Effect of levosimendan therapy on myocardial infarct size and left ventricular function after acute coronary occlusion
BackgroundLevosimendan is an inotropic agent with cardioprotective and vasodilating properties used for the management of acutely decompensated heart failure. We studied the effects of levosimendan treatment on the size of myocardial infarction (MI) and left ventricular (LV) function in experimental...
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| Veröffentlicht in: | Heart (British Cardiac Society) 2016-03, Vol.102 (6), p.465-471 |
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| creator | Tarkia, Miikka Stark, Christoffer Haavisto, Matti Kentala, Rasmus Vähäsilta, Tommi Savunen, Timo Strandberg, Marjatta Saunavaara, Virva Tolvanen, Tuula Teräs, Mika Pietilä, Mikko Nyman, Leena Duvall, Emma Saukko, Pekka Levijoki, Jouko Roivainen, Anne Saraste, Antti Knuuti, Juhani |
| description | BackgroundLevosimendan is an inotropic agent with cardioprotective and vasodilating properties used for the management of acutely decompensated heart failure. We studied the effects of levosimendan treatment on the size of myocardial infarction (MI) and left ventricular (LV) function in experimental pig model of post MI heart failure.MethodsAfter occlusion of the left anterior descending (LAD) coronary artery, animals received levosimendan 5 mg/kg/day orally for 8 weeks (n=7) or no treatment (n=18). One week after stopping treatment, transthoracic echocardiography, CT scan and positron emission tomography were performed to evaluate myocardial function, perfusion and oxidative metabolism. Histology was used to confirm the size of MI and features of LV remodelling.ResultsThe size of MI was significantly smaller in the levosimendan group than in the controls (12±13% vs 27±15% of the LV, p=0.03). End-diastolic volume (EDV) and end-systolic volume (ESV) were smaller in the levosimendan than in the control group (EDV 161±29 mL vs 245±84 mL, p=0.06; ESV 81±18 mL vs 149±67 mL, p=0.03), whereas ejection fraction tended to be higher in the levosimendan group (50±6% vs 41±8%, p=0.06).ConclusionsEight weeks of levosimendan therapy after recent LAD occlusion decreases the size of MI and leads to better preservation of LV function as well as reduced LV remodelling. |
| doi_str_mv | 10.1136/heartjnl-2015-308137 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1768557375</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1768557375</sourcerecordid><originalsourceid>FETCH-LOGICAL-b375t-42b4f10d7054de1b5d8af002daf59e58274fea16dcb77af85f7cd9c44fdb056f3</originalsourceid><addsrcrecordid>eNqNkU9LHDEYxkOxVN32G5QS8NLLdJOZ_NtjEasFoZcK3oZM8r44y0yyTTIL9tObZdWDJ08Jye958udHyFfOfnDeqfUD2FS2YWpaxmXTMcM7_YGccaHMYen-pM47KRvFOn1KznPeMsbExqhP5LRVWrVtZ87I_goRXKER6QT7mMcZgreBlgdIdvdIY6DzY3Q2-dFOdAxoU6Xz-B-oDb5msNA9hJJGt0w2UVyCK2NNWSyQqHVLAepiisGm2ubctOS6_Zl8RDtl-PI8rsjdr6u_lzfN7Z_r35c_b5uh07I0oh0EcuY1k8IDH6Q3FhlrvUW5AWlaLRAsV94NWls0ErXzGycE-oFJhd2KfD_27lL8t0Au_TxmB9NkA8Ql91wrI6Wuh1X04g26jUsK9XaVMrx-qRK8UuJIuRRzToD9Lo1zfVvPWX_w0r946Q9e-qOXGvv2XL4MM_jX0IuICqyPwDBv31f5BD7FnTQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1781201641</pqid></control><display><type>article</type><title>Effect of levosimendan therapy on myocardial infarct size and left ventricular function after acute coronary occlusion</title><source>MEDLINE</source><source>BMJ Journals - NESLi2</source><source>PubMed Central</source><creator>Tarkia, Miikka ; Stark, Christoffer ; Haavisto, Matti ; Kentala, Rasmus ; Vähäsilta, Tommi ; Savunen, Timo ; Strandberg, Marjatta ; Saunavaara, Virva ; Tolvanen, Tuula ; Teräs, Mika ; Pietilä, Mikko ; Nyman, Leena ; Duvall, Emma ; Saukko, Pekka ; Levijoki, Jouko ; Roivainen, Anne ; Saraste, Antti ; Knuuti, Juhani</creator><creatorcontrib>Tarkia, Miikka ; Stark, Christoffer ; Haavisto, Matti ; Kentala, Rasmus ; Vähäsilta, Tommi ; Savunen, Timo ; Strandberg, Marjatta ; Saunavaara, Virva ; Tolvanen, Tuula ; Teräs, Mika ; Pietilä, Mikko ; Nyman, Leena ; Duvall, Emma ; Saukko, Pekka ; Levijoki, Jouko ; Roivainen, Anne ; Saraste, Antti ; Knuuti, Juhani</creatorcontrib><description>BackgroundLevosimendan is an inotropic agent with cardioprotective and vasodilating properties used for the management of acutely decompensated heart failure. We studied the effects of levosimendan treatment on the size of myocardial infarction (MI) and left ventricular (LV) function in experimental pig model of post MI heart failure.MethodsAfter occlusion of the left anterior descending (LAD) coronary artery, animals received levosimendan 5 mg/kg/day orally for 8 weeks (n=7) or no treatment (n=18). One week after stopping treatment, transthoracic echocardiography, CT scan and positron emission tomography were performed to evaluate myocardial function, perfusion and oxidative metabolism. Histology was used to confirm the size of MI and features of LV remodelling.ResultsThe size of MI was significantly smaller in the levosimendan group than in the controls (12±13% vs 27±15% of the LV, p=0.03). End-diastolic volume (EDV) and end-systolic volume (ESV) were smaller in the levosimendan than in the control group (EDV 161±29 mL vs 245±84 mL, p=0.06; ESV 81±18 mL vs 149±67 mL, p=0.03), whereas ejection fraction tended to be higher in the levosimendan group (50±6% vs 41±8%, p=0.06).ConclusionsEight weeks of levosimendan therapy after recent LAD occlusion decreases the size of MI and leads to better preservation of LV function as well as reduced LV remodelling.</description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/heartjnl-2015-308137</identifier><identifier>PMID: 26762238</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>Acute Disease ; Animals ; Cardiomyocytes ; Cardiotonic Agents - therapeutic use ; Coronary Occlusion - complications ; Coronary vessels ; Diastole ; Disease Models, Animal ; Drug dosages ; Follow-Up Studies ; Heart attacks ; Heart failure ; Hogs ; Hydrazones - therapeutic use ; Male ; Medical imaging ; Medical research ; Metabolites ; Myocardial Contraction - drug effects ; Myocardial Contraction - physiology ; Myocardial Infarction - drug therapy ; Myocardial Infarction - etiology ; Myocardial Infarction - physiopathology ; Myocardium - pathology ; Pyridazines - therapeutic use ; Rodents ; Stroke Volume - drug effects ; Stroke Volume - physiology ; Studies ; Swine ; Systole ; Veins & arteries ; Ventricular Function, Left - drug effects ; Ventricular Function, Left - physiology ; Ventricular Remodeling - drug effects</subject><ispartof>Heart (British Cardiac Society), 2016-03, Vol.102 (6), p.465-471</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><rights>Copyright: 2016 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b375t-42b4f10d7054de1b5d8af002daf59e58274fea16dcb77af85f7cd9c44fdb056f3</citedby><cites>FETCH-LOGICAL-b375t-42b4f10d7054de1b5d8af002daf59e58274fea16dcb77af85f7cd9c44fdb056f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://heart.bmj.com/content/102/6/465.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttps://heart.bmj.com/content/102/6/465.