Carbon-11 hydroxyephedrine with positron emission tomography for serial assessment of cardiac adrenergic neuronal function after acute myocardial infarction in humans

Objectives. The purpose of this study was to assess the extent and reversibility of neuronal abnormalities in patients with an acute myocardial infarction. Background. Previous experimental studies have described ischemic injury to sympathetic neurons exceeding the area of myocardial necrosis. Carbo...

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Veröffentlicht in:Journal of the American College of Cardiology 1993-08, Vol.22 (2), p.368-375
Hauptverfasser: Allman, Kevin C., Wieland, Donald M., Muzik, Otto, Degrado, Timothy R., Wolfe, Edwin R., Schwaiger, Markus
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container_end_page 375
container_issue 2
container_start_page 368
container_title Journal of the American College of Cardiology
container_volume 22
creator Allman, Kevin C.
Wieland, Donald M.
Muzik, Otto
Degrado, Timothy R.
Wolfe, Edwin R.
Schwaiger, Markus
description Objectives. The purpose of this study was to assess the extent and reversibility of neuronal abnormalities in patients with an acute myocardial infarction. Background. Previous experimental studies have described ischemic injury to sympathetic neurons exceeding the area of myocardial necrosis. Carbon-11 (C-11) hydroxyephedrine (HED) is a norepinephrine analogue that can be used for the noninvasive evaluation of neuronal integrity using positron emission tomography. Methods. We studied 14 volunteers and 16 patients experiencing a first acute myocardial infarction. Positron emission tomographic imaging was used to quantitatively compare regional perfusion, as assessed with nitrogen-13 ammonia, with myocardial retention of C-11 hydroxyephedrine early after myocardial infarction as well as >6 months after the acute event. Results. C-11 hydroxyephedrine and flow images demonstrated homogeneous tracer retention in volunteers but were abnormal in all patients. C-11 hydroxyephedrine abnormalities were more extensive than those for blood flow assessed by semiquantitative polar map analysis (31 ± 15% vs. 17 ± 17% left ventricle; p < 0.05), particularly in five patients with non-Q wave infarction (31 ± 11% vs. 3.5 ± 2.5% left ventricle; p = 0.008). Eleven patients with Q wave infarction had matched defects (28 ± 17% vs. 21 ± 17% left ventricle; p = NS). C-11 hydroxyephedrine tissue retention fraction was quantified in three tissue zones: zone 1 (abnormal rest flow) had retention fraction 0.037 ± 0.02−min; zone 2 (normal rest flow but decreased carbon-11 hydroxyephedrine retention) had retention fraction 0.068 ± .034−min, and zone 3 (normal flow and carbon-11 hydroxyephedrine retention) had retention fraction 0.087 ± 0.041−min(p = 0.0004). Follow-up studies at 8 ± 3 months in eight patients revealed no change in extent of abnormalities or absolute tissue tracer retention in infarct and peri-infarct territories. Conclusions. The results of abnormal regional sympathetic innervation in patients with infarction confirm previous experimental data and suggest persistent neuronal damage in infarct and peri-infarct territories, without evidence of reinnervation of reversibly injured myocardium.
