Myocardial Substrate Utilization and Left Ventricular Function in Adriamycin Cardiomyopathy
We evaluated alterations of substrate utilization in a rat model of adriamycin cardiomyopathy with deteriorating left ventricular function. Rats were treated with adriamycin (2 mg/kg), once a week for 6, 8, 9 and 10 wk. Fluorine-18-F-deoxyglucose (18F-FDG) and 125I-beta-methyl-branched fatty acid (1...
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| Veröffentlicht in: | The Journal of nuclear medicine (1978) 1993-09, Vol.34 (9), p.1529 |
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| creator | Wakasugi, Shigetoshi Fischman, Alan J Babich, John W Callahan, Ronald J Elmaleh, David R Wilkinson, Robert Strauss, H. William |
| description | We evaluated alterations of substrate utilization in a rat model of adriamycin cardiomyopathy with deteriorating left ventricular function. Rats were treated with adriamycin (2 mg/kg), once a week for 6, 8, 9 and 10 wk. Fluorine-18-F-deoxyglucose (18F-FDG) and 125I-beta-methyl-branched fatty acid (125I-BMIPP) were used as tracers of glucose and fatty acid metabolism and 99mTc-hexakis (2-methoxyisobutyl-isonitrile) (99mTc-MIBI) was used as a myocardial blood flow tracer. Left ventricular ejection fraction (LVEF) calculated from gated blood pool images was used as an indicator of cardiac function. LVEF was normal in the 6-wk group (78.0% +/- 4.8%), abruptly decreased in the 8-wk group (43.1% +/- 10.1%) and further deteriorated in the 9-wk group (27.6% +/- 13.4%). Accumulation of 18F-FDG (%kgID/g) in the hearts of adriamycin treated animals progressively decreased compared to controls (2.19% +/- 0.38%); 1.47% +/- 0.42% (p < 0.01) at 6 wk, 1.22% +/- 0.27% (p < 0.001) at 8 wk, 0.69% +/- 0.56% (p < 0.001) at 9 wk and 0.50% +/- 0.08% (p < 0.001) at 10 wk. This decrease occurred earlier than the deterioration in LVEF. Myocardial accumulation of 125I-BMIPP decreased in the advanced stages of adriamycin cardiomyopathy and was well correlated with the decrease in 18F-FDG accumulation. However, the decrease was less profound than for 18F-FDG; 53.7% +/- 9.8% versus 31.6% +/- 25.4% of control at 9 wk (p = NS), 49.5% +/- 15.3% versus 22.6% +/- 3.5% of control at 10 wk (p < 0.05). Accumulation of 99mTc-MIBI did not differ between controls and the adriamycin treated groups. There were no differences in blood glucose levels between controls and adriamycin treatment groups. Both glucose and fatty acid utilization are decreased in adriamycin-induced cardiomyopathy and these critical impairments in energy metabolism are associated with heart failure. Impaired myocardial glucose utilization measured with 18F-FDG may be a particularly sensitive marker of adriamycin cardiomyopathy. |
| format | Article |
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William</creator><creatorcontrib>Wakasugi, Shigetoshi ; Fischman, Alan J ; Babich, John W ; Callahan, Ronald J ; Elmaleh, David R ; Wilkinson, Robert ; Strauss, H. William</creatorcontrib><description>We evaluated alterations of substrate utilization in a rat model of adriamycin cardiomyopathy with deteriorating left ventricular function. Rats were treated with adriamycin (2 mg/kg), once a week for 6, 8, 9 and 10 wk. Fluorine-18-F-deoxyglucose (18F-FDG) and 125I-beta-methyl-branched fatty acid (125I-BMIPP) were used as tracers of glucose and fatty acid metabolism and 99mTc-hexakis (2-methoxyisobutyl-isonitrile) (99mTc-MIBI) was used as a myocardial blood flow tracer. Left ventricular ejection fraction (LVEF) calculated from gated blood pool images was used as an indicator of cardiac function. LVEF was normal in the 6-wk group (78.0% +/- 4.8%), abruptly decreased in the 8-wk