AUTHOR AFFILIATIONS .uk



Invited EditorialCan Imaging Improve our Understanding ofCardiovascular Pathophysiology?Marc R Dweck MD PhD1,2 Fabien Hyafil MD PhD3AUTHOR AFFILIATIONS1 Translation Molecular Imaging Institute, Icahn School of Medicine at Mount-Sinai, New York2 British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom 3 Department of Nuclear Medicine, Bichat University Hospital, Assistance Publique –H?pitaux de Paris, Département Hospitalo-Universitaire FIRE, Inserm 1148, Paris, FranceWord Count: 1494References:13CORRESPONDING AUTHORMarc Dweck, MD PhDChancellor’s BuildingUniversity of Edinburgh49 Little France CrescentEH16 4SBEmail: marc.dweck@ed.ac.ukFINANCIAL SUPPORTMRD is supported by the British Heart Foundation (FS/14/78/31020) and is the recipient of the Sir Jules Thorn Award for Biomedical Research 2015 (15/JTA). CONFLICTS OF INTERESTNoneRecent advances in non-invasive imaging technology now allow us to simultaneously investigate cardiovascular anatomy, soft tissue characteristics and disease activity as pathological processes occur in the body. Moreover this can be performed at different anatomical locations so that the interplay between different organ systems can be interrogated. This offers us a powerful tool with which to improve our understanding of the mechanisms underlying cardiovascular disease and the adverse events that ensue. This is the focus of the manuscript by Figueroa and colleagues in the current edition of Circulation Cardiovascular Imaging, ADDIN PAPERS2_CITATIONS <citation><uuid>922B0872-DB7C-40B6-B70A-DE8318E6C363</uuid><priority>0</priority><publications><publication><endpage>9:e004043</endpage><title>Relationship between Measures of Adiposity, Arterial Inflammation and Subsequent Cardiovascular Events</title><startpage>2016</startpage><type>400</type><subtype>400</subtype><uuid>8538F3C0-7B69-40BA-ADFE-23117A334C40</uuid><bundle><publication><title>Circulation. Cardiovascular imaging</title><type>-100</type><subtype>-100</subtype><uuid>EA3448B4-90CC-4FA2-8570-7BA609D5B4B0</uuid></publication></bundle><authors><author><firstName>A</firstName><middleNames>L</middleNames><lastName>FIguero</lastName></author><author><firstName>RAP</firstName><lastName>Takx</lastName></author><author><firstName>M</firstName><middleNames>H</middleNames><lastName>McNabb</lastName></author><author><firstName>A</firstName><lastName>Abdelbaky</lastName></author><author><firstName>Z</firstName><middleNames>R</middleNames><lastName>Lavender</lastName></author><author><firstName>R</firstName><middleNames>S</middleNames><lastName>Kaplan</lastName></author><author><firstName>Q</firstName><middleNames>A</middleNames><lastName>Truong</lastName></author><author><firstName>J</firstName><lastName>Lo</lastName></author><author><firstName>B</firstName><middleNames>B</middleNames><lastName>Ghoshhajra</lastName></author><author><firstName>S</firstName><middleNames>K</middleNames><lastName>Grinspoon</lastName></author><author><firstName>U</firstName><lastName>HOFFMANN</lastName></author><author><firstName>A</firstName><lastName>Tawakol</lastName></author></authors></publication></publications><cites></cites></citation>1 where the authors have used both anatomical computed tomography (CT) assessments and positron emission tomography (PET) measures of disease activity to investigate the relationship between visceral adiposity, vascular inflammation and cardiovascular events. Recently the view on adipose visceral tissue has evolved from a passive lipid storage compartment towards an active endocrine organ able to secrete large amounts of bioactive factors and pro-inflammatory cytokines, which might play a role in the progression of atherosclerosis ADDIN PAPERS2_CITATIONS <citation><uuid>6EC79543-B54A-4983-9586-C738B6B8041E</uuid><priority>0</priority><publications><publication><uuid>A7D5362B-E3D6-4C90-A983-FFA35EE7B3C3</uuid><volume>444</volume><doi>10.1038/nature05487</doi><startpage>875</startpage><publication_date>99200612141200000000222000</publication_date><url> linking obesity with cardiovascular disease.