Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people
Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease a...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Taglieri, Nevio [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s) 2021 |
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| Übergeordnetes Werk: |
Enthalten in: Journal of nuclear cardiology - New York, NY : Springer, 1994, 29(2021), 4 vom: 10. Feb., Seite 1566-1575 |
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| Übergeordnetes Werk: |
volume:29 ; year:2021 ; number:4 ; day:10 ; month:02 ; pages:1566-1575 |
| Links: |
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| DOI / URN: |
10.1007/s12350-020-02522-5 |
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| Katalog-ID: |
SPR047748141 |
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| 041 | |a eng | ||
| 100 | 1 | |a Taglieri, Nevio |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people |
| 264 | 1 | |c 2021 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
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| 500 | |a © The Author(s) 2021 | ||
| 520 | |a Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. | ||
| 650 | 4 | |a HIV |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a F-fluorodeoxyglucose-positron emission tomography |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Arterial inflammation |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Bonfiglioli, Rachele |4 aut | |
| 700 | 1 | |a Bon, Isabella |4 aut | |
| 700 | 1 | |a Malosso, Pietro |4 aut | |
| 700 | 1 | |a Corovic, Andrej |4 aut | |
| 700 | 1 | |a Bruno, Matteo |4 aut | |
| 700 | 1 | |a Le, Elizabeth |4 aut | |
| 700 | 1 | |a Granozzi, Bianca |4 aut | |
| 700 | 1 | |a Palmerini, Tullio |4 aut | |
| 700 | 1 | |a Ghetti, Gabriele |4 aut | |
| 700 | 1 | |a Tamburello, Martina |4 aut | |
| 700 | 1 | |a Bruno, Antonio Giulio |4 aut | |
| 700 | 1 | |a Saia, Francesco |4 aut | |
| 700 | 1 | |a Tarkin, Jason M. |4 aut | |
| 700 | 1 | |a Rudd, James H. F. |4 aut | |
| 700 | 1 | |a Calza, Leonardo |4 aut | |
| 700 | 1 | |a Fanti, Stefano |4 aut | |
| 700 | 1 | |a Re, Maria Carla |4 aut | |
| 700 | 1 | |a Galié, Nazzareno |4 aut | |
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10.1007/s12350-020-02522-5 doi (DE-627)SPR047748141 (SPR)s12350-020-02522-5-e DE-627 ger DE-627 rakwb eng Taglieri, Nevio verfasserin aut Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. HIV (dpeaa)DE-He213 F-fluorodeoxyglucose-positron emission tomography (dpeaa)DE-He213 Arterial inflammation (dpeaa)DE-He213 Bonfiglioli, Rachele aut Bon, Isabella aut Malosso, Pietro aut Corovic, Andrej aut Bruno, Matteo aut Le, Elizabeth aut Granozzi, Bianca aut Palmerini, Tullio aut Ghetti, Gabriele aut Tamburello, Martina aut Bruno, Antonio Giulio aut Saia, Francesco aut Tarkin, Jason M. aut Rudd, James H. F. aut Calza, Leonardo aut Fanti, Stefano aut Re, Maria Carla aut Galié, Nazzareno aut Enthalten in Journal of nuclear cardiology New York, NY : Springer, 1994 29(2021), 4 vom: 10. Feb., Seite 1566-1575 (DE-627)329395173 (DE-600)2048325-9 1532-6551 nnns volume:29 year:2021 number:4 day:10 month:02 pages:1566-1575 https://dx.doi.org/10.1007/s12350-020-02522-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 29 2021 4 10 02 1566-1575 |
| spelling |
10.1007/s12350-020-02522-5 doi (DE-627)SPR047748141 (SPR)s12350-020-02522-5-e DE-627 ger DE-627 rakwb eng Taglieri, Nevio verfasserin aut Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. HIV (dpeaa)DE-He213 F-fluorodeoxyglucose-positron emission tomography (dpeaa)DE-He213 Arterial inflammation (dpeaa)DE-He213 Bonfiglioli, Rachele aut Bon, Isabella aut Malosso, Pietro aut Corovic, Andrej aut Bruno, Matteo aut Le, Elizabeth aut Granozzi, Bianca aut Palmerini, Tullio aut Ghetti, Gabriele aut Tamburello, Martina aut Bruno, Antonio Giulio aut Saia, Francesco aut Tarkin, Jason M. aut Rudd, James H. F. aut Calza, Leonardo aut Fanti, Stefano aut Re, Maria Carla aut Galié, Nazzareno aut Enthalten in Journal of nuclear cardiology New York, NY : Springer, 1994 29(2021), 4 vom: 10. Feb., Seite 1566-1575 (DE-627)329395173 (DE-600)2048325-9 1532-6551 nnns volume:29 year:2021 number:4 day:10 month:02 pages:1566-1575 https://dx.doi.org/10.1007/s12350-020-02522-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 29 2021 4 10 02 1566-1575 |
