Chronic heart rate reduction with ivabradine improves systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term increase in FKBP12/12.6 expression
Aims To investigate the adaptations of left ventricular function and calcium handling to chronic heart rate reduction with ivabradine in the reperfused heart. Methods and results Rabbits underwent 20 min coronary artery occlusion followed by 3 weeks of reperfusion. Throughout reperfusion, rabbits re...
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| Veröffentlicht in: | European heart journal 2010-06, Vol.31 (12), p.1529-1537 |
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| creator | Couvreur, Nicolas Tissier, Renaud Pons, Sandrine Chetboul, Valérie Gouni, Vassiliky Bruneval, Patrick Mandet, Chantal Pouchelon, Jean-Louis Berdeaux, Alain Ghaleh, Bijan |
| description | Aims To investigate the adaptations of left ventricular function and calcium handling to chronic heart rate reduction with ivabradine in the reperfused heart. Methods and results Rabbits underwent 20 min coronary artery occlusion followed by 3 weeks of reperfusion. Throughout reperfusion, rabbits received ivabradine (10 mg/kg/day) or vehicle (control). Ivabradine reduced heart rate by about 20% and improved both ejection fraction (+35%) and systolic displacement (+26%) after 3 weeks of treatment. Interestingly, this was associated with a two-fold increase expression of FKBP12/12.6. There was no difference in the expressions of phospholamban, SERCA2a, calsequestrin, ryanodine, phospho-ryanodine, and Na2+/Ca2+ exchanger in the two groups. Infarct scar and vascular density were similar in both groups. Administration of a single intravenous bolus of ivabradine (1 mg/kg) in control rabbits at 3 weeks of reperfusion also significantly improved acutely ejection fraction and systolic displacement. Conclusion Chronic heart rate reduction protects the myocardium against ventricular dysfunction induced by myocardial ischaemia followed by 3 weeks of reperfusion. Beyond pure heart rate reduction, ivabradine improves global and regional systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term adaptation in calcium handling, as supported by the increase in FKBP12/12.6 expression. |
| doi_str_mv | 10.1093/eurheartj/ehp554 |
| format | Article |
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Methods and results Rabbits underwent 20 min coronary artery occlusion followed by 3 weeks of reperfusion. Throughout reperfusion, rabbits received ivabradine (10 mg/kg/day) or vehicle (control). Ivabradine reduced heart rate by about 20% and improved both ejection fraction (+35%) and systolic displacement (+26%) after 3 weeks of treatment. Interestingly, this was associated with a two-fold increase expression of FKBP12/12.6. There was no difference in the expressions of phospholamban, SERCA2a, calsequestrin, ryanodine, phospho-ryanodine, and Na2+/Ca2+ exchanger in the two groups. Infarct scar and vascular density were similar in both groups. Administration of a single intravenous bolus of ivabradine (1 mg/kg) in control rabbits at 3 weeks of reperfusion also significantly improved acutely ejection fraction and systolic displacement. Conclusion Chronic heart rate reduction protects the myocardium against ventricular dysfunction induced by myocardial ischaemia followed by 3 weeks of reperfusion. Beyond pure heart rate reduction, ivabradine improves global and regional systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term adaptation in calcium handling, as supported by the increase in FKBP12/12.6 expression.</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehp554</identifier><identifier>PMID: 20028694</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animals ; Anti-Arrhythmia Agents - pharmacology ; Benzazepines - pharmacology ; Biochemistry, Molecular Biology ; Biological and medical sciences ; Blotting, Western ; Calcium handling ; Calcium-Binding Proteins - metabolism ; Cardiology. Vascular system ; Chronic heart rate reduction ; Coronary heart disease ; Coronary Occlusion - physiopathology ; Heart ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Heart Rate - drug effects ; If-channel ; Infarction ; Ivabradine ; Left ventricular dysfunction ; Life Sciences ; Medical sciences ; Myocardial Infarction - physiopathology ; Myocardial Reperfusion - methods ; Rabbits ; Stroke Volume - drug effects ; Tacrolimus Binding Protein 1A - metabolism ; Ventricular Dysfunction, Left - drug therapy ; Ventricular Dysfunction, Left - physiopathology</subject><ispartof>European heart journal, 2010-06, Vol.31 (12), p.1529-1537</ispartof><rights>2015 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c500t-dba881090a3be5f7cfa32c100d391385e608999147dd43033469b28c06a021203</citedby><cites>FETCH-LOGICAL-c500t-dba881090a3be5f7cfa32c100d391385e608999147dd43033469b28c06a021203</cites><orcidid>0000-0001-7891-1814 ; 0000-0001-6602-939X ; 0000-0002-2350-2914 ; 0000-0001-7561-9869 ; 