Reduced Sympathetic Innervation Underlies Adjacent Noninfarcted Region Dysfunction During Left Ventricular Remodeling
Objectives. We examined the association of sympathetic denervation and reduced blood flow with mechanical dysfunction in adjacent noninfarcted regions late after myocardial infarction (MI). Background. Using a well characterized ovine model of left ventricular (LV) remodeling after transmural antero...
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| Veröffentlicht in: | Journal of the American College of Cardiology 1997-10, Vol.30 (4), p.1079-1085 |
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| creator | Kramer, Christopher M Nicol, Philip D Rogers, Walter J Suzuki, Mark M Shaffer, Amy Theobald, Therese M Reichek, Nathaniel |
| description | Objectives. We examined the association of sympathetic denervation and reduced blood flow with mechanical dysfunction in adjacent noninfarcted regions late after myocardial infarction (MI).
Background. Using a well characterized ovine model of left ventricular (LV) remodeling after transmural anteroapical MI, we previously showed that histologically normal adjacent noninfarcted regions demonstrate mechanical dysfunction.
Methods. Ten sheep underwent coronary ligation. Magnetic resonance imaging was performed before and 8 weeks after infarction for measurement of LV mass, volumes, ejection fraction and regional intramyocardial circumferential shortening (%S). Iodine-123 metaiodobenzylguanidine (I-123 MIBG) and fluorescent microspheres before and after administration of adenosine were infused before death for measurement of sympathetic innervation, blood flow and blood flow reserve from matched postmortem regions.
Results. From baseline to 8 weeks after infarction, LV end-diastolic volume increased from (mean ± SD) 1.5 ± 0.3 to 2.6 ± 0.5 ml/kg (p < 0.001), and LV mass increased from 2.0 ± 0.3 to 2.6 ± 0.5 g/kg (p = 0.001). Regionally, the decline in subendocardial %S was greater in adjacent (19 ± 5% to 8 ± 5%) than in remote noninfarcted regions (20 ± 6% to 19 ± 6%, p < 0.002). No difference in regional blood flow or blood flow reserve was found between adjacent and remote regions, whereas I-123 MIBG uptake was lower in adjacent than in remote myocardium (1.09 ± 0.30 vs. 1.31 ± 0.40 nmol/g, p < 0.003). Topographically, from apex to base at 8 weeks after infarction, %S correlated closely with I-123 MIBG uptake (r = 0.93, p = 0.003).
Conclusions. In mechanically dysfunctional noninfarcted regions adjacent to chronic transmural myocardial infarction in the remodeled left ventricle, blood flow and blood flow reserve are preserved, yet sympathetic innervation is reduced. Chronic sympathetic denervation in adjacent noninfarcted regions, in association with regional mechanical dysfunction, may contribute to LV remodeling after infarction. |
| doi_str_mv | 10.1016/S0735-1097(97)00244-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_79317303</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0735109797002441</els_id><sourcerecordid>79317303</sourcerecordid><originalsourceid>FETCH-LOGICAL-c490t-a9317703cd15fa60e6ed0f0ebd1d2535dda1aff7c37c3b79be4193fe8e7982b53</originalsourceid><addsrcrecordid>eNqFkU1r3DAQhkVpSbdpf0LAh1Kag9PRyrKsUwlJ2gaWFpKmVyFLo1TBlreSHNh_X-0Hew0M6DDPqxmeIeSMwgUF2n65B8F4TUGKz1KcAyybpqavyIJy3tWMS_GaLI7IW_IupScAaDsqT8iJZLTlDVuQ-Q7tbNBW95txrfNfzN5UtyFgfNbZT6F6CBbj4DFVl_ZJGwy5-jkFH5yOJpfcHT5usetNcnMwu8j1HH14rFbocvWnBKI386BjQcfJ4lB678kbp4eEHw7vKXn4dvP76ke9-vX99upyVZtGQq51WVMIYMZS7nQL2KIFB9hbapeccWs11c4Jw0r1QvbYUMkcdihkt-w5OyWf9v-u4_RvxpTV6JPBYdABpzkpsR3AgBWQ70ETp5QiOrWOftRxoyiorW610622LlWpnW5FS-7sMGDuR7TH1MFv6X889HUyenBRB-PTEVt2DDraFezrHsMi49ljVMl4DOUuPqLJyk7-hUX-A3l2ntI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>79317303</pqid></control><display><type>article</type><title>Reduced Sympathetic Innervation Underlies Adjacent Noninfarcted Region Dysfunction During Left Ventricular Remodeling</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Kramer, Christopher M ; Nicol, Philip D ; Rogers, Walter J ; Suzuki, Mark M ; Shaffer, Amy ; Theobald, Therese M ; Reichek, Nathaniel</creator><creatorcontrib>Kramer, Christopher M ; Nicol, Philip D ; Rogers, Walter J ; Suzuki, Mark M ; Shaffer, Amy ; Theobald, Therese M ; Reichek, Nathaniel</creatorcontrib><description>Objectives. We examined the association of sympathetic denervation and reduced blood flow with mechanical dysfunction in adjacent noninfarcted regions late after myocardial infarction (MI).