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10.1007/s12350-020-02522-5 doi (DE-627)SPR047748141 (SPR)s12350-020-02522-5-e DE-627 ger DE-627 rakwb eng Taglieri, Nevio verfasserin aut Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. HIV (dpeaa)DE-He213 F-fluorodeoxyglucose-positron emission tomography (dpeaa)DE-He213 Arterial inflammation (dpeaa)DE-He213 Bonfiglioli, Rachele aut Bon, Isabella aut Malosso, Pietro aut Corovic, Andrej aut Bruno, Matteo aut Le, Elizabeth aut Granozzi, Bianca aut Palmerini, Tullio aut Ghetti, Gabriele aut Tamburello, Martina aut Bruno, Antonio Giulio aut Saia, Francesco aut Tarkin, Jason M. aut Rudd, James H. F. aut Calza, Leonardo aut Fanti, Stefano aut Re, Maria Carla aut Galié, Nazzareno aut Enthalten in Journal of nuclear cardiology New York, NY : Springer, 1994 29(2021), 4 vom: 10. Feb., Seite 1566-1575 (DE-627)329395173 (DE-600)2048325-9 1532-6551 nnns volume:29 year:2021 number:4 day:10 month:02 pages:1566-1575 https://dx.doi.org/10.1007/s12350-020-02522-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 29 2021 4 10 02 1566-1575 |
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10.1007/s12350-020-02522-5 doi (DE-627)SPR047748141 (SPR)s12350-020-02522-5-e DE-627 ger DE-627 rakwb eng Taglieri, Nevio verfasserin aut Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. HIV (dpeaa)DE-He213 F-fluorodeoxyglucose-positron emission tomography (dpeaa)DE-He213 Arterial inflammation (dpeaa)DE-He213 Bonfiglioli, Rachele aut Bon, Isabella aut Malosso, Pietro aut Corovic, Andrej aut Bruno, Matteo aut Le, Elizabeth aut Granozzi, Bianca aut Palmerini, Tullio aut Ghetti, Gabriele aut Tamburello, Martina aut Bruno, Antonio Giulio aut Saia, Francesco aut Tarkin, Jason M. aut Rudd, James H. F. aut Calza, Leonardo aut Fanti, Stefano aut Re, Maria Carla aut Galié, Nazzareno aut Enthalten in Journal of nuclear cardiology New York, NY : Springer, 1994 29(2021), 4 vom: 10. Feb., Seite 1566-1575 (DE-627)329395173 (DE-600)2048325-9 1532-6551 nnns volume:29 year:2021 number:4 day:10 month:02 pages:1566-1575 https://dx.doi.org/10.1007/s12350-020-02522-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 29 2021 4 10 02 1566-1575 |
| allfieldsSound |
10.1007/s12350-020-02522-5 doi (DE-627)SPR047748141 (SPR)s12350-020-02522-5-e DE-627 ger DE-627 rakwb eng Taglieri, Nevio verfasserin aut Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2021 Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. HIV (dpeaa)DE-He213 F-fluorodeoxyglucose-positron emission tomography (dpeaa)DE-He213 Arterial inflammation (dpeaa)DE-He213 Bonfiglioli, Rachele aut Bon, Isabella aut Malosso, Pietro aut Corovic, Andrej aut Bruno, Matteo aut Le, Elizabeth aut Granozzi, Bianca aut Palmerini, Tullio aut Ghetti, Gabriele aut Tamburello, Martina aut Bruno, Antonio Giulio aut Saia, Francesco aut Tarkin, Jason M. aut Rudd, James H. F. aut Calza, Leonardo aut Fanti, Stefano aut Re, Maria Carla aut Galié, Nazzareno aut Enthalten in Journal of nuclear cardiology New York, NY : Springer, 1994 29(2021), 4 vom: 10. Feb., Seite 1566-1575 (DE-627)329395173 (DE-600)2048325-9 1532-6551 nnns volume:29 year:2021 number:4 day:10 month:02 pages:1566-1575 https://dx.doi.org/10.1007/s12350-020-02522-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 29 2021 4 10 02 1566-1575 |
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Enthalten in Journal of nuclear cardiology 29(2021), 4 vom: 10. Feb., Seite 1566-1575 volume:29 year:2021 number:4 day:10 month:02 pages:1566-1575 |
