Noninvasive in vivo measurement of vascular inflammation with F-18 fluorodeoxyglucose positron emission tomography
Fluorine 18 fluorodeoxyglucose (FDG) has been shown to accumulate in inflamed tissues. However, it is not known whether vascular inflammation can be measured noninvasively. The aim of this study was to test the hypothesis that vascular inflammation can be measured noninvasively by use of positron em...
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| description | Fluorine 18 fluorodeoxyglucose (FDG) has been shown to accumulate in inflamed tissues. However, it is not known whether vascular inflammation can be measured noninvasively. The aim of this study was to test the hypothesis that vascular inflammation can be measured noninvasively by use of positron emission tomography (PET) with FDG.
Inflamed atherosclerotic lesions were induced in 9 male New Zealand white rabbits via balloon injury of the aortoiliac arterial segment and exposure to a high cholesterol diet. Ten rabbits fed standard chow served as controls. Three to six months after balloon injury, the rabbits were injected with FDG (1 mCi/kg), after which aortic uptake of FDG was assessed (3 hours after injection). Biodistribution of FDG activity within aortic segments was obtained by use of standard well gamma counting. FDG uptake was also determined noninvasively in a subset of 6 live atherosclerotic rabbits and 5 normal rabbits, via PET imaging and measurement of standardized uptake values over the abdominal aorta. Plaque macrophage density and smooth muscle cell density were determined by planimetric analysis of RAM-11 and smooth muscle actin staining, respectively. Biodistribution of FDG within nontarget organs was similar between atherosclerotic and control rabbits. However, well counter measurements of FDG uptake were significantly higher within atherosclerotic aortas compared with control aortas (
P < .001). Within the upper abdominal aorta of the atherosclerotic group (area of greatest plaque formation), there was an approximately 19-fold increase in FDG uptake compared with controls (108.9 ± 55.6 percent injected dose [%ID]/g × 10
3 vs 5.7 ± 1.2 %ID/g × 10
3 [mean ± SEM],
P < .001). In parallel with these findings, FDG uptake, as determined by PET, was higher in atherosclerotic aortas (standardized uptake value for atherosclerotic aortas vs control aortas, 0.68 ± 0.06 vs 0.13 ± 0.01;
P < .001). Moreover, macrophage density, assessed histologically, correlated with noninvasive (PET) measurements of FDG uptake (
r = 0.93,
P < .0001). In contrast to this finding, FDG uptake did not correlate with either aortic wall thickness or smooth muscle cell staining of the specimens.
These data show that FDG accumulates in macrophage-rich atherosclerotic plaques and demonstrate that vascular macrophage activity can be quantified noninvasively with FDG-PET. As such, measurement of vascular FDG uptake with PET holds promise for the noninvasive characterization of |
| doi_str_mv | 10.1016/j.nuclcard.2005.03.002 |
| format | Article |
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Inflamed atherosclerotic lesions were induced in 9 male New Zealand white rabbits via balloon injury of the aortoiliac arterial segment and exposure to a high cholesterol diet. Ten rabbits fed standard chow served as controls. Three to six months after balloon injury, the rabbits were injected with FDG (1 mCi/kg), after which aortic uptake of FDG was assessed (3 hours after injection). Biodistribution of FDG activity within aortic segments was obtained by use of standard well gamma counting. FDG uptake was also determined noninvasively in a subset of 6 live atherosclerotic rabbits and 5 normal rabbits, via PET imaging and measurement of standardized uptake values over the abdominal aorta. Plaque macrophage density and smooth muscle cell density were determined by planimetric analysis of RAM-11 and smooth muscle actin staining, respectively. Biodistribution of FDG within nontarget organs was similar between atherosclerotic and control rabbits. However, well counter measurements of FDG uptake were significantly higher within atherosclerotic aortas compared with control aortas (
P < .001). Within the upper abdominal aorta of the atherosclerotic group (area of greatest plaque formation), there was an approximately 19-fold increase in FDG uptake compared with controls (108.9 ± 55.6 percent injected dose [%ID]/g × 10
3 vs 5.7 ± 1.2 %ID/g × 10
3 [mean ± SEM],
P < .001). In parallel with these findings, FDG uptake, as determined by PET, was higher in atherosclerotic aortas (standardized uptake value for atherosclerotic aortas vs control aortas, 0.68 ± 0.06 vs 0.13 ± 0.01;
P < .001). Moreover, macrophage density, assessed histologically, correlated with noninvasive (PET) measurements of FDG uptake (
r = 0.93,
P < .0001). In contrast to this finding, FDG uptake did not correlate with either aortic wall thickness or smooth muscle cell staining of the specimens.