group (43.1% +/- 10.1%) and further deteriorated in the 9-wk group (27.6% +/- 13.4%). Accumulation of 18F-FDG (%kgID/g) in the hearts of adriamycin treated animals progressively decreased compared to controls (2.19% +/- 0.38%); 1.47% +/- 0.42% (p < 0.01) at 6 wk, 1.22% +/- 0.27% (p < 0.001) at 8 wk, 0.69% +/- 0.56% (p < 0.001) at 9 wk and 0.50% +/- 0.08% (p < 0.001) at 10 wk. This decrease occurred earlier than the deterioration in LVEF. Myocardial accumulation of 125I-BMIPP decreased in the advanced stages of adriamycin cardiomyopathy and was well correlated with the decrease in 18F-FDG accumulation. However, the decrease was less profound than for 18F-FDG; 53.7% +/- 9.8% versus 31.6% +/- 25.4% of control at 9 wk (p = NS), 49.5% +/- 15.3% versus 22.6% +/- 3.5% of control at 10 wk (p < 0.05). Accumulation of 99mTc-MIBI did not differ between controls and the adriamycin treated groups. There were no differences in blood glucose levels between controls and adriamycin treatment groups. Both glucose and fatty acid utilization are decreased in adriamycin-induced cardiomyopathy and these critical impairments in energy metabolism are associated with heart failure. Impaired myocardial glucose utilization measured with 18F-FDG may be a particularly sensitive marker of adriamycin cardiomyopathy.</description><identifier>ISSN: 0161-5505</identifier><identifier>EISSN: 1535-5667</identifier><identifier>PMID: 8355075</identifier><language>eng</language><publisher>United States: Soc Nuclear Med</publisher><subject>Animals ; Deoxyglucose - analogs & derivatives ; Doxorubicin - adverse effects ; Fatty Acids ; Fluorine Radioisotopes ; Fluorodeoxyglucose F18 ; Gated Blood-Pool Imaging ; Heart - diagnostic imaging ; Heart Failure - chemically induced ; Heart Failure - diagnostic imaging ; Iodine Radioisotopes ; Iodobenzenes ; Male ; Myocardium - metabolism ; Rats ; Rats, Wistar ; Technetium Tc 99m Sestamibi ; Ventricular Function, Left - drug effects</subject><ispartof>The Journal of nuclear medicine (1978), 1993-09, Vol.34 (9), p.1529</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8355075$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wakasugi, Shigetoshi</creatorcontrib><creatorcontrib>Fischman, Alan J</creatorcontrib><creatorcontrib>Babich, John W</creatorcontrib><creatorcontrib>Callahan, Ronald J</creatorcontrib><creatorcontrib>Elmaleh, David R</creatorcontrib><creatorcontrib>Wilkinson, Robert</creatorcontrib><creatorcontrib>Strauss, H. William</creatorcontrib><title>Myocardial Substrate Utilization and Left Ventricular Function in Adriamycin Cardiomyopathy</title><title>The Journal of nuclear medicine (1978)</title><addtitle>J Nucl Med</addtitle><description>We evaluated alterations of substrate utilization in a rat model of adriamycin cardiomyopathy with deteriorating left ventricular function. Rats were treated with adriamycin (2 mg/kg), once a week for 6, 8, 9 and 10 wk. Fluorine-18-F-deoxyglucose (18F-FDG) and 125I-beta-methyl-branched fatty acid (125I-BMIPP) were used as tracers of glucose and fatty acid metabolism and 99mTc-hexakis (2-methoxyisobutyl-isonitrile) (99mTc-MIBI) was used as a myocardial blood flow tracer. Left ventricular ejection fraction (LVEF) calculated from gated blood pool images was used as an indicator of cardiac function. LVEF was normal in the 6-wk group (78.0% +/- 4.8%), abruptly decreased in the 8-wk group (43.1% +/- 10.1%) and further deteriorated in the 9-wk group (27.6% +/- 13.4%). Accumulation of 18F-FDG (%kgID/g) in the hearts of adriamycin treated animals progressively decreased compared to controls (2.19% +/- 0.38%); 1.47% +/- 0.42% (p < 0.01) at 6 wk, 1.22% +/- 0.27% (p < 0.001) at 8 wk, 0.69% +/- 0.56% (p < 0.001) at 9 wk and 0.50% +/- 0.08% (p < 0.001) at 10 wk. This decrease occurred earlier than the deterioration in LVEF. Myocardial accumulation of 125I-BMIPP decreased in the advanced stages of adriamycin cardiomyopathy and was well correlated with the decrease in 18F-FDG accumulation. However, the decrease was less profound than for 18F-FDG; 53.7% +/- 9.8% versus 31.6% +/- 25.4% of control at 9 wk (p = NS), 49.5% +/- 15.3% versus 22.6% +/- 3.5% of control at 10 wk (p < 0.05). Accumulation of 99mTc-MIBI did not differ between controls and the adriamycin treated groups. There were no differences in blood glucose levels between controls and adriamycin treatment groups. Both glucose and fatty acid utilization are decreased in adriamycin-induced cardiomyopathy and these critical impairments in energy metabolism are associated with heart failure. Impaired myocardial glucose utilization measured with 18F-FDG may be a particularly sensitive marker of adriamycin cardiomyopathy.</description><subject>Animals</subject><subject>Deoxyglucose - analogs & derivatives</subject><subject>Doxorubicin - adverse effects</subject><subject>Fatty Acids</subject><subject>Fluorine Radioisotopes</subject><subject>Fluorodeoxyglucose F18</subject><subject>Gated Blood-Pool Imaging</subject><subject>Heart - diagnostic imaging</subject><subject>Heart Failure - chemically induced</subject><subject>Heart Failure - diagnostic imaging</subject><subject>Iodine Radioisotopes</subject><subject>Iodobenzenes</subject><subject>Male</subject><subject>Myocardium - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Technetium Tc 99m Sestamibi</subject><subject>Ventricular Function, Left - drug effects</subject><issn>0161-5505</issn><issn>1535-5667</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNotj09LxDAUxIMo67r6EYTcPBWSzZ8mx2VxVah40PXiobw2qc3SpiVNkfrp7bp7esP8huHNBVpSwUQipEwv0ZJQSRMhiLhGN8NwIIRIpdQCLRSb3VQs0dfr1JUQjIMGv4_FEANEi_fRNe4Xous8Bm9wZquIP62PwZVjAwHvRl_-U-fxxgQH7VTOcnts6tqp6yHW0y26qqAZ7N35rtB-9_ixfU6yt6eX7SZL6jVTMRHV_PGaK1ZoIokWnBeacUV5mc6-TYWQ1jJhJBilZWFTIBUFrrWmRAMYtkL3p95-LFpr8j64FsKUn0fO_OHEa_dd_7hgcz-WjYVwDB98y3iucyrWmv0BU6JdDg</recordid><startdate>19930901</startdate><enddate>19930901</enddate><creator>Wakasugi, Shigetoshi</creator><creator>Fischman, Alan J</creator><creator>Babich, John W</creator><creator>Callahan, Ronald J</creator><creator>Elmaleh, David R</creator><creator>Wilkinson, Robert</creator><creator>Strauss, H. William</creator><general>Soc Nuclear Med</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>19930901</creationdate><title>Myocardial Substrate Utilization and Left Ventricular Function in Adriamycin Cardiomyopathy</title><author>Wakasugi, Shigetoshi ; Fischman, Alan J ; Babich, John W ; Callahan, Ronald J ; Elmaleh, David R ; Wilkinson, Robert ; Strauss, H. William</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h238t-5f5352483b90609544b934814c7352e7556ee35d6ad896be7a0f1a4999109aad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Deoxyglucose - analogs & derivatives</topic><topic>Doxorubicin - adverse effects</topic><topic>Fatty Acids</topic><topic>Fluorine Radioisotopes</topic><topic>Fluorodeoxyglucose F18</topic><topic>Gated Blood-Pool Imaging</topic><topic>Heart - diagnostic imaging</topic><topic>Heart Failure - chemically induced</topic><topic>Heart Failure - diagnostic imaging</topic><topic>Iodine Radioisotopes</topic><topic>Iodobenzenes</topic><topic>Male</topic><topic>Myocardium - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Technetium Tc 99m Sestamibi</topic><topic>Ventricular Function, Left - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wakasugi, Shigetoshi</creatorcontrib><creatorcontrib>Fischman, Alan