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Enthalten in Journal of nuclear cardiology 29(2021), 4 vom: 10. Feb., Seite 1566-1575 volume:29 year:2021 number:4 day:10 month:02 pages:1566-1575 |
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Taglieri, Nevio @@aut@@ Bonfiglioli, Rachele @@aut@@ Bon, Isabella @@aut@@ Malosso, Pietro @@aut@@ Corovic, Andrej @@aut@@ Bruno, Matteo @@aut@@ Le, Elizabeth @@aut@@ Granozzi, Bianca @@aut@@ Palmerini, Tullio @@aut@@ Ghetti, Gabriele @@aut@@ Tamburello, Martina @@aut@@ Bruno, Antonio Giulio @@aut@@ Saia, Francesco @@aut@@ Tarkin, Jason M. @@aut@@ Rudd, James H. F. @@aut@@ Calza, Leonardo @@aut@@ Fanti, Stefano @@aut@@ Re, Maria Carla @@aut@@ Galié, Nazzareno @@aut@@ |
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Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. 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Taglieri, Nevio |
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Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people HIV (dpeaa)DE-He213 F-fluorodeoxyglucose-positron emission tomography (dpeaa)DE-He213 Arterial inflammation (dpeaa)DE-He213 |
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Taglieri, Nevio Bonfiglioli, Rachele Bon, Isabella Malosso, Pietro Corovic, Andrej Bruno, Matteo Le, Elizabeth Granozzi, Bianca Palmerini, Tullio Ghetti, Gabriele Tamburello, Martina Bruno, Antonio Giulio Saia, Francesco Tarkin, Jason M. Rudd, James H. F. Calza, Leonardo Fanti, Stefano Re, Maria Carla Galié, Nazzareno |
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Taglieri, Nevio |
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10.1007/s12350-020-02522-5 |
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pattern of arterial inflammation and inflammatory markers in people living with hiv compared with uninfected people |
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Pattern of arterial inflammation and inflammatory markers in people living with HIV compared with uninfected people |
| abstract |
Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. © The Author(s) 2021 |
| abstractGer |
Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. © The Author(s) 2021 |
| abstract_unstemmed |
Study Design To compare arterial inflammation (AI) between people living with HIV (PLWH) and uninfected people as assessed by 18F-Fluorodeoxyglucose (18F-FDG)-positron emission tomography (PET). Methods We prospectively enrolled 20 PLWH and 20 uninfected people with no known cardiovascular disease and at least 3 traditional cardiovascular risk factors. All patients underwent 18F-FDG-PET/computed tomography (CT) of the thorax and neck. Biomarkers linked to inflammation and atherosclerosis were also determined. The primary outcome was AI in ascending aorta (AA) measured as mean maximum target-to-background ratio ($ TBR_{max} $). The independent relationships between HIV status and both $ TBR_{max} $ and biomarkers were evaluated by multivariable linear regression adjusted for body mass index, creatinine, statin therapy, and atherosclerotic cardiovascular 10-year estimated risk (ASCVD). Results Unadjusted mean $ TBR_{max} $ in AA was slightly higher but not statistically different (P = .18) in PLWH (2.07; IQR 1.97, 2.32]) than uninfected people (2.01; IQR 1.85, 2.16]). On multivariable analysis, PLWH had an independent risk of increased mean log-$ TBR_{max} $ in AA (coef = 0.12; 95%CI 0.01,0.22; P = .032). HIV infection was independently associated with higher values of interleukin-10 (coef = 0.83; 95%CI 0.34, 1.32; P = .001), interferon-γ (coef. = 0.90; 95%CI 0.32, 1.47; P = .003), and vascular cell adhesion molecule-1 (VCAM-1) (coef. = 0.75; 95%CI: 0.42, 1.08, P < .001). Conclusions In patients with high cardiovascular risk, HIV status was an independent predictor of increased $ TBR_{max} $ in AA. PLWH also had an increased independent risk of IFN-γ, IL-10, and VCAM-1 levels. © The Author(s) 2021 |
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| score |
7.4030848 |