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,778,782,3185,23554,27907,27908,77351,77382</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26762238$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tarkia, Miikka</creatorcontrib><creatorcontrib>Stark, Christoffer</creatorcontrib><creatorcontrib>Haavisto, Matti</creatorcontrib><creatorcontrib>Kentala, Rasmus</creatorcontrib><creatorcontrib>Vähäsilta, Tommi</creatorcontrib><creatorcontrib>Savunen, Timo</creatorcontrib><creatorcontrib>Strandberg, Marjatta</creatorcontrib><creatorcontrib>Saunavaara, Virva</creatorcontrib><creatorcontrib>Tolvanen, Tuula</creatorcontrib><creatorcontrib>Teräs, Mika</creatorcontrib><creatorcontrib>Pietilä, Mikko</creatorcontrib><creatorcontrib>Nyman, Leena</creatorcontrib><creatorcontrib>Duvall, Emma</creatorcontrib><creatorcontrib>Saukko, Pekka</creatorcontrib><creatorcontrib>Levijoki, Jouko</creatorcontrib><creatorcontrib>Roivainen, Anne</creatorcontrib><creatorcontrib>Saraste, Antti</creatorcontrib><creatorcontrib>Knuuti, Juhani</creatorcontrib><title>Effect of levosimendan therapy on myocardial infarct size and left ventricular function after acute coronary occlusion</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><description>BackgroundLevosimendan is an inotropic agent with cardioprotective and vasodilating properties used for the management of acutely decompensated heart failure. We studied the effects of levosimendan treatment on the size of myocardial infarction (MI) and left ventricular (LV) function in experimental pig model of post MI heart failure.MethodsAfter occlusion of the left anterior descending (LAD) coronary artery, animals received levosimendan 5 mg/kg/day orally for 8 weeks (n=7) or no treatment (n=18). One week after stopping treatment, transthoracic echocardiography, CT scan and positron emission tomography were performed to evaluate myocardial function, perfusion and oxidative metabolism. Histology was used to confirm the size of MI and features of LV remodelling.ResultsThe size of MI was significantly smaller in the levosimendan group than in the controls (12±13% vs 27±15% of the LV, p=0.03). End-diastolic volume (EDV) and end-systolic volume (ESV) were smaller in the levosimendan than in the control group (EDV 161±29 mL vs 245±84 mL, p=0.06; ESV 81±18 mL vs 149±67 mL, p=0.03), whereas ejection fraction tended to be higher in the levosimendan group (50±6% vs 41±8%, p=0.06).ConclusionsEight weeks of levosimendan therapy after recent LAD occlusion decreases the size of MI and leads to better preservation of LV function as well as reduced LV remodelling.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Cardiomyocytes</subject><subject>Cardiotonic Agents - therapeutic use</subject><subject>Coronary Occlusion - complications</subject><subject>Coronary vessels</subject><subject>Diastole</subject><subject>Disease Models, Animal</subject><subject>Drug dosages</subject><subject>Follow-Up Studies</subject><subject>Heart attacks</subject><subject>Heart failure</subject><subject>Hogs</subject><subject>Hydrazones - therapeutic use</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Medical research</subject><subject>Metabolites</subject><subject>Myocardial Contraction - drug effects</subject><subject>Myocardial Contraction - physiology</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - etiology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardium - pathology</subject><subject>Pyridazines - therapeutic use</subject><subject>Rodents</subject><subject>Stroke Volume - drug effects</subject><subject>Stroke Volume - physiology</subject><subject>Studies</subject><subject>Swine</subject><subject>Systole</subject><subject>Veins & arteries</subject><subject>Ventricular Function, Left - drug effects</subject><subject>Ventricular Function, Left - physiology</subject><subject>Ventricular Remodeling - drug