J</creatorcontrib><creatorcontrib>Babich, John W</creatorcontrib><creatorcontrib>Callahan, Ronald J</creatorcontrib><creatorcontrib>Elmaleh, David R</creatorcontrib><creatorcontrib>Wilkinson, Robert</creatorcontrib><creatorcontrib>Strauss, H. William</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>The Journal of nuclear medicine (1978)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wakasugi, Shigetoshi</au><au>Fischman, Alan J</au><au>Babich, John W</au><au>Callahan, Ronald J</au><au>Elmaleh, David R</au><au>Wilkinson, Robert</au><au>Strauss, H. William</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocardial Substrate Utilization and Left Ventricular Function in Adriamycin Cardiomyopathy</atitle><jtitle>The Journal of nuclear medicine (1978)</jtitle><addtitle>J Nucl Med</addtitle><date>1993-09-01</date><risdate>1993</risdate><volume>34</volume><issue>9</issue><spage>1529</spage><pages>1529-</pages><issn>0161-5505</issn><eissn>1535-5667</eissn><abstract>We evaluated alterations of substrate utilization in a rat model of adriamycin cardiomyopathy with deteriorating left ventricular function. Rats were treated with adriamycin (2 mg/kg), once a week for 6, 8, 9 and 10 wk. Fluorine-18-F-deoxyglucose (18F-FDG) and 125I-beta-methyl-branched fatty acid (125I-BMIPP) were used as tracers of glucose and fatty acid metabolism and 99mTc-hexakis (2-methoxyisobutyl-isonitrile) (99mTc-MIBI) was used as a myocardial blood flow tracer. Left ventricular ejection fraction (LVEF) calculated from gated blood pool images was used as an indicator of cardiac function. LVEF was normal in the 6-wk group (78.0% +/- 4.8%), abruptly decreased in the 8-wk group (43.1% +/- 10.1%) and further deteriorated in the 9-wk group (27.6% +/- 13.4%). Accumulation of 18F-FDG (%kgID/g) in the hearts of adriamycin treated animals progressively decreased compared to controls (2.19% +/- 0.38%); 1.47% +/- 0.42% (p < 0.01) at 6 wk, 1.22% +/- 0.27% (p < 0.001) at 8 wk, 0.69% +/- 0.56% (p < 0.001) at 9 wk and 0.50% +/- 0.08% (p < 0.001) at 10 wk. This decrease occurred earlier than the deterioration in LVEF. Myocardial accumulation of 125I-BMIPP decreased in the advanced stages of adriamycin cardiomyopathy and was well correlated with the decrease in 18F-FDG accumulation. However, the decrease was less profound than for 18F-FDG; 53.7% +/- 9.8% versus 31.6% +/- 25.4% of control at 9 wk (p = NS), 49.5% +/- 15.3% versus 22.6% +/- 3.5% of control at 10 wk (p < 0.05). Accumulation of 99mTc-MIBI did not differ between controls and the adriamycin treated groups. There were no differences in blood glucose levels between controls and adriamycin treatment groups. Both glucose and fatty acid utilization are decreased in adriamycin-induced cardiomyopathy and these critical impairments in energy metabolism are associated with heart failure. Impaired myocardial glucose utilization measured with 18F-FDG may be a particularly sensitive marker of adriamycin cardiomyopathy.</abstract><cop>United States</cop><pub>Soc Nuclear Med</pub><pmid>8355075</pmid></addata></record> |
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| subjects | Animals Deoxyglucose - analogs & derivatives Doxorubicin - adverse effects Fatty Acids Fluorine Radioisotopes Fluorodeoxyglucose F18 Gated Blood-Pool Imaging Heart - diagnostic imaging Heart Failure - chemically induced Heart Failure - diagnostic imaging Iodine Radioisotopes Iodobenzenes Male Myocardium - metabolism Rats Rats, Wistar Technetium Tc 99m Sestamibi Ventricular Function, Left - drug effects |
| title | Myocardial Substrate Utilization and Left Ventricular Function in Adriamycin Cardiomyopathy |
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