Reproducible model of post-infarction left ventricular dysfunction: haemodynamic characterization by conductance catheter
Objective: The understanding of pathophysiology and cellular mechanisms of chronic heart failure requires the creation of appropriate and accurately characterized animal models, thus enabling meaningful evaluation of evolving medical and surgical therapies. Methods: The left anterior descending and...
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| Veröffentlicht in: | European journal of cardio-thoracic surgery 2003-07, Vol.24 (1), p.98-104 |
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| container_title | European journal of cardio-thoracic surgery |
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| creator | Hasnat, A.K. van der Velde, Enno T. Hon, Jimmy K.F. Yacoub, Magdi H. |
| description | Objective: The understanding of pathophysiology and cellular mechanisms of chronic heart failure requires the creation of appropriate and accurately characterized animal models, thus enabling meaningful evaluation of evolving medical and surgical therapies. Methods: The left anterior descending and its diagonal branch were ligated in 12 sheep to induce left ventricular dysfunction. Results: Study of left ventricular pressure–volume loops 3 months post-operatively showed a significant deterioration of both systolic and diastolic indexes of left ventricular function. The left ventricular end-diastolic pressure increased from 3±1 to 7±1 mmHg (P |
| doi_str_mv | 10.1016/S1010-7940(03)00261-6 |
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Methods: The left anterior descending and its diagonal branch were ligated in 12 sheep to induce left ventricular dysfunction. Results: Study of left ventricular pressure–volume loops 3 months post-operatively showed a significant deterioration of both systolic and diastolic indexes of left ventricular function. The left ventricular end-diastolic pressure increased from 3±1 to 7±1 mmHg (P<0.001) along with a substantial increase in end-diastolic volume from 78±8 to 121±6 ml (P=0.002) and a significant decrease in cardiac output from 2±0.2 to 1.5±0.2 l/min (P=0.001). The left ventricular end-systolic pressure–volume relationship deteriorated from 2.7±0.37 to 0.7±0.16 mmHg/ml (P=0.0002) along with a significant reduction in the pre-load recruitable stroke work (P=0.001). The ejection fraction decreased from 34±2% to 16±4% (P<0.001) with a significant decrease in +dp/dt and −dp/dt (P=0.009). The mean systemic blood pressure, however, was maintained due to a substantial increase in the systemic vascular resistance (P=0.007). Conclusion: This study describes a reproducible large animal model of left ventricular dysfunction. This model is potentially useful to study the pathogenesis of remodelling, surgical management of heart failure and development of novel treatment strategies.</description><identifier>ISSN: 1010-7940</identifier><identifier>EISSN: 1873-734X</identifier><identifier>DOI: 10.1016/S1010-7940(03)00261-6</identifier><identifier>PMID: 12853052</identifier><identifier>CODEN: EJCSE7</identifier><language>eng</language><publisher>Amsterdam: Elsevier Science B.V</publisher><subject>Animals ; Biological and medical sciences ; Cardiac Catheterization ; Cardiology. Vascular system ; Coronary heart disease ; End-systolic pressure–volume relationship ; Heart ; Hemodynamics ; Left ventricle ; Medical sciences ; Models, Animal ; Myocardial Infarction - complications ; Myocardial Infarction - pathology ; Myocardium - pathology ; Pre-load recruitable stroke work ; Sheep ; Time Factors ; Ventricular dysfunction ; Ventricular Dysfunction, Left - diagnosis ; Ventricular Dysfunction, Left - etiology</subject><ispartof>European journal of cardio-thoracic surgery, 2003-07, Vol.24 (1), p.98-104</ispartof><rights>Elsevier Science B.V. © 2003 Elsevier Science B.V. 2003</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-50c3c71a2a42a00bfa74c9378128cf628d31f30f2753c91c9cc76f7efc6161653</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14991427$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12853052$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hasnat, A.K.