18F-Fluorodeoxyglucose Positron Emission Tomography for the Detection of Myocardial Inflammation in Arrhythmogenic Left Ventricular Cardiomyopathy
2022; Lippincott Williams & Wilkins; Volume: 15; Issue: 7 Linguagem: Inglês
10.1161/circimaging.122.014065
ISSN1942-0080
AutoresRoxane Tessier, Lara Marteau, Marc Vivien, Béatrice Guyomarch, Aurélie Thollet, Imen Fellah, Bastien Jamet, Jean Charles Sébille, Thomas Eugène, Jean Michel Serfaty, Vincent Probst, Jean‐Noël Trochu, Claire Toquet, K. Warin-Fresse, Nicolas Piriou,
Tópico(s)Cardiomyopathy and Myosin Studies
ResumoHomeCirculation: Cardiovascular ImagingVol. 15, No. 718F-Fluorodeoxyglucose Positron Emission Tomography for the Detection of Myocardial Inflammation in Arrhythmogenic Left Ventricular Cardiomyopathy Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUB18F-Fluorodeoxyglucose Positron Emission Tomography for the Detection of Myocardial Inflammation in Arrhythmogenic Left Ventricular Cardiomyopathy Roxane Tessier, Lara Marteau, Marc Vivien, Béatrice Guyomarch, Aurélie Thollet, Imen Fellah, Bastien Jamet, Jean Charles Sébille, Thomas Eugene, Jean Michel Serfaty, Vincent Probst, Jean Noël Trochu, Claire Toquet, Karine Warin-Fresse and Nicolas Piriou Roxane TessierRoxane Tessier CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. , Lara MarteauLara Marteau https://orcid.org/0000-0002-4904-1810 CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. Department of Cardiovascular Radiology (L.M., J.M.S., K.W.-F.), CHU Nantes, Nantes Université, France. , Marc VivienMarc Vivien CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. , Béatrice GuyomarchBéatrice Guyomarch CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. , Aurélie TholletAurélie Thollet CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. , Imen FellahImen Fellah CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. , Bastien JametBastien Jamet Department of Nuclear Medicine (B.J., J.C.S., T.E., N.P.), CHU Nantes, Nantes Université, France. , Jean Charles SébilleJean Charles Sébille https://orcid.org/0000-0002-8234-6456 Department of Nuclear Medicine (B.J., J.C.S., T.E., N.P.), CHU Nantes, Nantes Université, France. , Thomas EugeneThomas Eugene Department of Nuclear Medicine (B.J., J.C.S., T.E., N.P.), CHU Nantes, Nantes Université, France. , Jean Michel SerfatyJean Michel Serfaty Department of Cardiovascular Radiology (L.M., J.M.S., K.W.-F.), CHU Nantes, Nantes Université, France. , Vincent ProbstVincent Probst https://orcid.org/0000-0002-5492-8619 CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. , Jean Noël TrochuJean Noël Trochu https://orcid.org/0000-0003-4742-281X CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. , Claire ToquetClaire Toquet CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. Department of Pathology (C.T.), CHU Nantes, Nantes Université, France. , Karine Warin-FresseKarine Warin-Fresse Department of Cardiovascular Radiology (L.M., J.M.S., K.W.-F.), CHU Nantes, Nantes Université, France. and Nicolas PiriouNicolas Piriou Correspondence to: Nicolas Piriou, MD, Service de Médecine Nucléaire, CHU de Nantes, Hôpital Laënnec, 44093 Nantes Cedex 1, France. Email E-mail Address: [email protected] https://orcid.org/0000-0002-6677-6552 CNRS, INSERM, l'institut du thorax (R.T., L.M., M.V., B.G., A.T., I.F., V.P., J.N., C.T., N.P.), CHU Nantes, Nantes Université, France. Department of Nuclear Medicine (B.J., J.C.S., T.E., N.P.), CHU Nantes, Nantes Université, France. Originally published30 Jun 2022https://doi.org/10.1161/CIRCIMAGING.122.014065Circulation: Cardiovascular Imaging. 2022;15Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: June 30, 2022: Ahead of Print In recently updated classification and diagnostic criteria for arrhythmogenic cardiomyopathy (AC), presence of subepicardial or midmyocardial late gadolinium enhancement (LGE) of septal, inferior, or lateral left ventricular (LV) walls on cardiac magnetic resonance (CMR; Figure [A]) is one of the 2 major diagnostic criteria for arrhythmogenic LV cardiomyopathy (ALVC), a particular AC phenotype with isolated or predominant LV involvement.1 Evidence of a pathogenic genetic variant is required to confirm the diagnosis of the genetic syndrome. Some studies have shown that myocarditis and chronic myocardial inflammation can be associated to ALVC.2 Apart from endomyocardial biopsy, diagnosing