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The purpose of this study was to assess the extent and reversibility of neuronal abnormalities in patients with an acute myocardial infarction. Background. Previous experimental studies have described ischemic injury to sympathetic neurons exceeding the area of myocardial necrosis. Carbon-11 (C-11) hydroxyephedrine (HED) is a norepinephrine analogue that can be used for the noninvasive evaluation of neuronal integrity using positron emission tomography. Methods. We studied 14 volunteers and 16 patients experiencing a first acute myocardial infarction. Positron emission tomographic imaging was used to quantitatively compare regional perfusion, as assessed with nitrogen-13 ammonia, with myocardial retention of C-11 hydroxyephedrine early after myocardial infarction as well as &gt;6 months after the acute event. Results. C-11 hydroxyephedrine and flow images demonstrated homogeneous tracer retention in volunteers but were abnormal in all patients. C-11 hydroxyephedrine abnormalities were more extensive than those for blood flow assessed by semiquantitative polar map analysis (31 ± 15% vs. 17 ± 17% left ventricle; p &lt; 0.05), particularly in five patients with non-Q wave infarction (31 ± 11% vs. 3.5 ± 2.5% left ventricle; p = 0.008). Eleven patients with Q wave infarction had matched defects (28 ± 17% vs. 21 ± 17% left ventricle; p = NS). C-11 hydroxyephedrine tissue retention fraction was quantified in three tissue zones: zone 1 (abnormal rest flow) had retention fraction 0.037 ± 0.02−min; zone 2 (normal rest flow but decreased carbon-11 hydroxyephedrine retention) had retention fraction 0.068 ± .034−min, and zone 3 (normal flow and carbon-11 hydroxyephedrine retention) had retention fraction 0.087 ± 0.041−min(p = 0.0004). Follow-up studies at 8 ± 3 months in eight patients revealed no change in extent of abnormalities or absolute tissue tracer retention in infarct and peri-infarct territories. Conclusions. The results of abnormal regional sympathetic innervation in patients with infarction confirm previous experimental data and suggest persistent neuronal damage in infarct and peri-infarct territories, without evidence of reinnervation of reversibly injured myocardium.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/0735-1097(93)90039-4</identifier><identifier>PMID: 8335806</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adrenergic Fibers - physiology ; Adult ; Aged ; Autonomic Nervous System Diseases - diagnostic imaging ; Autonomic Nervous System Diseases - etiology ; Biological and medical sciences ; Carbon Radioisotopes ; Cardiology. 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The purpose of this study was to assess the extent and reversibility of neuronal abnormalities in patients with an acute myocardial infarction. Background. Previous experimental studies have described ischemic injury to sympathetic neurons exceeding the area of myocardial necrosis. Carbon-11 (C-11) hydroxyephedrine (HED) is a norepinephrine analogue that can be used for the noninvasive evaluation of neuronal integrity using positron emission tomography. Methods. We studied 14 volunteers and 16 patients experiencing a first acute myocardial infarction. Positron emission tomographic imaging was used to quantitatively compare regional perfusion, as assessed with nitrogen-13 ammonia, with myocardial retention of C-11 hydroxyephedrine early after myocardial infarction as well as &gt;6 months after the acute event. Results. C-11 hydroxyephedrine and flow images demonstrated homogeneous tracer retention in volunteers but were abnormal in all patients. C-11 hydroxyephedrine abnormalities were more extensive than those for blood flow assessed by semiquantitative polar map analysis (31 ± 15% vs. 17 ± 17% left ventricle; p &lt; 0.05), particularly in five patients with non-Q wave infarction (31 ± 11% vs. 3.5 ± 2.5% left ventricle; p = 0.008). Eleven patients with Q wave infarction had matched defects (28 ± 17% vs. 21 ± 17% left ventricle; p = NS). C-11 hydroxyephedrine tissue retention fraction was quantified in three