Background. Using a well characterized ovine model of left ventricular (LV) remodeling after transmural anteroapical MI, we previously showed that histologically normal adjacent noninfarcted regions demonstrate mechanical dysfunction.
Methods. Ten sheep underwent coronary ligation. Magnetic resonance imaging was performed before and 8 weeks after infarction for measurement of LV mass, volumes, ejection fraction and regional intramyocardial circumferential shortening (%S). Iodine-123 metaiodobenzylguanidine (I-123 MIBG) and fluorescent microspheres before and after administration of adenosine were infused before death for measurement of sympathetic innervation, blood flow and blood flow reserve from matched postmortem regions.
Results. From baseline to 8 weeks after infarction, LV end-diastolic volume increased from (mean ± SD) 1.5 ± 0.3 to 2.6 ± 0.5 ml/kg (p < 0.001), and LV mass increased from 2.0 ± 0.3 to 2.6 ± 0.5 g/kg (p = 0.001). Regionally, the decline in subendocardial %S was greater in adjacent (19 ± 5% to 8 ± 5%) than in remote noninfarcted regions (20 ± 6% to 19 ± 6%, p < 0.002). No difference in regional blood flow or blood flow reserve was found between adjacent and remote regions, whereas I-123 MIBG uptake was lower in adjacent than in remote myocardium (1.09 ± 0.30 vs. 1.31 ± 0.40 nmol/g, p < 0.003). Topographically, from apex to base at 8 weeks after infarction, %S correlated closely with I-123 MIBG uptake (r = 0.93, p = 0.003).
Conclusions. In mechanically dysfunctional noninfarcted regions adjacent to chronic transmural myocardial infarction in the remodeled left ventricle, blood flow and blood flow reserve are preserved, yet sympathetic innervation is reduced. Chronic sympathetic denervation in adjacent noninfarcted regions, in association with regional mechanical dysfunction, may contribute to LV remodeling after infarction.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/S0735-1097(97)00244-1</identifier><identifier>PMID: 9316543</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>3-Iodobenzylguanidine ; Adrenergic Fibers - pathology ; Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Contrast Media ; Coronary Circulation - physiology ; Coronary heart disease ; Disease Models, Animal ; Female ; Heart ; Heart - innervation ; Hemodynamics ; Magnetic Resonance Imaging ; Medical sciences ; Myocardial Infarction - diagnostic imaging ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Radionuclide Imaging ; Sheep</subject><ispartof>Journal of the American College of Cardiology, 1997-10, Vol.30 (4), p.1079-1085</ispartof><rights>1997 The American College of Cardiology</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-a9317703cd15fa60e6ed0f0ebd1d2535dda1aff7c37c3b79be4193fe8e7982b53</citedby><cites>FETCH-LOGICAL-c490t-a9317703cd15fa60e6ed0f0ebd1d2535dda1aff7c37c3b79be4193fe8e7982b53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0735109797002441$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2830818$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9316543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kramer, Christopher M</creatorcontrib><creatorcontrib>Nicol, Philip D</creatorcontrib><creatorcontrib>Rogers, Walter J</creatorcontrib><creatorcontrib>Suzuki, Mark M</creatorcontrib><creatorcontrib>Shaffer, Amy</creatorcontrib><creatorcontrib>Theobald, Therese M</creatorcontrib><creatorcontrib>Reichek, Nathaniel</creatorcontrib><title>Reduced Sympathetic Innervation Underlies Adjacent Noninfarcted Region Dysfunction During Left Ventricular Remodeling</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>Objectives. We examined the association of sympathetic denervation and reduced blood flow with mechanical dysfunction in adjacent noninfarcted regions late after myocardial infarction (MI).