myocardial inflammation associated to ALVC is challenging. In CMR, LGE is strongly suggestive of fibrotic replacement associated to AC, but tissue characterization tools are known to be less sensitive to distinguish between LGE only due to fibrosis or associated to inflammation in arrhythmogenic and cardiomyopathic clinical presentations of myocarditis.3 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET), widely used in cardiac sarcoidosis, could be of interest to increase imaging sensitivity in detecting myocardial inflammation in ALVC.Download figureDownload PowerPointFigure. Comparison of contrast-enhanced cardiac magnetic resonance (CMR) and 18F-fluorodeoxyglucose-positron emission tomography (FDG-PET) findings in arrhythmogenic left ventricular cardiomyopathy (ALVC). A, Contrast-enhanced CMR (left) and FDG-PET (right) in a patient with DSP (desmoplakin) pathogenic variant. CMR shows typical features of ALVC with subepicardial late gadolinium enhancement (LGE) on lateral and inferior left ventricular (LV) walls and midmyocardial LGE of the inferoseptal wall. PET shows concordant FDG uptake in corresponding areas with subepicardial LGE. B, Bulls eyes representations of the percentages of patients with subepicardial LGE (left) and FDG uptake (right) for each LV segment.We retrospectively analyzed data from 17 patients with a final diagnosis of ALVC who had benefited from a cardiac FDG-PET scan after prolonged fasting and low carbohydrates diet to suppress physiological cardiomyocytes glucose uptake, so that residual myocardial FDG hypermetabolism can reflect areas of myocardial inflammation. FDG-PET was performed in the course of routine diagnostic work-up to rule out phenocopies such as nonhereditary inflammatory AC. The study was approved by the institutional review committee and participants gave informed consent. The data that support the findings of this study are available from the corresponding author upon reasonable request.Seventy-one percent of patients were women, mean age was 45±14 years. Mean LVEF was 42±15%. Genetic variants were classified as pathogenic following the 5-tier terminology system of the American College of Medical Genetics and Genomics.4 DSP, coding for the desmosomal protein Desmoplakin, was the most common gene involved (n=10; 59%). Other genotypes were PKP2 (plakophilin-2 [desmosome], n=2), FLNC (filamin C [cytoskeleton], n=2), LMNA (lamin A/C [nuclear envelope], n=1), DES (desmin ([intermediate filament], n=1), Ryr2 (ryanodine receptor 2 [sarcoplasmic reticulum], n=1). Five patients (31%) had a previous history of myocarditis.Ten out of 17 patients had a significant LV myocardial FDG uptake assessed visually. FDG uptake pattern was focal in 7 patients (Figure [A]), diffuse in 3. LVEF was not significantly different between patients with and patients without LV FDG (respectively 38±14%, n=10, and 47±15%, respectively, n=7, P=0.22, Mann-Whitney U test). Myocarditis was significantly associated with the presence of FDG uptake (n=5/10 patients with FDG uptake had a history of myocarditis, n=0/7 patients without FDG uptake, P=0.04, Fisher exact test). Two patients with clinically suspected myocarditis had an endomyocardial biopsy that revealed no signs of myocardial inflammation but cardiomyocyte dystrophy and fibrosis.Mixed logistic models with random effects showed that FDG uptake was significantly more present on lateral and inferior LV walls (P=0.037; Figure [B]). There was a weak correlation between the presence of FDG and subepicardial or midmyocardial locations of LGE on CMR in the same segment (Spearman correlation coefficient ρ=0.44; P=0.08). For subepicardial-only LGE locations (111 segments/289 total), the presence of FDG uptake in a segment was significantly correlated with the presence of LGE (ρ=0.71; P=0.01; Figure [B]).Significant co-location of FDG uptake and subepicardial LGE in LV lateral and inferior walls, a typical CMR feature of myocarditis, as well as the consistent FDG positivity in patients with previous history of myocarditis, suggest that FDG-PET could be of interest to noninvasively detect sub-acute or chronic myocardial inflammation in patients with ALVC.This largest reported sample of patients with ALVC with FDG-PET myocardial characterization carries several limitations. FDG-PET indication was based on clinical or CMR findings