These data show that FDG accumulates in macrophage-rich atherosclerotic plaques and demonstrate that vascular macrophage activity can be quantified noninvasively with FDG-PET. As such, measurement of vascular FDG uptake with PET holds promise for the noninvasive characterization of vascular inflammation.</description><identifier>ISSN: 1071-3581</identifier><identifier>EISSN: 1532-6551</identifier><identifier>DOI: 10.1016/j.nuclcard.2005.03.002</identifier><identifier>PMID: 15944534</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Arteriosclerosis - complications ; Arteriosclerosis - diagnostic imaging ; Arteriosclerosis - metabolism ; Atherosclerosis ; Biodistribution ; Carotid Stenosis - complications ; Carotid Stenosis - diagnostic imaging ; Carotid Stenosis - metabolism ; Cells ; Coronary vessels ; fluorodeoxyglucose ; Fluorodeoxyglucose F18 - pharmacokinetics ; Inflammation ; macrophage ; Male ; Muscular system ; Nuclear Medicine - methods ; Nuclear Medicine - trends ; Organ Specificity ; Positron-Emission Tomography - methods ; Practice Guidelines as Topic ; Practice Patterns, Physicians ; Prognosis ; Proteins ; Rabbits ; Radionuclide Imaging - methods ; Radionuclide Imaging - trends ; Radiopharmaceuticals ; Risk Assessment - methods ; Risk Factors ; Smooth muscle ; Tissue Distribution ; Tomography ; Vasculitis - diagnostic imaging ; Vasculitis - etiology ; Vasculitis - metabolism ; vulnerable plaque</subject><ispartof>Journal of nuclear cardiology, 2005-05, Vol.12 (3), p.294-301</ispartof><rights>2005 American Society of Nuclear Cardiology</rights><rights>American Society of Nuclear Cardiology 2005.</rights><rights>American Society of Nuclear Cardiology 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-d4540acf667cc3bf1bb735321f003654f9cc02390d5a08364928bbb285bb0c43</citedby><cites>FETCH-LOGICAL-c453t-d4540acf667cc3bf1bb735321f003654f9cc02390d5a08364928bbb285bb0c43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15944534$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tawakol, Ahmed</creatorcontrib><creatorcontrib>Migrino, Raymond Q.</creatorcontrib><creatorcontrib>Hoffmann, Udo</creatorcontrib><creatorcontrib>Abbara, Suhny</creatorcontrib><creatorcontrib>Houser, Stuart</creatorcontrib><creatorcontrib>Gewirtz, Henry</creatorcontrib><creatorcontrib>Muller, James E.</creatorcontrib><creatorcontrib>Brady, Thomas J.</creatorcontrib><creatorcontrib>Fischman, Alan J.</creatorcontrib><title>Noninvasive in vivo measurement of vascular inflammation with F-18 fluorodeoxyglucose positron emission tomography</title><title>Journal of nuclear cardiology</title><addtitle>J Nucl Cardiol</addtitle><description>Fluorine 18 fluorodeoxyglucose (FDG) has been shown to accumulate in inflamed tissues. However, it is not known whether vascular inflammation can be measured noninvasively. The aim of this study was to test the hypothesis that vascular inflammation can be measured noninvasively by use of positron emission tomography (PET) with FDG.