effects</subject><issn>1355-6037</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkU9LHDEYxkOxVN32G5QS8NLLdJOZ_NtjEasFoZcK3oZM8r44y0yyTTIL9tObZdWDJ08Jye958udHyFfOfnDeqfUD2FS2YWpaxmXTMcM7_YGccaHMYen-pM47KRvFOn1KznPeMsbExqhP5LRVWrVtZ87I_goRXKER6QT7mMcZgreBlgdIdvdIY6DzY3Q2-dFOdAxoU6Xz-B-oDb5msNA9hJJGt0w2UVyCK2NNWSyQqHVLAepiisGm2ubctOS6_Zl8RDtl-PI8rsjdr6u_lzfN7Z_r35c_b5uh07I0oh0EcuY1k8IDH6Q3FhlrvUW5AWlaLRAsV94NWls0ErXzGycE-oFJhd2KfD_27lL8t0Au_TxmB9NkA8Ql91wrI6Wuh1X04g26jUsK9XaVMrx-qRK8UuJIuRRzToD9Lo1zfVvPWX_w0r946Q9e-qOXGvv2XL4MM_jX0IuICqyPwDBv31f5BD7FnTQ</recordid><startdate>201603</startdate><enddate>201603</enddate><creator>Tarkia, Miikka</creator><creator>Stark, Christoffer</creator><creator>Haavisto, Matti</creator><creator>Kentala, Rasmus</creator><creator>Vähäsilta, Tommi</creator><creator>Savunen, Timo</creator><creator>Strandberg, Marjatta</creator><creator>Saunavaara, Virva</creator><creator>Tolvanen, Tuula</creator><creator>Teräs, Mika</creator><creator>Pietilä, Mikko</creator><creator>Nyman, Leena</creator><creator>Duvall, Emma</creator><creator>Saukko, Pekka</creator><creator>Levijoki, Jouko</creator><creator>Roivainen, Anne</creator><creator>Saraste, Antti</creator><creator>Knuuti, Juhani</creator><general>BMJ Publishing Group LTD</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>201603</creationdate><title>Effect of levosimendan therapy on myocardial infarct size and left ventricular function after acute coronary occlusion</title><author>Tarkia, Miikka ; Stark, Christoffer ; Haavisto, Matti ; Kentala, Rasmus ; Vähäsilta, Tommi ; Savunen, Timo ; Strandberg, Marjatta ; Saunavaara, Virva ; Tolvanen, Tuula ; Teräs, Mika ; Pietilä, Mikko ; Nyman, Leena ; Duvall, Emma ; Saukko, Pekka ; Levijoki, Jouko ; Roivainen, Anne ; Saraste, Antti ; Knuuti, Juhani</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b375t-42b4f10d7054de1b5d8af002daf59e58274fea16dcb77af85f7cd9c44fdb056f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Cardiomyocytes</topic><topic>Cardiotonic Agents - therapeutic use</topic><topic>Coronary Occlusion - complications</topic><topic>Coronary vessels</topic><topic>Diastole</topic><topic>Disease Models, Animal</topic><topic>Drug dosages</topic><topic>Follow-Up Studies</topic><topic>Heart attacks</topic><topic>Heart failure</topic><topic>Hogs</topic><topic>Hydrazones - therapeutic use</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Medical research</topic><topic>Metabolites</topic><topic>Myocardial Contraction - drug effects</topic><topic>Myocardial Contraction - physiology</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - etiology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardium - pathology</topic><topic>Pyridazines - therapeutic use</topic><topic>Rodents</topic><topic>Stroke Volume - drug effects</topic><topic>Stroke Volume - physiology</topic><topic>Studies</topic><topic>Swine</topic><topic>Systole</topic><topic>Veins & arteries</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Ventricular Function, Left - physiology</topic><topic>Ventricular Remodeling - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tarkia, Miikka</creatorcontrib><creatorcontrib>Stark, Christoffer</creatorcontrib><creatorcontrib>Haavisto, Matti</creatorcontrib><creatorcontrib>Kentala, Rasmus</creatorcontrib><creatorcontrib>Vähäsilta, Tommi</creatorcontrib><creatorcontrib>Savunen, Timo</creatorcontrib><creatorcontrib>Strandberg, Marjatta</creatorcontrib><creatorcontrib>Saunavaara, Virva</creatorcontrib><creatorcontrib>Tolvanen, Tuula</creatorcontrib><creatorcontrib>Teräs, Mika</creatorcontrib><creatorcontrib>Pietilä, Mikko</creatorcontrib><creatorcontrib>Nyman, Leena</creatorcontrib><creatorcontrib>Duvall, Emma</creatorcontrib><creatorcontrib>Saukko, Pekka</creatorcontrib><creatorcontrib>Levijoki, Jouko</creatorcontrib><creatorcontrib>Roivainen, Anne</creatorcontrib><creatorcontrib>Saraste, Antti</creatorcontrib><creatorcontrib>Knuuti, Juhani</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database (ProQuest)</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 (British Cardiac Society)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tarkia, Miikka</au><au>Stark, Christoffer</au><au>Haavisto, Matti</au><au>Kentala, Rasmus</au><au>Vähäsilta, Tommi</au><au>Savunen, Timo</au><au>Strandberg, Marjatta</au><au>Saunavaara, Virva</au><au>Tolvanen, Tuula</au><au>Teräs, Mika</au><au>Pietilä, Mikko</au><au>Nyman, Leena</au><au>Duvall, Emma</au><au>Saukko, Pekka</au><au>Levijoki, Jouko</au><au>Roivainen, Anne</au><au>Saraste, Antti</au><au>Knuuti, Juhani</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of levosimendan therapy on myocardial infarct size and left ventricular function after acute coronary occlusion</atitle><jtitle>Heart (British Cardiac Society)</jtitle><addtitle>Heart</addtitle><date>2016-03</date><risdate>2016</risdate><volume>102</volume><issue>6</issue><spage>465</spage><epage>471</epage><pages>465-471</pages><issn>1355-6037</issn><eissn>1468-201X</eissn><abstract>BackgroundLevosimendan is an inotropic agent with cardioprotective and vasodilating properties used for the management of acutely decompensated heart failure. We studied the effects of levosimendan treatment on the size of myocardial infarction (MI) and left ventricular (LV) function in experimental pig model of post MI heart failure.MethodsAfter occlusion of the left anterior descending (LAD) coronary artery, animals received levosimendan 5 mg/kg/day orally for 8 weeks (n=7) or no treatment (n=18). One week after stopping treatment, transthoracic echocardiography, CT scan and positron emission tomography were performed to evaluate myocardial function, perfusion and oxidative metabolism. Histology was used to confirm the size of MI and features of LV remodelling.ResultsThe size of MI was significantly smaller in the levosimendan group than in the controls (12±13% vs 27±15% of the LV, p=0.03). End-diastolic volume (EDV) and end-systolic volume (ESV) were smaller in the levosimendan than in the control group (EDV 161±29 mL vs 245±84 mL, p=0.06; ESV 81±18 mL vs 149±67 mL, p=0.03), whereas ejection fraction tended to be higher in the levosimendan group (50±6% vs 41±8%, p=0.06).ConclusionsEight weeks of levosimendan therapy after recent LAD occlusion decreases the size of MI and leads to better preservation of LV function as well as reduced LV remodelling.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>26762238</pmid><doi>10.1136/heartjnl-2015-308137</doi><tpages>7</tpages></addata></record> |
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| subjects | Acute Disease Animals Cardiomyocytes Cardiotonic Agents - therapeutic use Coronary Occlusion - complications Coronary vessels Diastole Disease Models, Animal Drug dosages Follow-Up Studies Heart attacks Heart failure Hogs Hydrazones - therapeutic use Male Medical imaging Medical research Metabolites Myocardial Contraction - drug effects Myocardial Contraction - physiology Myocardial Infarction - drug therapy Myocardial Infarction - etiology Myocardial Infarction - physiopathology Myocardium - pathology Pyridazines - therapeutic use Rodents Stroke Volume - drug effects Stroke Volume - physiology Studies Swine Systole Veins & arteries Ventricular Function, Left - drug effects Ventricular Function, Left - physiology Ventricular Remodeling - drug effects |
| title | Effect of levosimendan therapy on myocardial infarct size and left ventricular function after acute coronary occlusion |
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