Background. Using a well characterized ovine model of left ventricular (LV) remodeling after transmural anteroapical MI, we previously showed that histologically normal adjacent noninfarcted regions demonstrate mechanical dysfunction.
Methods. Ten sheep underwent coronary ligation. Magnetic resonance imaging was performed before and 8 weeks after infarction for measurement of LV mass, volumes, ejection fraction and regional intramyocardial circumferential shortening (%S). Iodine-123 metaiodobenzylguanidine (I-123 MIBG) and fluorescent microspheres before and after administration of adenosine were infused before death for measurement of sympathetic innervation, blood flow and blood flow reserve from matched postmortem regions.
Results. From baseline to 8 weeks after infarction, LV end-diastolic volume increased from (mean ± SD) 1.5 ± 0.3 to 2.6 ± 0.5 ml/kg (p < 0.001), and LV mass increased from 2.0 ± 0.3 to 2.6 ± 0.5 g/kg (p = 0.001). Regionally, the decline in subendocardial %S was greater in adjacent (19 ± 5% to 8 ± 5%) than in remote noninfarcted regions (20 ± 6% to 19 ± 6%, p < 0.002). No difference in regional blood flow or blood flow reserve was found between adjacent and remote regions, whereas I-123 MIBG uptake was lower in adjacent than in remote myocardium (1.09 ± 0.30 vs. 1.31 ± 0.40 nmol/g, p < 0.003). Topographically, from apex to base at 8 weeks after infarction, %S correlated closely with I-123 MIBG uptake (r = 0.93, p = 0.003).
Conclusions. In mechanically dysfunctional noninfarcted regions adjacent to chronic transmural myocardial infarction in the remodeled left ventricle, blood flow and blood flow reserve are preserved, yet sympathetic innervation is reduced. Chronic sympathetic denervation in adjacent noninfarcted regions, in association with regional mechanical dysfunction, may contribute to LV remodeling after infarction.</description><subject>3-Iodobenzylguanidine</subject><subject>Adrenergic Fibers - pathology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Contrast Media</subject><subject>Coronary Circulation - physiology</subject><subject>Coronary heart disease</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Heart</subject><subject>Heart - innervation</subject><subject>Hemodynamics</subject><subject>Magnetic Resonance Imaging</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - diagnostic imaging</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Radionuclide Imaging</subject><subject>Sheep</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1r3DAQhkVpSbdpf0LAh1Kag9PRyrKsUwlJ2gaWFpKmVyFLo1TBlreSHNh_X-0Hew0M6DDPqxmeIeSMwgUF2n65B8F4TUGKz1KcAyybpqavyIJy3tWMS_GaLI7IW_IupScAaDsqT8iJZLTlDVuQ-Q7tbNBW95txrfNfzN5UtyFgfNbZT6F6CBbj4DFVl_ZJGwy5-jkFH5yOJpfcHT5usetNcnMwu8j1HH14rFbocvWnBKI386BjQcfJ4lB678kbp4eEHw7vKXn4dvP76ke9-vX99upyVZtGQq51WVMIYMZS7nQL2KIFB9hbapeccWs11c4Jw0r1QvbYUMkcdihkt-w5OyWf9v-u4_RvxpTV6JPBYdABpzkpsR3AgBWQ70ETp5QiOrWOftRxoyiorW610622LlWpnW5FS-7sMGDuR7TH1MFv6X889HUyenBRB-PTEVt2DDraFezrHsMi49ljVMl4DOUuPqLJyk7-hUX-A3l2ntI</recordid><startdate>19971001</startdate><enddate>19971001</enddate><creator>Kramer, Christopher M</creator><creator>Nicol, Philip D</creator><creator>Rogers, Walter J</creator><creator>Suzuki, Mark M</creator><creator>Shaffer, Amy</creator><creator>Theobald, Therese M</creator><creator>Reichek, Nathaniel</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>6I.</scope><scope>AAFTH</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>19971001</creationdate><title>Reduced Sympathetic Innervation Underlies Adjacent Noninfarcted Region Dysfunction During Left Ventricular Remodeling</title><author>Kramer, Christopher M ; Nicol, Philip D ; Rogers, Walter J ; Suzuki, Mark M ; Shaffer, Amy ; Theobald, Therese M ; Reichek, Nathaniel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-a9317703cd15fa60e6ed0f0ebd1d2535dda1aff7c37c3b79be4193fe8e7982b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>3-Iodobenzylguanidine</topic><topic>Adrenergic Fibers - pathology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Contrast Media</topic><topic>Coronary Circulation - physiology</topic><topic>Coronary heart