular ejection fraction (LVEF) was similar in group A (47.9±13.0%) and group B (56.9±9.0%). The SV correlated inversely with IVST + PWT (r=-0.62, p<0.01), and directly with both the LVDd (r=0.95, p<0.0001) and LVEF (r=0.64, p<0.01). The LVDd correlated inversely with IVST + PWT (r=-0.62, p<0.01). In conclusion, the reduction in SV that occurs during the acute phase of myocarditis is not only the result of systolic dysfunction, but also of the concentric left ventricular wall thickening associated with myocardial interstitial edema, which results in narrowing of the left ventricular cavity at end diastole. (Circ J 2003; 67: 490 - 494)]]></description><subject>Acute Disease</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Child</subject><subject>Convalescence</subject><subject>Diastole</subject><subject>Echocardiography</subject><subject>Edema</subject><subject>Edema - etiology</subject><subject>Female</subject><subject>Heart</subject><subject>Heart Septum - pathology</subject><subject>Heart Ventricles - diagnostic imaging</subject><subject>Heart Ventricles - pathology</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocarditis</subject><subject>Myocarditis - complications</subject><subject>Myocarditis - diagnostic imaging</subject><subject>Myocarditis - pathology</subject><subject>Myocarditis - physiopathology</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Myocardium - pathology</subject><subject>Retrospective Studies</subject><subject>Stroke Volume</subject><subject>Ultrasonography</subject><subject>Ventricular Dysfunction, Left - diagnostic imaging</subject><subject>Ventricular Dysfunction, Left - etiology</subject><subject>Ventricular Dysfunction, Left - pathology</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><subject>Wall thickness</subject><issn>1346-9843</issn><issn>1347-4820</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUtvEzEUhS0EoiWwY428gRUTPOPHeJZRBAUpPAShXVqufd04dcbF9hTll_B3mXQiIjbXV_Lnc6xzEHpZk3ndcPrO-GS2c9HOWUceofOasrZisiGPH3ZRdZLRM_Qs5y0hTUd49xSd1Y0kshHsHP35olOKv31_g6PDZQN4Ba7gS-hL8mYIOuGlvvdljxc5R-N1AYuvfNngddJ99iP3H3ylQ8DrjTe30B9Ev4MdDGT8o6R4C_gyhmEH2Pf4my6Hx3kSW5ihAP68j0Yn64vPz9ETp0OGF8dzhn5-eL9efqxWXy8-LRerynBCS2W5FLV0UgpHuXS8bYTk3FkuBLSGN_zaSgPMCOs6ZjtmAKhjglFKeatlQ2fozaR7l-KvAXJRO58NhKB7iENWLaWtEGPOM_R2Ak2KOSdw6i75nU57VRN1KEI9FKFEq8YiRvzVUXe43oE9wcfkR-D1EdDZ6ODGNI3PJ47JThJ2-OBi4ra56Bv4B-hUvAlwchXTGM1PdxudFPT0L689q_I</recordid><startdate>20030601</startdate><enddate>20030601</enddate><creator>Morimoto, Shin-ichiro</creator><creator>Kato, Shigeru</creator><creator>Hiramitsu, Shinya</creator><creator>Uemura, Akihisa</creator><creator>Ohtsuki, Masatsugu</creator><creator>Kato, Yasuchika</creator><creator>Sugiura, Atsushi</creator><creator>Miyagishima, Kenji</creator><creator>Iwase, Masatsugu</creator><creator>Ito, Teruo</creator><creator>Hishida, Hitoshi</creator><general>The Japanese Circulation Society</general><general>Japanese Circulation Society</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20030601</creationdate><title>Narrowing of the Left Ventricular Cavity Associated With Transient Ventricular Wall Thickening Reduces Stroke Volume in Patients With Acute Myocarditis</title><author>Morimoto, Shin-ichiro ; Kato, Shigeru ; Hiramitsu, Shinya ; Uemura, Akihisa ; Ohtsuki, Masatsugu ; Kato, Yasuchika ; Sugiura, Atsushi ; Miyagishima, Kenji ; Iwase, Masatsugu ; Ito, Teruo ; Hishida, Hitoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-d58618f886f358f5726855fd566e7c525bd8ce4c6df94d94cee3f46433357a823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acute Disease</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Child</topic><topic>Convalescence</topic><topic>Diastole</topic><topic>Echocardiography</topic><topic>Edema</topic><topic>Edema - etiology</topic><topic>Female</topic><topic>Heart</topic><topic>Heart Septum - pathology</topic><topic>Heart Ventricles - diagnostic imaging</topic><topic>Heart Ventricles - pathology</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocarditis</topic><topic>Myocarditis - complications</topic><topic>Myocarditis - diagnostic imaging</topic><topic>Myocarditis - pathology</topic><topic>Myocarditis - physiopathology</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Myocardium - pathology</topic><topic>Retrospective