suggestive of an inflammatory cardiomyopathy representing a selection bias. FDG-PET and CMR interpretation were not blinded. In the absence of control group and pathological correlation in all patients, FDG uptake may reflect nonspecific findings associated to insufficient physiological uptake suppression or myocardial metabolic shift due to several pathological conditions. Two patients had negative endomyocardial biopsy that do not necessarily mean that FDG avidity was not because of myocardial inflammation as they were performed on the RV side of the septum whereas FDG uptake was located on the lateral LV walls in both patients, as in the whole cohort.Given increasing evidences that inflammation plays a role in AC,5 we think that these results must encourage further prospective studies with consecutive ALVC patients to determine whether FDG-PET can become a routine imaging tool to noninvasively detect myocardial inflammation.Article InformationSources of FundingNone.Disclosures None.FootnotesFor Sources of Funding and Disclosures, see page 562.Correspondence to: Nicolas Piriou, MD, Service de Médecine Nucléaire, CHU de Nantes, Hôpital Laënnec, 44093 Nantes Cedex 1, France. Email nicolas.piriou@chu-nantes.frReferences1. Corrado D, Zorzi A, Cipriani A, Bauce B, Bariani R, Beffagna G, De Lazzari M, Migliore F, Pilichou K, Rampazzo A, et al. Evolving diagnostic criteria for arrhythmogenic cardiomyopathy.J Am Heart Assoc. 2021; 10:e021987. doi: 10.1161/JAHA.121.021987LinkGoogle Scholar2. Smith ED, Lakdawala NK, Papoutsidakis N, Aubert G, Mazzanti A, McCanta AC, Agarwal PP, Arscott P, Dellefave-Castillo LM, Vorovich EE, et al. Desmoplakin cardiomyopathy, a fibrotic and inflammatory form of cardiomyopathy distinct from typical dilated or arrhythmogenic right ventricular cardiomyopathy.Circulation. 2020; 141:1872–1884. doi: 10.1161/CIRCULATIONAHA.119.044934LinkGoogle Scholar3. Francone M, Chimenti C, Galea N, Scopelliti F, Verardo R, Galea R, Carbone I, Catalano C, Fedele F, Frustaci A. CMR sensitivity varies with clinical presentation and extent of cell necrosis in biopsy-proven acute myocarditis.JACC Cardiovasc Imaging. 2014; 7:254–263. doi: 10.1016/j.jcmg.2013.10.011CrossrefMedlineGoogle Scholar4. Richards S, Aziz N, Bale S, Bick D, Das S, Gastier-Foster J, Grody WW, Hegde M, Lyon E, Spector E, et al; ACMG Laboratory Quality Assurance Committee.Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology.Genet Med. 2015; 17:405–424. doi: 10.1038/gim.2015.30CrossrefMedlineGoogle Scholar5. Asatryan B, Asimaki A, Landstrom AP, Khanji MY, Odening KE, Cooper LT, Marchlinski FE, Gelzer AR, Semsarian C, Reichlin T, et al. Inflammation and immune response in arrhythmogenic cardiomyopathy: state-of-the-art review.Circulation. 2021; 144:1646–1655. doi: 10.1161/CIRCULATIONAHA.121.055890LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Protonotarios A and Wicks E (2023) The role of FDG-PET imaging in arrhythmogenic cardiomyopathy, International Journal of Cardiology, 10.1016/j.ijcard.2023.131275, 391, (131275), Online publication date: 1-Nov-2023. 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Lazzeroni D, Crocamo A, Ziveri V, Notarangelo M, Rizzello D, Spoladori M, Donelli D, Cacciola G, Ardissino D, Niccoli G and Peretto G (2023) Personalized Management of Sudden Death Risk in Primary Cardiomyopathies: From Clinical Evaluation and Multimodality Imaging to Ablation and Cardioverter-Defibrillator Implant, Journal of Personalized Medicine, 10.3390/jpm13050877, 13:5, (877) Monda E, Rubino M, Palmiero G, Verrillo F, Lioncino M, Diana G, Cirillo A, Fusco A, Dongiglio F, Caiazza M, Altobelli I, Mauriello A, Guarnaccia N, Scatteia A, Cesaro A, Pacileo G, Sarubbi B, Frisso G, Bauce B, D'Andrea A, Dellegrottaglie S, Russo M, Calabrò P and Limongelli G (2023) Multimodality Imaging in Arrhythmogenic Left Ventricular Cardiomyopathy, Journal of Clinical Medicine, 10.3390/jcm12041568, 12:4, (1568) July 2022Vol 15, Issue 7 Advertisement Article InformationMetrics © 2022 American Heart Association, Inc.https://doi.org/10.1161/CIRCIMAGING.122.014065PMID: 35770631 Originally publishedJune 30, 2022 Keywordsarrhythmogenic cardiomyopathyinflammationMRImyocarditisPET-CTPDF download Advertisement SubjectsCardiomyopathyGeneticsInflammatory Heart DiseaseNuclear Cardiology and PET
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