Inflamed atherosclerotic lesions were induced in 9 male New Zealand white rabbits via balloon injury of the aortoiliac arterial segment and exposure to a high cholesterol diet. Ten rabbits fed standard chow served as controls. Three to six months after balloon injury, the rabbits were injected with FDG (1 mCi/kg), after which aortic uptake of FDG was assessed (3 hours after injection). Biodistribution of FDG activity within aortic segments was obtained by use of standard well gamma counting. FDG uptake was also determined noninvasively in a subset of 6 live atherosclerotic rabbits and 5 normal rabbits, via PET imaging and measurement of standardized uptake values over the abdominal aorta. Plaque macrophage density and smooth muscle cell density were determined by planimetric analysis of RAM-11 and smooth muscle actin staining, respectively. Biodistribution of FDG within nontarget organs was similar between atherosclerotic and control rabbits. However, well counter measurements of FDG uptake were significantly higher within atherosclerotic aortas compared with control aortas (
P < .001). Within the upper abdominal aorta of the atherosclerotic group (area of greatest plaque formation), there was an approximately 19-fold increase in FDG uptake compared with controls (108.9 ± 55.6 percent injected dose [%ID]/g × 10
3 vs 5.7 ± 1.2 %ID/g × 10
3 [mean ± SEM],
P < .001). In parallel with these findings, FDG uptake, as determined by PET, was higher in atherosclerotic aortas (standardized uptake value for atherosclerotic aortas vs control aortas, 0.68 ± 0.06 vs 0.13 ± 0.01;
P < .001). Moreover, macrophage density, assessed histologically, correlated with noninvasive (PET) measurements of FDG uptake (
r = 0.93,
P < .0001). In contrast to this finding, FDG uptake did not correlate with either aortic wall thickness or smooth muscle cell staining of the specimens.
These data show that FDG accumulates in macrophage-rich atherosclerotic plaques and demonstrate that vascular macrophage activity can be quantified noninvasively with FDG-PET. As such, measurement of vascular FDG uptake with PET holds promise for the noninvasive characterization of vascular inflammation.</description><subject>Animals</subject><subject>Arteriosclerosis - complications</subject><subject>Arteriosclerosis - diagnostic imaging</subject><subject>Arteriosclerosis - metabolism</subject><subject>Atherosclerosis</subject><subject>Biodistribution</subject><subject>Carotid Stenosis - complications</subject><subject>Carotid Stenosis - diagnostic imaging</subject><subject>Carotid Stenosis - metabolism</subject><subject>Cells</subject><subject>Coronary vessels</subject><subject>fluorodeoxyglucose</subject><subject>Fluorodeoxyglucose F18 - pharmacokinetics</subject><subject>Inflammation</subject><subject>macrophage</subject><subject>Male</subject><subject>Muscular system</subject><subject>Nuclear Medicine - methods</subject><subject>Nuclear Medicine - trends</subject><subject>Organ Specificity</subject><subject>Positron-Emission Tomography - methods</subject><subject>Practice Guidelines as Topic</subject><subject>Practice Patterns, Physicians</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Rabbits</subject><subject>Radionuclide Imaging - methods</subject><subject>Radionuclide Imaging - trends</subject><subject>Radiopharmaceuticals</subject><subject>Risk Assessment - methods</subject><subject>Risk Factors</subject><subject>Smooth muscle</subject><subject>Tissue Distribution</subject><subject>Tomography</subject><subject>Vasculitis - diagnostic imaging</subject><subject>Vasculitis - etiology</subject><subject>Vasculitis - metabolism</subject><subject>vulnerable plaque</subject><issn>1071-3581</issn><issn>1532-6551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkU9v1DAQxSMEoqXwFaoIDpwSxv-TG6iigFTBpXfLccatV0m82HFgvz1e7SIkJMRpLM1v3rzxq6prAi0BIt_t2iXbyZo4thRAtMBaAPqkuiSC0UYKQZ6WNyjSMNGRi-pFSjsA6FnfP68uiOg5F4xfVvFrWPyymeQ3rP1Sb34L9Ywm5YgzLmsdXF26Nk8mlr6bzDyb1Yel_uHXx_q2IV3tphxiGDH8PDxM2YaE9T4kv8ZC4exTOuJrmMNDNPvHw8vqmTNTwlfnelXd3368v_nc3H379OXmw11ji7W1GbngYKyTUlnLBkeGQbFyHHEATAruemuBsh5GYaBjkve0G4aBdmIYwHJ2Vb09ye5j-J4xrbpYsThNZsGQk1aCd0p1ShTy9V_kLuS4FG9aMS4JlUoV6M2_IFpUqABCSaHkibIxpBTR6X30s4kHTUAfg9M7_Ts4fQxOA9MluDJ4fZbPw4zjn7FzUgV4fwKwfNnmMepkPS4WRx_RrnoM_n87fgHaO64O</recordid><startdate>20050501</startdate><enddate>20050501</enddate><creator>Tawakol, Ahmed</creator><creator>Migrino, Raymond Q.