</title><institution>University of Antwerp, Faculty of Medicine, Department of Diabetology, Metabolism and Clinical Nutrition, Antwerp University Hospital, Wilrijkstraat 10, B-2650 Edegem, Belgium. luc.van.gaal@uza.be</institution><number>7121</number><subtype>400</subtype><endpage>880</endpage><bundle><publication><publisher>Nature Publishing Group</publisher><title>Nature</title><type>-100</type><subtype>-100</subtype><uuid>63198680-FA84-4014-9D05-052D25FC19A6</uuid></publication></bundle><authors><author><lastName>Gaal</lastName><nonDroppingParticle>Van</nonDroppingParticle><firstName>Luc</firstName><middleNames>F</middleNames></author><author><firstName>Ilse</firstName><middleNames>L</middleNames><lastName>Mertens</lastName></author><author><lastName>Block</lastName><nonDroppingParticle>De</nonDroppingParticle><firstName>Christophe</firstName><middleNames>E</middleNames></author></authors></publication></publications><cites></cites></citation>2 The current study is therefore both timely and of clinical relevance, especially given the worldwide epidemic in obesity rates and the acceptance that obesity represents a major modifiable risk factor for coronary artery disease. ADDIN PAPERS2_CITATIONS <citation><uuid>EF00E16B-B15D-4604-8E45-4FDB5B380B24</uuid><priority>0</priority><publications><publication><volume>113</volume><publication_date>99200606271200000000222000</publication_date><number>25</number><doi>10.1161/CIRCULATIONAHA.106.176583</doi><startpage>2943</startpage><title>Preventing cardiovascular disease and diabetes: a call to action from the American Diabetes Association and the American Heart Association.</title><uuid>4CC12E16-81E7-45C4-843B-93258626076A</uuid><subtype>400</subtype><endpage>2946</endpage><type>400</type><url> The strength and originality of this work is that the Authors have tested their hypothesis in a large cohort of more than 400 patients imaged with 18F-fluorodeoxyglucose (FDG) PET with a median follow-up of 4 years for the development of cardiovascular events. This builds upon this research group’s extensive experience and expertise in evaluating vascular inflammation with FDG-PET that has provided a series of key pathological insights. Ultimately they have here demonstrated that CT measures of visceral fat demonstrate an association with vascular inflammation (the modest correlation is perhaps not unexpected given the multitude of factors with pro-inflammatory effects), and that patients with a combination of both elevated visceral fat and vascular inflammation have an increased rate of subsequent vascular events. Importantly the imaging assessment of visceral fat provided incremental information to simpler and cheaper assessments such as the body mass index, which did not demonstrate the same associations and predictive capability. This therefore adds credence to the growing argument that visceral fat is an important player in the progression of systemic atherosclerosis and worthy of study beyond more generalized measures of systemic adiposity. Moreover it adds support to the expanding body of evidence indicating that assessments of vascular inflammation with 18F-FDG are of prognostic value. The authors are to be congratulated on these two important additions to the literature. Whilst such retrospective studies are of undoubted value in establishing potential pathological associations, there are limitations to the conclusions they allow us to draw. For example the correlation between visceral adiposity and vascular inflammation cannot establish causality. Therefore whilst it is interesting to speculate that visceral fat directly secretes factors that promote vascular inflammation, progression and adverse events, this conclusion cannot be established directly from this data. Moreover as the authors clearly acknowledge the study of cancer patients will always be prone to referral bias limiting generalizability. The major value of these retrospective observational data is therefore in generating novel hypotheses, to then be tested in prospective and definitive mechanistic studies. The design of definitive mechanistic imaging studies is challenging and has been limited by concerns regarding the radiation exposure associated with multiple time-point studies. Perhaps the best model focuses on imaging a chosen parameter both before and after an intervention, allowing the effect of that intercession to be assessed in isolation. Indeed this approach has been used by the authors’ research group and others to investigate the impact of drug therapy on atherosclerotic plaque anatomy and activity. Statins for example have been demonstrated to reduce both carotid atherosclerotic plaque burden, ADDIN PAPERS2_CITATIONS <citation><uuid>E87ADD77-4C36-446E-88C7-66FD57D4C783</uuid><priority>0</priority><publications><publication><volume>104</volume><publication_date>99200107171200000000222000</publication_date><number>3</number><institution>Cardiovascular Biology Research Laboratory, the Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY, USA.