Atherosclerosis Burdens in Diabetes Mellitus: Assessment by PET Imaging
Arteriosclerosis and its sequelae are the most common cause of death in diabetic patients and one of the reasons why diabetes has entered the top 10 causes of death worldwide, fatalities having doubled since 2000. The literature in the field claims almost unanimously that arteriosclerosis is more fr...
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Published in | International journal of molecular sciences Vol. 23; no. 18; p. 10268 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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06.09.2022
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ISSN | 1422-0067 1661-6596 1422-0067 |
DOI | 10.3390/ijms231810268 |
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Abstract | Arteriosclerosis and its sequelae are the most common cause of death in diabetic patients and one of the reasons why diabetes has entered the top 10 causes of death worldwide, fatalities having doubled since 2000. The literature in the field claims almost unanimously that arteriosclerosis is more frequent or develops more rapidly in diabetic than non-diabetic subjects, and that the disease is caused by arterial inflammation, the control of which should therefore be the goal of therapeutic efforts. These views are mostly based on indirect methodologies, including studies of artery wall thickness or stiffness, or on conventional CT-based imaging used to demonstrate tissue changes occurring late in the disease process. In contrast, imaging with positron emission tomography and computed tomography (PET/CT) applying the tracers 18F-fluorodeoxyglucose (FDG) or 18F-sodium fluoride (NaF) mirrors arterial wall inflammation and microcalcification, respectively, early in the course of the disease, potentially enabling in vivo insight into molecular processes. The present review provides an overview of the literature from the more than 20 and 10 years, respectively, that these two tracers have been used for the study of atherosclerosis, with emphasis on what new information they have provided in relation to diabetes and which questions remain insufficiently elucidated. |
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AbstractList | Arteriosclerosis and its sequelae are the most common cause of death in diabetic patients and one of the reasons why diabetes has entered the top 10 causes of death worldwide, fatalities having doubled since 2000. The literature in the field claims almost unanimously that arteriosclerosis is more frequent or develops more rapidly in diabetic than non-diabetic subjects, and that the disease is caused by arterial inflammation, the control of which should therefore be the goal of therapeutic efforts. These views are mostly based on indirect methodologies, including studies of artery wall thickness or stiffness, or on conventional CT-based imaging used to demonstrate tissue changes occurring late in the disease process. In contrast, imaging with positron emission tomography and computed tomography (PET/CT) applying the tracers 18F-fluorodeoxyglucose (FDG) or 18F-sodium fluoride (NaF) mirrors arterial wall inflammation and microcalcification, respectively, early in the course of the disease, potentially enabling in vivo insight into molecular processes. The present review provides an overview of the literature from the more than 20 and 10 years, respectively, that these two tracers have been used for the study of atherosclerosis, with emphasis on what new information they have provided in relation to diabetes and which questions remain insufficiently elucidated. Arteriosclerosis and its sequelae are the most common cause of death in diabetic patients and one of the reasons why diabetes has entered the top 10 causes of death worldwide, fatalities having doubled since 2000. The literature in the field claims almost unanimously that arteriosclerosis is more frequent or develops more rapidly in diabetic than non-diabetic subjects, and that the disease is caused by arterial inflammation, the control of which should therefore be the goal of therapeutic efforts. These views are mostly based on indirect methodologies, including studies of artery wall thickness or stiffness, or on conventional CT-based imaging used to demonstrate tissue changes occurring late in the disease process. In contrast, imaging with positron emission tomography and computed tomography (PET/CT) applying the tracers 18F-fluorodeoxyglucose (FDG) or 18F-sodium fluoride (NaF) mirrors arterial wall inflammation and microcalcification, respectively, early in the course of the disease, potentially enabling in vivo insight into molecular processes. The present review provides an overview of the literature from the more than 20 and 10 years, respectively, that these two tracers have been used for the study of atherosclerosis, with emphasis on what new information they have provided in relation to diabetes and which questions remain insufficiently elucidated.Arteriosclerosis and its sequelae are the most common cause of death in diabetic patients and one of the reasons why diabetes has entered the top 10 causes of death worldwide, fatalities having doubled since 2000. The literature in the field claims