</creatorcontrib><creatorcontrib>van der Velde, Enno T.</creatorcontrib><creatorcontrib>Hon, Jimmy K.F.</creatorcontrib><creatorcontrib>Yacoub, Magdi H.</creatorcontrib><title>Reproducible model of post-infarction left ventricular dysfunction: haemodynamic characterization by conductance catheter</title><title>European journal of cardio-thoracic surgery</title><addtitle>Eur J Cardiothorac Surg</addtitle><addtitle>Eur J Cardiothorac Surg</addtitle><description>Objective: The understanding of pathophysiology and cellular mechanisms of chronic heart failure requires the creation of appropriate and accurately characterized animal models, thus enabling meaningful evaluation of evolving medical and surgical therapies. Methods: The left anterior descending and its diagonal branch were ligated in 12 sheep to induce left ventricular dysfunction. Results: Study of left ventricular pressure–volume loops 3 months post-operatively showed a significant deterioration of both systolic and diastolic indexes of left ventricular function. The left ventricular end-diastolic pressure increased from 3±1 to 7±1 mmHg (P<0.001) along with a substantial increase in end-diastolic volume from 78±8 to 121±6 ml (P=0.002) and a significant decrease in cardiac output from 2±0.2 to 1.5±0.2 l/min (P=0.001). The left ventricular end-systolic pressure–volume relationship deteriorated from 2.7±0.37 to 0.7±0.16 mmHg/ml (P=0.0002) along with a significant reduction in the pre-load recruitable stroke work (P=0.001). The ejection fraction decreased from 34±2% to 16±4% (P<0.001) with a significant decrease in +dp/dt and −dp/dt (P=0.009). The mean systemic blood pressure, however, was maintained due to a substantial increase in the systemic vascular resistance (P=0.007). Conclusion: This study describes a reproducible large animal model of left ventricular dysfunction. This model is potentially useful to study the pathogenesis of remodelling, surgical management of heart failure and development of novel treatment strategies.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiac Catheterization</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>End-systolic pressure–volume relationship</subject><subject>Heart</subject><subject>Hemodynamics</subject><subject>Left ventricle</subject><subject>Medical sciences</subject><subject>Models, Animal</subject><subject>Myocardial Infarction - complications</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardium - pathology</subject><subject>Pre-load recruitable stroke work</subject><subject>Sheep</subject><subject>Time Factors</subject><subject>Ventricular dysfunction</subject><subject>Ventricular Dysfunction, Left - diagnosis</subject><subject>Ventricular Dysfunction, Left - etiology</subject><issn>1010-7940</issn><issn>1873-734X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkF2L1DAUhoso7of-BCU3ynoRPWnapPVOB50VFgQ_cNmbcOY0YaKddkxSsf56Mx-6CBJIAnnevJynKB4JeC5AqBcf8w5ctxVcgHwGUCrB1Z3iVDRaci2r67v5_gc5Kc5i_AoASpb6fnEiyqaWUJenxfzBbsPYTeRXvWWbsbM9Gx3bjjFxPzgMlPw4sN66xH7YIQVPU4-BdXN007B_fMnWaHNyHnDjidEaA1Kywf_CfXY1MxqHXJFwIMsI09rm5wfFPYd9tA-P53nx-e2bT4tLfvV--W7x6opT1daJ10CStMASqxIBVg51Ra3UTZ6BnCqbTgonwZW6ltQKaom0cto6UiKvWp4XTw__5jm_TzYms_GRbN_jYMcpmuxKtdA2GawPIIUxxmCd2Qa_wTAbAWbn3Oydm51QA9LsnRuVc4-PBdNqY7vb1FFyBp4cAYyEvQvZg4-3XNW2oip15uDAjdP2_938n26-6-aHiI_J_vwbwvDNKC11bS6vb8zrBdwsG_hilvI3F2qpTg</recordid><startdate>20030701</startdate><enddate>20030701</enddate><creator>Hasnat, A.K.</creator><creator>van der Velde, Enno T.</creator><creator>Hon, Jimmy K.F.</creator><creator>Yacoub, Magdi H.