{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T09:46:15Z","timestamp":1791884775518,"version":"4.3.4"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Cardiovascular Imaging"],"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>\n                      Myocardial\n                      <jats:sup>18<\/jats:sup>\n                      fluorodeoxyglucose (\n                      <jats:sup>18<\/jats:sup>\n                      FDG)-avidity is frequently seen in patients with genetic cardiomyopathy, as well as a growing \u201cidiopathic\n                      <jats:sup>18<\/jats:sup>\n                      FDG-avidity\u201d group of genotype-negative patients who do not clearly have cardiac sarcoidosis. The prognostic implications of\n                      <jats:sup>18<\/jats:sup>\n                      FDG-avidity in patients with and without genetic cardiomyopathy, and the effects of immunosuppression in the latter, remain uncertain.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      This multicenter, retrospective study included all patients who were referred for both\n                      <jats:sup>18<\/jats:sup>\n                      FDG-PET and cardiomyopathy genetic testing. Patients with acute myocarditis, biopsy-proven sarcoidosis, or extracardiac\n                      <jats:sup>18<\/jats:sup>\n                      FDG-avidity were excluded. We investigated heart failure (HF) composite (left ventricular assist device, heart transplant, HF hospitalization, or death) and arrhythmia composite (sustained ventricular arrhythmias [ventricular tachycardia\/VF], atrioventricular block, or death) outcomes using survival analysis, including Cox proportional hazards modeling and inverse probability of treatment weighting.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Among 372 patients, 142 (38%) were\n                      <jats:sup>18<\/jats:sup>\n                      FDG-avid. The prevalence of genetic cardiomyopathy among\n                      <jats:sup>18<\/jats:sup>\n                      FDG-avid patients (12%) was similar to that of\n                      <jats:sup>18<\/jats:sup>\n                      FDG-negative patients (18%;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.11). Unadjusted,\n                      <jats:sup>18<\/jats:sup>\n                      FDG-avidity was associated with an increased risk of HF composite (hazard ratio, 1.69 [95% CI, 1.04\u20132.75];\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.034) and arrhythmia composite (hazard ratio, 1.63 [95% CI, 1.1\u20132.4];\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.014) outcomes compared with\n                      <jats:sup>18<\/jats:sup>\n                      FDG-negative patients. However, these associations were not statistically significant after multivariable adjustment, nor were there significant differences in\n                      <jats:sup>18<\/jats:sup>\n                      FDG-associated risks in patients with genetic cardiomyopathy versus genotype-negative patients. After inverse probability of treatment weighting, immunosuppression of\n                      <jats:sup>18<\/jats:sup>\n                      FDG-avid patients (n=49) was not associated with a reduction in HF or arrhythmia composite outcomes compared with those who were not immunosuppressed (n=93).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      Myocardial-only\n                      <jats:sup>18<\/jats:sup>\n                      FDG-avidity is not significantly associated with HF or arrhythmia risk in patients who do not clearly have cardiac sarcoidosis (including those with genetic cardiomyopathy). Immunosuppression therapy does not seem to modify the disease course, suggesting that not all myocardial\n                      <jats:sup>18<\/jats:sup>\n                      FDG uptake reflects clinically significant inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circimaging.126.019970","type":"journal-article","created":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T09:00:20Z","timestamp":1791882020000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Impact of\n                    <sup>18<\/sup>\n                    FDG-Avidity and Immunosuppression on Idiopathic and Genetic Cardiomyopathies"],"prefix":"10.1161","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0098-6706","authenticated-orcid":true,"given":"Shiva","family":"Tabaghi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Graham H.","family":"Bevan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-1869-3333","authenticated-orcid":true,"given":"Stephen","family":"Hankinson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2639-2949","authenticated-orcid":true,"given":"Esra D.","family":"Gumuser","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Heart and Vascular Institute, Mass General Brigham, Brigham and Women\u2019s Hospital, Boston, MA (E.D.G., N.K.L., R.B., M.F.D.C., S.D.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mallika","family":"Lal","sequence":"additional","affiliation":[{"name":"Knight Cardiovascular Institute, Oregon Health &amp; Science University, Portland (M.L., M.P., B.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8536-3991","authenticated-orcid":true,"given":"Madison","family":"Pico","sequence":"additional","affiliation":[{"name":"Knight Cardiovascular Institute, Oregon Health &amp; Science University, Portland (M.L., M.P., B.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8290-127X","authenticated-orcid":true,"given":"Neal","family":"Chatterjee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1380-5364","authenticated-orcid":true,"given":"Alexi","family":"Vasbinder","sequence":"additional","affiliation":[{"name":"Department of Biobehavioral Nursing and Health Informatics, University of Washington School of Nursing, Seattle (A.V.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5994-5998","authenticated-orcid":true,"given":"Richard K.","family":"Cheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6976-6512","authenticated-orcid":true,"given":"April","family":"Stempien-Otero","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6458-5421","authenticated-orcid":true,"given":"Neal K.","family":"Lakdawala","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Heart and Vascular Institute, Mass General Brigham, Brigham and Women\u2019s Hospital, Boston, MA (E.D.G., N.K.L., R.B., M.F.D.C., S.D.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8393-6562","authenticated-orcid":true,"given":"Ron","family":"Blankstein","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Heart and Vascular Institute, Mass General Brigham, Brigham and Women\u2019s Hospital, Boston, MA (E.D.G., N.K.L., R.B., M.F.D.C., S.D.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3119-025X","authenticated-orcid":true,"given":"Marcelo F.","family":"Di Carli","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Heart and Vascular Institute, Mass General Brigham, Brigham and Women\u2019s Hospital, Boston, MA (E.D.G., N.K.L., R.B., M.F.D.C., S.D.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1742-8030","authenticated-orcid":true,"given":"Benjamin","family":"Levin","sequence":"additional","affiliation":[{"name":"Knight Cardiovascular Institute, Oregon Health &amp; 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