</institution><startpage>249</startpage><title>Effects of lipid-lowering by simvastatin on human atherosclerotic lesions: a longitudinal study by high-resolution, noninvasive magnetic resonance imaging.</title><uuid>F1285E0B-30DC-4C83-A6D9-D689764F6004</uuid><subtype>400</subtype><endpage>252</endpage><type>400</type><url> lowering by simvastatin induces regression of human atherosclerotic lesions: two years' follow-up by high-resolution noninvasive magnetic resonance imaging.</title><institution>Cardiovascular Biology Research Laboratory, Mount Sinai School of Medicine, New York, NY 10029, USA.</institution><number>23</number><subtype>400</subtype><endpage>2887</endpage><bundle><publication><title>Circulation</title><type>-100</type><subtype>-100</subtype><uuid>720785A6-8FCF-440D-A26F-FCA94EE0FEC7</uuid></publication></bundle><authors><author><firstName>Roberto</firstName><lastName>Corti</lastName></author><author><firstName>Valentin</firstName><lastName>Fuster</lastName></author><author><firstName>Zahi</firstName><middleNames>a</middleNames><lastName>Fayad</lastName></author><author><firstName>Stephen</firstName><middleNames>G</middleNames><lastName>Worthley</lastName></author><author><firstName>Gerard</firstName><lastName>Helft</lastName></author><author><firstName>Donald</firstName><lastName>Smith</lastName></author><author><firstName>Jesse</firstName><lastName>Weinberger</lastName></author><author><firstName>Jolanda</firstName><lastName>Wentzel</lastName></author><author><firstName>Gabor</firstName><lastName>Mizsei</lastName></author><author><firstName>Michele</firstName><lastName>Mercuri</lastName></author><author><firstName>Juan</firstName><middleNames>J</middleNames><lastName>Badimon</lastName></author></authors></publication></publications><cites></cites></citation>4,5 and plaque composition ADDIN PAPERS2_CITATIONS <citation><uuid>E90DEBC9-EB51-431D-8693-3A7C1B35129E</uuid><priority>0</priority><publications><publication><uuid>923B5552-960E-4BD1-B2E7-2EEBDB7E71C4</uuid><volume>155</volume><accepted_date>99200711121200000000222000</accepted_date><doi>10.1016/j.ahj.2007.11.018</doi><startpage>584.e1</startpage><publication_date>99200803001200000000220000</publication_date><url> of rosuvastatin therapy on carotid plaque morphology and composition in moderately hypercholesterolemic patients: a high-resolution magnetic resonance imaging trial.</title><submission_date>99200708031200000000222000</submission_date><number>3</number><institution>Department of Radiology, University of Washington, Seattle, WA 98109, USA.</institution><subtype>400</subtype><endpage>8</endpage><bundle><publication><publisher>Mosby, Inc.</publisher><title>American heart journal</title><type>-100</type><subtype>-100</subtype><uuid>4A157322-7514-40A9-8EF0-43E03FFC139A</uuid></publication></bundle><authors><author><firstName>Hunter</firstName><middleNames>R</middleNames><lastName>Underhill</lastName></author><author><firstName>Chun</firstName><lastName>Yuan</lastName></author><author><firstName>Xue-Qiao</firstName><lastName>Zhao</lastName></author><author><firstName>Larry</firstName><middleNames>W</middleNames><lastName>Kraiss</lastName></author><author><firstName>Dennis</firstName><middleNames>L</middleNames><lastName>Parker</lastName></author><author><firstName>Tobias</firstName><lastName>Saam</lastName></author><author><firstName>Baocheng</firstName><lastName>Chu</lastName></author><author><firstName>Norihide</firstName><lastName>Takaya</lastName></author><author><firstName>Fei</firstName><lastName>Liu</lastName></author><author><firstName>Nayak</firstName><middleNames>L</middleNames><lastName>Polissar</lastName></author><author><firstName>Blazej</firstName><lastName>Neradilek</lastName></author><author><firstName>Joel</firstName><middleNames>S</middleNames><lastName>Raichlen</lastName></author><author><firstName>Valerie</firstName><middleNames>A</middleNames><lastName>Cain</lastName></author><author><firstName>John</firstName><middleNames>C</middleNames><lastName>Waterton</lastName></author><author><firstName>Wendy</firstName><lastName>Hamar</lastName></author><author><firstName>Thomas</firstName><middleNames>S</middleNames><lastName>Hatsukami</lastName></author></authors></publication></publications><cites></cites></citation>6 