disease</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Heart</topic><topic>Heart - innervation</topic><topic>Hemodynamics</topic><topic>Magnetic Resonance Imaging</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - diagnostic imaging</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Radionuclide Imaging</topic><topic>Sheep</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kramer, Christopher M</creatorcontrib><creatorcontrib>Nicol, Philip D</creatorcontrib><creatorcontrib>Rogers, Walter J</creatorcontrib><creatorcontrib>Suzuki, Mark M</creatorcontrib><creatorcontrib>Shaffer, Amy</creatorcontrib><creatorcontrib>Theobald, Therese M</creatorcontrib><creatorcontrib>Reichek, Nathaniel</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kramer, Christopher M</au><au>Nicol, Philip D</au><au>Rogers, Walter J</au><au>Suzuki, Mark M</au><au>Shaffer, Amy</au><au>Theobald, Therese M</au><au>Reichek, Nathaniel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced Sympathetic Innervation Underlies Adjacent Noninfarcted Region Dysfunction During Left Ventricular Remodeling</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>1997-10-01</date><risdate>1997</risdate><volume>30</volume><issue>4</issue><spage>1079</spage><epage>1085</epage><pages>1079-1085</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract>Objectives. We examined the association of sympathetic denervation and reduced blood flow with mechanical dysfunction in adjacent noninfarcted regions late after myocardial infarction (MI).
Background. Using a well characterized ovine model of left ventricular (LV) remodeling after transmural anteroapical MI, we previously showed that histologically normal adjacent noninfarcted regions demonstrate mechanical dysfunction.
Methods. Ten sheep underwent coronary ligation. Magnetic resonance imaging was performed before and 8 weeks after infarction for measurement of LV mass, volumes, ejection fraction and regional intramyocardial circumferential shortening (%S). Iodine-123 metaiodobenzylguanidine (I-123 MIBG) and fluorescent microspheres before and after administration of adenosine were infused before death for measurement of sympathetic innervation, blood flow and blood flow reserve from matched postmortem regions.
Results. From baseline to 8 weeks after infarction, LV end-diastolic volume increased from (mean ± SD) 1.5 ± 0.3 to 2.6 ± 0.5 ml/kg (p < 0.001), and LV mass increased from 2.0 ± 0.3 to 2.6 ± 0.5 g/kg (p = 0.001). Regionally, the decline in subendocardial %S was greater in adjacent (19 ± 5% to 8 ± 5%) than in remote noninfarcted regions (20 ± 6% to 19 ± 6%, p < 0.002). No difference in regional blood flow or blood flow reserve was found between adjacent and remote regions, whereas I-123 MIBG uptake was lower in adjacent than in remote myocardium (1.09 ± 0.30 vs. 1.31 ± 0.40 nmol/g, p < 0.003). Topographically, from apex to base at 8 weeks after infarction, %S correlated closely with I-123 MIBG uptake (r = 0.93, p = 0.003).
Conclusions. In mechanically dysfunctional noninfarcted regions adjacent to chronic transmural myocardial infarction in the remodeled left ventricle, blood flow and blood flow reserve are preserved, yet sympathetic innervation is reduced. Chronic sympathetic denervation in adjacent noninfarcted regions, in association with regional mechanical dysfunction, may contribute to LV remodeling after infarction.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>9316543</pmid><doi>10.1016/S0735-1097(97)00244-1</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3-Iodobenzylguanidine Adrenergic Fibers - pathology Animals Biological and medical sciences Cardiology. Vascular system Contrast Media Coronary Circulation - physiology Coronary heart disease Disease Models, Animal Female Heart Heart - innervation Hemodynamics Magnetic Resonance Imaging Medical sciences Myocardial Infarction - diagnostic imaging Myocardial Infarction - pathology Myocardial Infarction - physiopathology Radionuclide Imaging Sheep |
| title | Reduced Sympathetic Innervation Underlies Adjacent Noninfarcted Region Dysfunction During Left Ventricular Remodeling |
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