0000-0003-0061-5462</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22861961$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20028694$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://inserm.hal.science/inserm-00500900$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Couvreur, Nicolas</creatorcontrib><creatorcontrib>Tissier, Renaud</creatorcontrib><creatorcontrib>Pons, Sandrine</creatorcontrib><creatorcontrib>Chetboul, Valérie</creatorcontrib><creatorcontrib>Gouni, Vassiliky</creatorcontrib><creatorcontrib>Bruneval, Patrick</creatorcontrib><creatorcontrib>Mandet, Chantal</creatorcontrib><creatorcontrib>Pouchelon, Jean-Louis</creatorcontrib><creatorcontrib>Berdeaux, Alain</creatorcontrib><creatorcontrib>Ghaleh, Bijan</creatorcontrib><title>Chronic heart rate reduction with ivabradine improves systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term increase in FKBP12/12.6 expression</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description>Aims To investigate the adaptations of left ventricular function and calcium handling to chronic heart rate reduction with ivabradine in the reperfused heart. Methods and results Rabbits underwent 20 min coronary artery occlusion followed by 3 weeks of reperfusion. Throughout reperfusion, rabbits received ivabradine (10 mg/kg/day) or vehicle (control). Ivabradine reduced heart rate by about 20% and improved both ejection fraction (+35%) and systolic displacement (+26%) after 3 weeks of treatment. Interestingly, this was associated with a two-fold increase expression of FKBP12/12.6. There was no difference in the expressions of phospholamban, SERCA2a, calsequestrin, ryanodine, phospho-ryanodine, and Na2+/Ca2+ exchanger in the two groups. Infarct scar and vascular density were similar in both groups. Administration of a single intravenous bolus of ivabradine (1 mg/kg) in control rabbits at 3 weeks of reperfusion also significantly improved acutely ejection fraction and systolic displacement. Conclusion Chronic heart rate reduction protects the myocardium against ventricular dysfunction induced by myocardial ischaemia followed by 3 weeks of reperfusion. Beyond pure heart rate reduction, ivabradine improves global and regional systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term adaptation in calcium handling, as supported by the increase in FKBP12/12.6 expression.</description><subject>Animals</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Benzazepines - pharmacology</subject><subject>Biochemistry, Molecular Biology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Calcium handling</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Cardiology. Vascular system</subject><subject>Chronic heart rate reduction</subject><subject>Coronary heart disease</subject><subject>Coronary Occlusion - physiopathology</subject><subject>Heart</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Heart Rate - drug effects</subject><subject>If-channel</subject><subject>Infarction</subject><subject>Ivabradine</subject><subject>Left ventricular dysfunction</subject><subject>Life Sciences</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardial Reperfusion - methods</subject><subject>Rabbits</subject><subject>Stroke Volume - drug effects</subject><subject>Tacrolimus Binding Protein 1A - metabolism</subject><subject>Ventricular Dysfunction, Left - drug therapy</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkk-P0zAQxSMEYpeFOyfkC-JCtuM4ceML0lJYiqhEhRZUcbFcZ9J4SZ1iO2X3W_KRcEi3_PHFkt_vPc_YkyRPKZxTEGyCvWtQuXA9wWZXFPm95JQWWZYKnhf3k1Ogokg5L1cnySPvrwGg5JQ_TE4ygKzkIj9Nfs4a11mjye8c4lRA4rDqdTCdJT9MaIjZq7VTlbFIzHbnuj164m996Npoq3s7ol1NQjN4d-jq3mN1SAwxv980RJGqVy3Zom6UNX5LjN137d7YzSAZhzrciTpyWNfDibJVlNvObtKAbjBph8rHSiy5_PB6SbMJzc45wZudQ-9jIY-TB7VqPT457GfJ58u3V7N5uvj47v3sYpHqAiCk1VqVZXxDUGyNRT3VtWKZpgAVE5SVBXIohRA0n1ZVzoCxnIt1VmrgCjKaATtLXo25u369xUqjDU61cufMVrlb2Skj_1WsaeSm20sGPOfTMga8HAOa_2zzi4U01sd2JUAsVgDsacRfHO5z3fcefZBb4zW2rbLY9V5OWVwCeBZJGEntOu8d1sd0CnIYG3kcGzmOTbQ8-7uZo-FuTiLw_AAoH7-ndspq4_9wkaKCD1WmI2d8wJujrtw3yadsWsj56qt8s_ySr66Wn6RgvwANcuIp</recordid><startdate>20100601</startdate><enddate>20100601</enddate><creator>Couvreur, Nicolas</creator><creator>Tissier, Renaud</creator><creator>Pons, Sandrine</creator><creator>Chetboul, Valérie</creator><creator>Gouni, Vassiliky</creator><creator>Bruneval, Patrick</creator><creator>Mandet, Chantal</creator><creator>Pouchelon, Jean-Louis</creator><creator>Berdeaux, Alain</creator><creator>Ghaleh, Bijan</creator><general>Oxford University Press</general><general>Oxford University Press (OUP)</general><scope>BSCLL</scope><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><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7891-1814</orcidid><orcidid>https://orcid.org/0000-0001-6602-939X</orcidid><orcidid>https://orcid.org/0000-0002-2350-2914</orcidid><orcidid>https://orcid.org/0000-0001-7561-9869</orcidid><orcidid>https://orcid.org/0000-0003-0061-5462</orcidid></search><sort><creationdate>20100601</creationdate><title>Chronic heart rate reduction with ivabradine improves systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term increase in FKBP12/12.6 expression</title><author>Couvreur, Nicolas ; Tissier, Renaud ; Pons, Sandrine ; Chetboul, Valérie ; Gouni, Vassiliky ; Bruneval, Patrick ; Mandet, Chantal ; Pouchelon, Jean-Louis ; Berdeaux, Alain ; Ghaleh, Bijan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c500t-dba881090a3be5f7cfa32c100d391385e608999147dd43033469b28c06a021203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Benzazepines - pharmacology</topic><topic>Biochemistry, Molecular Biology</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Calcium handling</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Cardiology. Vascular system</topic><topic>Chronic heart rate reduction</topic><topic>Coronary heart disease</topic><topic>Coronary Occlusion - physiopathology</topic><topic>Heart</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Heart Rate - drug effects</topic><topic>If-channel</topic><topic>Infarction</topic><topic>Ivabradine</topic><topic>Left ventricular dysfunction</topic><topic>Life Sciences</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardial Reperfusion - methods</topic><topic>Rabbits</topic><topic>Stroke Volume - drug effects</topic><topic>Tacrolimus Binding Protein 1A - metabolism</topic><topic>Ventricular Dysfunction, Left - drug therapy</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Couvreur, Nicolas</creatorcontrib><creatorcontrib>Tissier, Renaud</creatorcontrib><creatorcontrib>Pons, Sandrine</creatorcontrib><creatorcontrib>Chetboul, Valérie</creatorcontrib><creatorcontrib>Gouni, Vassiliky</creatorcontrib><creatorcontrib>Bruneval, Patrick</creatorcontrib><creatorcontrib>Mandet, Chantal</creatorcontrib><creatorcontrib>Pouchelon, Jean-Louis</creatorcontrib><creatorcontrib>Berdeaux, Alain</creatorcontrib><creatorcontrib>Ghaleh, Bijan</creatorcontrib><collection>Istex</collection><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><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Couvreur, Nicolas</au><au>Tissier, Renaud</au><au>Pons, Sandrine</au><au>Chetboul, Valérie</au><au>Gouni, Vassiliky</au><au>Bruneval, Patrick</au><au>Mandet, Chantal</au><au>Pouchelon, Jean-Louis</au><au>Berdeaux, Alain</au><au>Ghaleh, Bijan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic heart rate reduction with ivabradine improves systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term increase in FKBP12/12.6 expression</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2010-06-01</date><risdate>2010</risdate><volume>31</volume><issue>12</issue><spage>1529</spage><epage>1537</epage><pages>1529-1537</pages><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>Aims To investigate the adaptations of left ventricular function and calcium handling to chronic heart rate reduction with ivabradine in the reperfused heart. Methods and results Rabbits underwent 20 min coronary artery occlusion followed by 3 weeks of reperfusion. Throughout reperfusion, rabbits received ivabradine (10 mg/kg/day) or vehicle (control). Ivabradine reduced heart rate by about 20% and improved both ejection fraction (+35%) and systolic displacement (+26%) after 3 weeks of treatment. Interestingly, this was associated with a two-fold increase expression of FKBP12/12.6. There was no difference in the expressions of phospholamban, SERCA2a, calsequestrin, ryanodine, phospho-ryanodine, and Na2+/Ca2+ exchanger in the two groups. Infarct scar and vascular density were similar in both groups. Administration of a single intravenous bolus of ivabradine (1 mg/kg) in control rabbits at 3 weeks of reperfusion also significantly improved acutely ejection fraction and systolic displacement. Conclusion Chronic heart rate reduction protects the myocardium against ventricular dysfunction induced by myocardial ischaemia followed by 3 weeks of reperfusion. Beyond pure heart rate reduction, ivabradine improves global and regional systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term adaptation in calcium handling, as supported by the increase in FKBP12/12.6 expression.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>20028694</pmid><doi>10.1093/eurheartj/ehp554</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-7891-1814</orcidid><orcidid>https://orcid.org/0000-0001-6602-939X</orcidid><orcidid>https://orcid.org/0000-0002-2350-2914</orcidid><orcidid>https://orcid.org/0000-0001-7561-9869</orcidid><orcidid>https://orcid.org/0000-0003-0061-5462</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Arrhythmia Agents - pharmacology Benzazepines - pharmacology Biochemistry, Molecular Biology Biological and medical sciences Blotting, Western Calcium handling Calcium-Binding Proteins - metabolism Cardiology. Vascular system Chronic heart rate reduction Coronary heart disease Coronary Occlusion - physiopathology Heart Heart failure, cardiogenic pulmonary edema, cardiac enlargement Heart Rate - drug effects If-channel Infarction Ivabradine Left ventricular dysfunction Life Sciences Medical sciences Myocardial Infarction - physiopathology Myocardial Reperfusion - methods Rabbits Stroke Volume - drug effects Tacrolimus Binding Protein 1A - metabolism Ventricular Dysfunction, Left - drug therapy Ventricular Dysfunction, Left - physiopathology |
| title | Chronic heart rate reduction with ivabradine improves systolic function of the reperfused heart through a dual mechanism involving a direct mechanical effect and a long-term increase in FKBP12/12.6 expression |
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