on magnetic resonance (MR) as well as reducing vascular 18F-FDG uptake on PET. ADDIN PAPERS2_CITATIONS <citation><uuid>795C0523-EEDD-4DD8-B612-73AC4FE3147D</uuid><priority>0</priority><publications><publication><uuid>51630575-85F6-4E37-A0F0-06AE50B8FB9C</uuid><volume>48</volume><accepted_date>99200603061200000000222000</accepted_date><doi>10.1016/j.jacc.2006.03.069</doi><startpage>1825</startpage><revision_date>99200603031200000000222000</revision_date><publication_date>99200611071200000000222000</publication_date><url> attenuates plaque inflammation: evaluation by fluorodeoxyglucose positron emission tomography.</title><submission_date>99200601101200000000222000</submission_date><number>9</number><institution>Department of Medicine/Cardiovascular Research Institute, Division of Cardio-Vascular Medicine, Kurume University School of Medicine, Kurume, Japan.</institution><subtype>400</subtype><endpage>1831</endpage><bundle><publication><title>Journal of the American College of Cardiology</title><type>-100</type><subtype>-100</subtype><uuid>F2907E42-9BB5-4F62-A62B-F3317DFF4CE7</uuid></publication></bundle><authors><author><firstName>Nobuhiro</firstName><lastName>Tahara</lastName></author><author><firstName>Hisashi</firstName><lastName>Kai</lastName></author><author><firstName>Masatoshi</firstName><lastName>Ishibashi</lastName></author><author><firstName>Hiroyuki</firstName><lastName>Nakaura</lastName></author><author><firstName>Hayato</firstName><lastName>Kaida</lastName></author><author><firstName>Kenkichi</firstName><lastName>Baba</lastName></author><author><firstName>Naofumi</firstName><lastName>Hayabuchi</lastName></author><author><firstName>Tsutomu</firstName><lastName>Imaizumi</lastName></author></authors></publication></publications><cites></cites></citation>7 Other medication such cholesterol ester transfer protein (CETP) inhibitors have by comparison failed to reduce 18F-FDG activity mirroring the similarly disappointing effects of these drugs on clinical outcomes. 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Electronic address: atawakol@.</institution><subtype>400</subtype><endpage>88</endpage><bundle><publication><title>Journal of the American College of Cardiology</title><type>-100</type><subtype>-100</subtype><uuid>F2907E42-9BB5-4F62-A62B-F3317DFF4CE7</uuid></publication></bundle><authors><author><firstName>Ahmed</firstName><lastName>Tawakol</lastName></author><author><firstName>Parmanand</firstName><lastName>Singh</lastName></author><author><firstName>James</firstName><middleNames>H F</middleNames><lastName>Rudd</lastName></author><author><firstName>Joseph</firstName><lastName>Soffer</lastName></author><author><firstName>Gengqian</firstName><lastName>Cai</lastName></author><author><firstName>Esad</firstName><lastName>Vucic</lastName></author><author><firstName>Sarah</firstName><middleNames>P</middleNames><lastName>Brannan</lastName></author><author><firstName>Elizabeth</firstName><middleNames>A</middleNames><lastName>Tarka</lastName></author><author><firstName>Bonnie</firstName><middleNames>C</middleNames><lastName>Shaddinger</lastName></author><author><firstName>Lea</firstName><lastName>Sarov-Blat</lastName></author><author><firstName>Paul</firstName><lastName>Matthews</lastName></author><author><firstName>Sharath</firstName><lastName>Subramanian</lastName></author><author><firstName>Michael</firstName><lastName>Farkouh</lastName></author><author><firstName>Zahi</firstName><middleNames>a</middleNames><lastName>Fayad</lastName></author></authors></publication></publications><cites></cites></citation>9 The recent emergence of hybrid PET/MR systems offers major potential in this field allowing combined, detailed assessment of large vessel plaque burden (MR), composition (MR) and activity (PET) at radiation doses considerably lower than possible with PET/CT (3-4mSv per scan). ADDIN PAPERS2_CITATIONS <citation><uuid>B1DB655C-47B8-406D-86BB-2A87DEF20934</uuid><priority>0</priority><publications><publication><uuid>A0C5B484-CDED-4DEC-B0CF-E41CC105D410</uuid><volume>26</volume><doi>10.1016/j.nic.2015.09.005</doi><startpage>55</startpage><publication_date>99201602001200000000220000</publication_date><url> of Combining PET and MR Imaging of Carotid Plaque.