Studies</topic><topic>Stroke Volume</topic><topic>Ultrasonography</topic><topic>Ventricular Dysfunction, Left - diagnostic imaging</topic><topic>Ventricular Dysfunction, Left - etiology</topic><topic>Ventricular Dysfunction, Left - pathology</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><topic>Wall thickness</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morimoto, Shin-ichiro</creatorcontrib><creatorcontrib>Kato, Shigeru</creatorcontrib><creatorcontrib>Hiramitsu, Shinya</creatorcontrib><creatorcontrib>Uemura, Akihisa</creatorcontrib><creatorcontrib>Ohtsuki, Masatsugu</creatorcontrib><creatorcontrib>Kato, Yasuchika</creatorcontrib><creatorcontrib>Sugiura, Atsushi</creatorcontrib><creatorcontrib>Miyagishima, Kenji</creatorcontrib><creatorcontrib>Iwase, Masatsugu</creatorcontrib><creatorcontrib>Ito, Teruo</creatorcontrib><creatorcontrib>Hishida, Hitoshi</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morimoto, Shin-ichiro</au><au>Kato, Shigeru</au><au>Hiramitsu, Shinya</au><au>Uemura, Akihisa</au><au>Ohtsuki, Masatsugu</au><au>Kato, Yasuchika</au><au>Sugiura, Atsushi</au><au>Miyagishima, Kenji</au><au>Iwase, Masatsugu</au><au>Ito, Teruo</au><au>Hishida, Hitoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Narrowing of the Left Ventricular Cavity Associated With Transient Ventricular Wall Thickening Reduces Stroke Volume in Patients With Acute Myocarditis</atitle><jtitle>Circulation Journal</jtitle><addtitle>Circ J</addtitle><date>2003-06-01</date><risdate>2003</risdate><volume>67</volume><issue>6</issue><spage>490</spage><epage>494</epage><pages>490-494</pages><issn>1346-9843</issn><eissn>1347-4820</eissn><abstract><![CDATA[It has been reported that some patients with acute myocarditis have transient ventricular thickening associated with narrowing of the left ventricular cavity caused by interstitial edema. The present study investigated this phenomenon in 20 patients with acute myocarditis. Based on the sum of the interventricular septal wall thickness and left ventricular posterior wall thickness (IVST + PWT), measured by M-mode echocardiography, patients were divided into group A (IVST + PWT ≥25 mm, n=12) and group B (IVST + PWT <25 mm, n=8). The IVST + PWT was 31.8 ±3.5 mm in group A and 21.9±2.7 mm in group B (p<0.0001). The left ventricular end-diastolic dimension (LVDd) was 42.3±6.0 mm in group A and 49.4±6.7 mm in group B (p<0.05). The stroke volume (SV) was 41.1±20.5 ml and 73.0±32.3 ml in groups A and B, respectively (p<0.05). The left ventricular ejection fraction (LVEF) was similar in group A (47.9±13.0%) and group B (56.9±9.0%). The SV correlated inversely with IVST + PWT (r=-0.62, p<0.01), and directly with both the LVDd (r=0.95, p<0.0001) and LVEF (r=0.64, p<0.01). The LVDd correlated inversely with IVST + PWT (r=-0.62, p<0.01). In conclusion, the reduction in SV that occurs during the acute phase of myocarditis is not only the result of systolic dysfunction, but also of the concentric left ventricular wall thickening associated with myocardial interstitial edema, which results in narrowing of the left ventricular cavity at end diastole. (Circ J 2003; 67: 490 - 494)]]></abstract><cop>Kyoto</cop><pub>The Japanese Circulation Society</pub><pmid>12808264</pmid><doi>10.1253/circj.67.490</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease Adolescent Adult Aged Biological and medical sciences Cardiology. Vascular system Child Convalescence Diastole Echocardiography Edema Edema - etiology Female Heart Heart Septum - pathology Heart Ventricles - diagnostic imaging Heart Ventricles - pathology Humans Male Medical sciences Middle Aged Myocarditis Myocarditis - complications Myocarditis - diagnostic imaging Myocarditis - pathology Myocarditis - physiopathology Myocarditis. Cardiomyopathies Myocardium - pathology Retrospective Studies Stroke Volume Ultrasonography Ventricular Dysfunction, Left - diagnostic imaging Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - pathology Ventricular Dysfunction, Left - physiopathology Wall thickness |
| title | Narrowing of the Left Ventricular Cavity Associated With Transient Ventricular Wall Thickening Reduces Stroke Volume in Patients With Acute Myocarditis |
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