tissue zones: zone 1 (abnormal rest flow) had retention fraction 0.037 ± 0.02−min; zone 2 (normal rest flow but decreased carbon-11 hydroxyephedrine retention) had retention fraction 0.068 ± .034−min, and zone 3 (normal flow and carbon-11 hydroxyephedrine retention) had retention fraction 0.087 ± 0.041−min(p = 0.0004). Follow-up studies at 8 ± 3 months in eight patients revealed no change in extent of abnormalities or absolute tissue tracer retention in infarct and peri-infarct territories. Conclusions. The results of abnormal regional sympathetic innervation in patients with infarction confirm previous experimental data and suggest persistent neuronal damage in infarct and peri-infarct territories, without evidence of reinnervation of reversibly injured myocardium.</description><subject>Adrenergic Fibers - physiology</subject><subject>Adult</subject><subject>Aged</subject><subject>Autonomic Nervous System Diseases - diagnostic imaging</subject><subject>Autonomic Nervous System Diseases - etiology</subject><subject>Biological and medical sciences</subject><subject>Carbon Radioisotopes</subject><subject>Cardiology. Vascular system</subject><subject>Case-Control Studies</subject><subject>Coronary Circulation</subject><subject>Coronary heart disease</subject><subject>Ephedrine - analogs &amp; derivatives</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Heart</subject><subject>Heart - diagnostic imaging</subject><subject>Heart - innervation</subject><subject>Heart - physiopathology</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - complications</subject><subject>Myocardial Infarction - diagnostic imaging</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Sympathomimetics</subject><subject>Tomography, Emission-Computed</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kV_LFCEYxSWKt23rGxR4EVEXU7rqjN4EsfQPXuimrsXVx3eMGZ10ppov1OfMbZa9DASF8zuHx-cg9JSS15TQ9g3pmGgoUd1LxV4pQphq-D20o0LIhgnV3Ue7K_IQPSrlOyGklVTdoBvJmJCk3aE_R5NPKTaU4n51Of1eYerB5RAB_wpzj6dUwpxTxDCGUkJ9zGlMd9lM_Yp9yrhADmbAphQoZYQ44-SxNdkFY7FxGSLku2BxhKXGVNIv0c7nIONnyNjYZQY8rmnzDDhEb_JGhIj7ZTSxPEYPvBkKPLnce_Ttw_uvx0_N7ZePn4_vbhvL23ZuOGVWcQOciYM88FZJAMV56ykFD8wQUIqLgz1R4qsqTpJbx2jnWuOUk4rt0Ystd8rpxwJl1vXXFobBREhL0Z2QXLJ69ohvoM2plAxeTzmMJq-aEn2uR593r8-714rpf_VoXm3PLvnLaQR3NV36qPrzi26KNYPPJtpQrhiXXLCWVOzthkHdxc8AWRcbIFpwIYOdtUvh_3P8BdcIsAg</recordid><startdate>19930801</startdate><enddate>19930801</enddate><creator>Allman, Kevin C.</creator><creator>Wieland, Donald M.</creator><creator>Muzik, Otto</creator><creator>Degrado, Timothy R.</creator><creator>Wolfe, Edwin R.</creator><creator>Schwaiger, Markus</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>19930801</creationdate><title>Carbon-11 hydroxyephedrine with positron emission tomography for serial assessment of cardiac adrenergic neuronal function after acute myocardial infarction in humans</title><author>Allman, Kevin C. ; Wieland, Donald M. ; Muzik, Otto ; Degrado, Timothy R. ; Wolfe, Edwin R. ; Schwaiger, Markus</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-413c94ae4352824698ee9446f11efe3a0e99452cb10f4695b84cd317d6ad9d893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adrenergic Fibers - physiology</topic><topic>Adult</topic><topic>Aged</topic><topic>Autonomic Nervous System Diseases - diagnostic imaging</topic><topic>Autonomic Nervous System Diseases - etiology</topic><topic>Biological and medical sciences</topic><topic>Carbon Radioisotopes</topic><topic>Cardiology. Vascular system</topic><topic>Case-Control Studies</topic><topic>Coronary Circulation</topic><topic>Coronary heart disease</topic><topic>Ephedrine - analogs &amp; derivatives</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Heart</topic><topic>Heart - diagnostic imaging</topic><topic>Heart - innervation</topic><topic>Heart - physiopathology</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - complications</topic><topic>Myocardial Infarction - diagnostic imaging</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Sympathomimetics</topic><topic>Tomography, Emission-Computed</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Allman, Kevin C.