</creator><creator>Hoffmann, Udo</creator><creator>Abbara, Suhny</creator><creator>Houser, Stuart</creator><creator>Gewirtz, Henry</creator><creator>Muller, James E.</creator><creator>Brady, Thomas J.</creator><creator>Fischman, Alan J.</creator><general>Elsevier Inc</general><general>Springer Nature B.V</general><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>K9.</scope><scope>NAPCQ</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20050501</creationdate><title>Noninvasive in vivo measurement of vascular inflammation with F-18 fluorodeoxyglucose positron emission tomography</title><author>Tawakol, Ahmed ; Migrino, Raymond Q. ; Hoffmann, Udo ; Abbara, Suhny ; Houser, Stuart ; Gewirtz, Henry ; Muller, James E. ; Brady, Thomas J. ; Fischman, Alan J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-d4540acf667cc3bf1bb735321f003654f9cc02390d5a08364928bbb285bb0c43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Arteriosclerosis - complications</topic><topic>Arteriosclerosis - diagnostic imaging</topic><topic>Arteriosclerosis - metabolism</topic><topic>Atherosclerosis</topic><topic>Biodistribution</topic><topic>Carotid Stenosis - complications</topic><topic>Carotid Stenosis - diagnostic imaging</topic><topic>Carotid Stenosis - metabolism</topic><topic>Cells</topic><topic>Coronary vessels</topic><topic>fluorodeoxyglucose</topic><topic>Fluorodeoxyglucose F18 - pharmacokinetics</topic><topic>Inflammation</topic><topic>macrophage</topic><topic>Male</topic><topic>Muscular system</topic><topic>Nuclear Medicine - methods</topic><topic>Nuclear Medicine - trends</topic><topic>Organ Specificity</topic><topic>Positron-Emission Tomography - methods</topic><topic>Practice Guidelines as Topic</topic><topic>Practice Patterns, Physicians</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Rabbits</topic><topic>Radionuclide Imaging - methods</topic><topic>Radionuclide Imaging - trends</topic><topic>Radiopharmaceuticals</topic><topic>Risk Assessment - methods</topic><topic>Risk Factors</topic><topic>Smooth muscle</topic><topic>Tissue Distribution</topic><topic>Tomography</topic><topic>Vasculitis - diagnostic imaging</topic><topic>Vasculitis - etiology</topic><topic>Vasculitis - metabolism</topic><topic>vulnerable plaque</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tawakol, Ahmed</creatorcontrib><creatorcontrib>Migrino, Raymond Q.</creatorcontrib><creatorcontrib>Hoffmann, Udo</creatorcontrib><creatorcontrib>Abbara, Suhny</creatorcontrib><creatorcontrib>Houser, Stuart</creatorcontrib><creatorcontrib>Gewirtz, Henry</creatorcontrib><creatorcontrib>Muller, James E.</creatorcontrib><creatorcontrib>Brady, Thomas J.</creatorcontrib><creatorcontrib>Fischman, Alan J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of nuclear cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tawakol, Ahmed</au><au>Migrino, Raymond Q.</au><au>Hoffmann, Udo</au><au>Abbara, Suhny</au><au>Houser, Stuart</au><au>Gewirtz, Henry</au><au>Muller, James E.</au><au>Brady, Thomas J.</au><au>Fischman, Alan J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Noninvasive in vivo measurement of vascular inflammation with F-18 fluorodeoxyglucose positron emission tomography</atitle><jtitle>Journal of nuclear cardiology</jtitle><addtitle>J Nucl Cardiol</addtitle><date>2005-05-01</date><risdate>2005</risdate><volume>12</volume><issue>3</issue><spage>294</spage><epage>301</epage><pages>294-301</pages><issn>1071-3581</issn><eissn>1532-6551</eissn><abstract>Fluorine 18 fluorodeoxyglucose (FDG) has been shown to accumulate in inflamed tissues. However, it is not known whether vascular inflammation can be measured noninvasively. The aim of this study was to test the hypothesis that vascular inflammation can be measured noninvasively by use of positron emission tomography (PET) with FDG.