</creator><general>Elsevier Science B.V</general><general>Elsevier Science</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></search><sort><creationdate>20030701</creationdate><title>Reproducible model of post-infarction left ventricular dysfunction: haemodynamic characterization by conductance catheter</title><author>Hasnat, A.K. ; van der Velde, Enno T. ; Hon, Jimmy K.F. ; Yacoub, Magdi H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c495t-50c3c71a2a42a00bfa74c9378128cf628d31f30f2753c91c9cc76f7efc6161653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiac Catheterization</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>End-systolic pressure–volume relationship</topic><topic>Heart</topic><topic>Hemodynamics</topic><topic>Left ventricle</topic><topic>Medical sciences</topic><topic>Models, Animal</topic><topic>Myocardial Infarction - complications</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardium - pathology</topic><topic>Pre-load recruitable stroke work</topic><topic>Sheep</topic><topic>Time Factors</topic><topic>Ventricular dysfunction</topic><topic>Ventricular Dysfunction, Left - diagnosis</topic><topic>Ventricular Dysfunction, Left - etiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hasnat, A.K.</creatorcontrib><creatorcontrib>van der Velde, Enno T.</creatorcontrib><creatorcontrib>Hon, Jimmy K.F.</creatorcontrib><creatorcontrib>Yacoub, Magdi H.</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><jtitle>European journal of cardio-thoracic surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hasnat, A.K.</au><au>van der Velde, Enno T.</au><au>Hon, Jimmy K.F.</au><au>Yacoub, Magdi H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reproducible model of post-infarction left ventricular dysfunction: haemodynamic characterization by conductance catheter</atitle><jtitle>European journal of cardio-thoracic surgery</jtitle><stitle>Eur J Cardiothorac Surg</stitle><addtitle>Eur J Cardiothorac Surg</addtitle><date>2003-07-01</date><risdate>2003</risdate><volume>24</volume><issue>1</issue><spage>98</spage><epage>104</epage><pages>98-104</pages><issn>1010-7940</issn><eissn>1873-734X</eissn><coden>EJCSE7</coden><abstract>Objective: The understanding of pathophysiology and cellular mechanisms of chronic heart failure requires the creation of appropriate and accurately characterized animal models, thus enabling meaningful evaluation of evolving medical and surgical therapies. Methods: The left anterior descending and its diagonal branch were ligated in 12 sheep to induce left ventricular dysfunction. Results: Study of left ventricular pressure–volume loops 3 months post-operatively showed a significant deterioration of both systolic and diastolic indexes of left ventricular function. The left ventricular end-diastolic pressure increased from 3±1 to 7±1 mmHg (P<0.001) along with a substantial increase in end-diastolic volume from 78±8 to 121±6 ml (P=0.002) and a significant decrease in cardiac output from 2±0.2 to 1.5±0.2 l/min (P=0.001). The left ventricular end-systolic pressure–volume relationship deteriorated from 2.7±0.37 to 0.7±0.16 mmHg/ml (P=0.0002) along with a significant reduction in the pre-load recruitable stroke work (P=0.001). The ejection fraction decreased from 34±2% to 16±4% (P<0.001) with a significant decrease in +dp/dt and −dp/dt (P=0.009). The mean systemic blood pressure, however, was maintained due to a substantial increase in the systemic vascular resistance (P=0.007). Conclusion: This study describes a reproducible large animal model of left ventricular dysfunction. This model is potentially useful to study the pathogenesis of remodelling, surgical management of heart failure and development of novel treatment strategies.</abstract><cop>Amsterdam</cop><pub>Elsevier Science B.V</pub><pmid>12853052</pmid><doi>10.1016/S1010-7940(03)00261-6</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Cardiac Catheterization Cardiology. Vascular system Coronary heart disease End-systolic pressure–volume relationship Heart Hemodynamics Left ventricle Medical sciences Models, Animal Myocardial Infarction - complications Myocardial Infarction - pathology Myocardium - pathology Pre-load recruitable stroke work Sheep Time Factors Ventricular dysfunction Ventricular Dysfunction, Left - diagnosis Ventricular Dysfunction, Left - etiology |
| title | Reproducible model of post-infarction left ventricular dysfunction: haemodynamic characterization by conductance catheter |
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