</creatorcontrib><creatorcontrib>Wieland, Donald M.</creatorcontrib><creatorcontrib>Muzik, Otto</creatorcontrib><creatorcontrib>Degrado, Timothy R.</creatorcontrib><creatorcontrib>Wolfe, Edwin R.</creatorcontrib><creatorcontrib>Schwaiger, Markus</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>Allman, Kevin C.</au><au>Wieland, Donald M.</au><au>Muzik, Otto</au><au>Degrado, Timothy R.</au><au>Wolfe, Edwin R.</au><au>Schwaiger, Markus</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Carbon-11 hydroxyephedrine with positron emission tomography for serial assessment of cardiac adrenergic neuronal function after acute myocardial infarction in humans</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>1993-08-01</date><risdate>1993</risdate><volume>22</volume><issue>2</issue><spage>368</spage><epage>375</epage><pages>368-375</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract>Objectives. The purpose of this study was to assess the extent and reversibility of neuronal abnormalities in patients with an acute myocardial infarction. Background. Previous experimental studies have described ischemic injury to sympathetic neurons exceeding the area of myocardial necrosis. Carbon-11 (C-11) hydroxyephedrine (HED) is a norepinephrine analogue that can be used for the noninvasive evaluation of neuronal integrity using positron emission tomography. Methods. We studied 14 volunteers and 16 patients experiencing a first acute myocardial infarction. Positron emission tomographic imaging was used to quantitatively compare regional perfusion, as assessed with nitrogen-13 ammonia, with myocardial retention of C-11 hydroxyephedrine early after myocardial infarction as well as &gt;6 months after the acute event. Results. C-11 hydroxyephedrine and flow images demonstrated homogeneous tracer retention in volunteers but were abnormal in all patients. C-11 hydroxyephedrine abnormalities were more extensive than those for blood flow assessed by semiquantitative polar map analysis (31 ± 15% vs. 17 ± 17% left ventricle; p &lt; 0.05), particularly in five patients with non-Q wave infarction (31 ± 11% vs. 3.5 ± 2.5% left ventricle; p = 0.008). Eleven patients with Q wave infarction had matched defects (28 ± 17% vs. 21 ± 17% left ventricle; p = NS). C-11 hydroxyephedrine tissue retention fraction was quantified in three tissue zones: zone 1 (abnormal rest flow) had retention fraction 0.037 ± 0.02−min; zone 2 (normal rest flow but decreased carbon-11 hydroxyephedrine retention) had retention fraction 0.068 ± .034−min, and zone 3 (normal flow and carbon-11 hydroxyephedrine retention) had retention fraction 0.087 ± 0.041−min(p = 0.0004). Follow-up studies at 8 ± 3 months in eight patients revealed no change in extent of abnormalities or absolute tissue tracer retention in infarct and peri-infarct territories. Conclusions. The results of abnormal regional sympathetic innervation in patients with infarction confirm previous experimental data and suggest persistent neuronal damage in infarct and peri-infarct territories, without evidence of reinnervation of reversibly injured myocardium.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8335806</pmid><doi>10.1016/0735-1097(93)90039-4</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects Adrenergic Fibers - physiology
Adult
Aged
Autonomic Nervous System Diseases - diagnostic imaging
Autonomic Nervous System Diseases - etiology
Biological and medical sciences
Carbon Radioisotopes
Cardiology. Vascular system
Case-Control Studies
Coronary Circulation
Coronary heart disease
Ephedrine - analogs & derivatives
Female
Follow-Up Studies
Heart
Heart - diagnostic imaging
Heart - innervation
Heart - physiopathology
Humans
Male
Medical sciences
Middle Aged
Myocardial Infarction - complications
Myocardial Infarction - diagnostic imaging
Myocardial Infarction - physiopathology
Sympathomimetics
Tomography, Emission-Computed
title Carbon-11 hydroxyephedrine with positron emission tomography for serial assessment of cardiac adrenergic neuronal function after acute myocardial infarction in humans
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