almost unanimously that arteriosclerosis is more frequent or develops more rapidly in diabetic than non-diabetic subjects, and that the disease is caused by arterial inflammation, the control of which should therefore be the goal of therapeutic efforts. These views are mostly based on indirect methodologies, including studies of artery wall thickness or stiffness, or on conventional CT-based imaging used to demonstrate tissue changes occurring late in the disease process. In contrast, imaging with positron emission tomography and computed tomography (PET/CT) applying the tracers 18F-fluorodeoxyglucose (FDG) or 18F-sodium fluoride (NaF) mirrors arterial wall inflammation and microcalcification, respectively, early in the course of the disease, potentially enabling in vivo insight into molecular processes. The present review provides an overview of the literature from the more than 20 and 10 years, respectively, that these two tracers have been used for the study of atherosclerosis, with emphasis on what new information they have provided in relation to diabetes and which questions remain insufficiently elucidated. Arteriosclerosis and its sequelae are the most common cause of death in diabetic patients and one of the reasons why diabetes has entered the top 10 causes of death worldwide, fatalities having doubled since 2000. The literature in the field claims almost unanimously that arteriosclerosis is more frequent or develops more rapidly in diabetic than non-diabetic subjects, and that the disease is caused by arterial inflammation, the control of which should therefore be the goal of therapeutic efforts. These views are mostly based on indirect methodologies, including studies of artery wall thickness or stiffness, or on conventional CT-based imaging used to demonstrate tissue changes occurring late in the disease process. In contrast, imaging with positron emission tomography and computed tomography (PET/CT) applying the tracers 18 F-fluorodeoxyglucose (FDG) or 18 F-sodium fluoride (NaF) mirrors arterial wall inflammation and microcalcification, respectively, early in the course of the disease, potentially enabling in vivo insight into molecular processes. The present review provides an overview of the literature from the more than 20 and 10 years, respectively, that these two tracers have been used for the study of atherosclerosis, with emphasis on what new information they have provided in relation to diabetes and which questions remain insufficiently elucidated. |
Author | Alavi, Abass Gerke, Oke Høilund-Carlsen, Poul F. Revheim, Mona-Elisabeth Werner, Thomas J. Piri, Reza Madsen, Per Lav Sturek, Michael |
AuthorAffiliation | 4 Division of Radiology and Nuclear Medicine, Oslo University Hospital, 0424 Oslo, Norway 1 Department of Nuclear Medicine, Odense University Hospital, 5000 Odense, Denmark 3 Department of Cardiology, Herlev Gentofte Hospital, 2900 Herlev, Denmark 5 Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, 0315 Oslo, Norway 6 Department of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA 2 Research Unit of Clinical Physiology and Nuclear Medicine, Department of Clinical Research, University of Southern Denmark, 5230 Odense, Denmark 7 Department of Anatomy, Cell Biology, Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA |
AuthorAffiliation_xml | – name: 6 Department of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA – name: 2 Research Unit of Clinical Physiology and Nuclear Medicine, Department of Clinical Research, University of Southern Denmark, 5230 Odense, Denmark – name: 7 Department of Anatomy, Cell Biology, Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA – name: 3 Department of Cardiology, Herlev Gentofte Hospital, 2900 Herlev, Denmark – name: 5 Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, 0315 Oslo, Norway – name: 1 Department of Nuclear Medicine, Odense University Hospital, 5000 Odense, Denmark – name: 4 Division of Radiology and Nuclear Medicine, Oslo University Hospital, 0424 Oslo, Norway |
Author_xml | – sequence: 1 givenname: Poul F. orcidid: 0000-0001-7420-2367 surname: Høilund-Carlsen fullname: Høilund-Carlsen, Poul F. – sequence: 2 givenname: Reza orcidid: 0000-0002-6379-3373 surname: Piri fullname: Piri, Reza – sequence: 3 givenname: Per Lav surname: Madsen fullname: Madsen, Per Lav – sequence: 4 givenname: Mona-Elisabeth orcidid: 0000-0003-3300-7420 surname: Revheim fullname: Revheim, Mona-Elisabeth – sequence: 5 givenname: Thomas J. surname: Werner fullname: Werner, Thomas J. – sequence: 6 givenname: Abass surname: Alavi fullname: Alavi, Abass – sequence: 7 givenname: Oke orcidid: 0000-0001-6335-3303 surname: Gerke fullname: Gerke, Oke – sequence: 8 givenname: Michael orcidid: 0000-0002-2920-7406 surname: Sturek fullname: Sturek, Michael |
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CitedBy_id | crossref_primary_10_1007_s12149_023_01875_4 crossref_primary_10_1021_acssensors_2c02590 crossref_primary_10_1016_j_cpcardiol_2023_101925 crossref_primary_10_62347_NLLM5784 crossref_primary_10_3390_ph17070929 crossref_primary_10_1152_ajpheart_00539_2024 crossref_primary_10_1016_j_atherosclerosis_2023_117275 crossref_primary_10_1021_acs_jmedchem_3c00720 |
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