</title><institution>British Heart Foundation Centre for Cardiovascular Science, College of Medicine and Veterinary Medicine, University of Edinburgh, Room Suite 305, The Chancellor's Building, 49 Little France Crescent, Edinburgh EH16 4SB, UK.</institution><number>1</number><subtype>400</subtype><endpage>68</endpage><bundle><publication><title>Neuroimaging clinics of North America</title><type>-100</type><subtype>-100</subtype><uuid>16521AC3-0129-469D-ACAD-A04AB594403E</uuid></publication></bundle><authors><author><firstName>Alex</firstName><middleNames>T</middleNames><lastName>Vesey</lastName></author><author><firstName>Marc</firstName><middleNames>R</middleNames><lastName>Dweck</lastName></author><author><firstName>Zahi</firstName><middleNames>a</middleNames><lastName>Fayad</lastName></author></authors></publication></publications><cites></cites></citation>10 As a consequence multiple time point studies become feasible. How could this technology be used to build upon the important study by Figueroa and colleagues and further investigate the relationship between visceral fat and atherosclerosis? One possibility would be to image patients before and after gastric banding. This operation results in major weight loss in patients with multiple risk factors for atherosclerosis and can be performed laparoscopically. A multiple time-point PET/MR study could be used to simultaneously assess the effect of this intervention on visceral fat, atherosclerotic burden, plaque composition and 18F-FDG activity. 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Large bore scanners would be preferential, as ultimately would more specific markers of vascular inflammation than 18F-FDG. Moreover it would be interesting to compare the activity of visceral fat with brown fat, the metabolic activity of which has also been studied using 18F-FDG. ADDIN PAPERS2_CITATIONS <citation><uuid>C293BB04-9D28-40E2-9865-4D915A9794C9</uuid><priority>0</priority><publications><publication><uuid>23AEF992-BFA9-40ED-9056-E462FED5BEA1</uuid><volume>360</volume><doi>10.1056/NEJMoa0808718</doi><startpage>1500</startpage><publication_date>99200904091200000000222000</publication_date><url> brown adipose tissue in healthy men.</title><institution>Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht, The Netherlands. markenlichtenbelt@hb.unimaas.nl</institution><number>15</number><subtype>400</subtype><endpage>1508</endpage><bundle><publication><title>The New England journal of medicine</title><type>-100</type><subtype>-100</subtype><uuid>72BCD25D-CFD3-4DAB-9494-31A8AE337CD7</uuid></publication></bundle><authors><author><lastName>Marken Lichtenbelt</lastName><nonDroppingParticle>van</nonDroppingParticle><firstName>Wouter</firstName><middleNames>D</middleNames></author><author><firstName>Joost</firstName><middleNames>W</middleNames><lastName>Vanhommerig</lastName></author><author><firstName>Nanda</firstName><middleNames>M</middleNames><lastName>Smulders</lastName></author><author><firstName>Jamie</firstName><middleNames>M A F L</middleNames><lastName>Drossaerts</lastName></author><author><firstName>Gerrit</firstName><middleNames>J</middleNames><lastName>Kemerink</lastName></author><author><firstName>Nicole</firstName><middleNames>D</middleNames><lastName>Bouvy</lastName></author><author><firstName>Patrick</firstName><lastName>Schrauwen</lastName></author><author><firstName>G</firstName><middleNames>J Jaap</middleNames><lastName>Teule</lastName></author></authors></publication></publications><cites></cites></citation>13 As we enter a new era of powerful non-invasive molecular imaging the availability of imaging systems will increase as will the range of tracers at our disposal, costs will come down and the scope for such studies will expand. 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