Inflamed atherosclerotic lesions were induced in 9 male New Zealand white rabbits via balloon injury of the aortoiliac arterial segment and exposure to a high cholesterol diet. Ten rabbits fed standard chow served as controls. Three to six months after balloon injury, the rabbits were injected with FDG (1 mCi/kg), after which aortic uptake of FDG was assessed (3 hours after injection). Biodistribution of FDG activity within aortic segments was obtained by use of standard well gamma counting. FDG uptake was also determined noninvasively in a subset of 6 live atherosclerotic rabbits and 5 normal rabbits, via PET imaging and measurement of standardized uptake values over the abdominal aorta. Plaque macrophage density and smooth muscle cell density were determined by planimetric analysis of RAM-11 and smooth muscle actin staining, respectively. Biodistribution of FDG within nontarget organs was similar between atherosclerotic and control rabbits. However, well counter measurements of FDG uptake were significantly higher within atherosclerotic aortas compared with control aortas (
P < .001). Within the upper abdominal aorta of the atherosclerotic group (area of greatest plaque formation), there was an approximately 19-fold increase in FDG uptake compared with controls (108.9 ± 55.6 percent injected dose [%ID]/g × 10
3 vs 5.7 ± 1.2 %ID/g × 10
3 [mean ± SEM],
P < .001). In parallel with these findings, FDG uptake, as determined by PET, was higher in atherosclerotic aortas (standardized uptake value for atherosclerotic aortas vs control aortas, 0.68 ± 0.06 vs 0.13 ± 0.01;
P < .001). Moreover, macrophage density, assessed histologically, correlated with noninvasive (PET) measurements of FDG uptake (
r = 0.93,
P < .0001). In contrast to this finding, FDG uptake did not correlate with either aortic wall thickness or smooth muscle cell staining of the specimens.
These data show that FDG accumulates in macrophage-rich atherosclerotic plaques and demonstrate that vascular macrophage activity can be quantified noninvasively with FDG-PET. As such, measurement of vascular FDG uptake with PET holds promise for the noninvasive characterization of vascular inflammation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15944534</pmid><doi>10.1016/j.nuclcard.2005.03.002</doi><tpages>8</tpages></addata></record> |
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| ispartof | Journal of nuclear cardiology, 2005-05, Vol.12 (3), p.294-301 |
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| subjects | Animals Arteriosclerosis - complications Arteriosclerosis - diagnostic imaging Arteriosclerosis - metabolism Atherosclerosis Biodistribution Carotid Stenosis - complications Carotid Stenosis - diagnostic imaging Carotid Stenosis - metabolism Cells Coronary vessels fluorodeoxyglucose Fluorodeoxyglucose F18 - pharmacokinetics Inflammation macrophage Male Muscular system Nuclear Medicine - methods Nuclear Medicine - trends Organ Specificity Positron-Emission Tomography - methods Practice Guidelines as Topic Practice Patterns, Physicians Prognosis Proteins Rabbits Radionuclide Imaging - methods Radionuclide Imaging - trends Radiopharmaceuticals Risk Assessment - methods Risk Factors Smooth muscle Tissue Distribution Tomography Vasculitis - diagnostic imaging Vasculitis - etiology Vasculitis - metabolism vulnerable plaque |
| title | Noninvasive in vivo measurement of vascular inflammation with F-18 fluorodeoxyglucose positron emission tomography |
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