Tomas Vita1, David R Okada1, Mahdi Veillet-Chowdhury1, Paco E Bravo1, Erin Mullins1, Edward Hulten1, Mukta Agrawal1, Rachna Madan1, Viviany R Taqueti1, Michael Steigner1, Hicham Skali1, Raymond Y Kwong1, Garrick C Stewart1, Sharmila Dorbala1, Marcelo F Di Carli1, Ron Blankstein2. 1. From the Cardiovascular Division, Department of Medicine, Cardiovascular Imaging Program (T.V., M.V.-C., P.E.B., E.M., E.H., V.R.T., M.S., H.S., R.Y.K., S.D., M.F.D.C., R.B.), Department of Radiology (T.V., M.V.-C., P.E.B., E.M., E.H., V.R.T., M.S., H.S., R.Y.K., S.D., M.F.D.C., R.B.), Division of Nuclear Medicine and Molecular Imaging, Department of Radiology (M.A., S.D., M.F.D.C., R.B.), Division of Thoracic Radiology, Department of Radiology (R.M.), and Cardiovascular Division (H.S., R.Y.K., G.S., M.F.D.C., R.B.), Brigham and Women's Hospital, Boston, MA; Division of Cardiology, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD (D.R.O.); Division of Medicine, Cardiology Service, Walter Reed National Military Medical Center, Bethesda, MD (E.H.); and Uniformed Services University of Health Sciences, Bethesda, MD (E.H.). 2. From the Cardiovascular Division, Department of Medicine, Cardiovascular Imaging Program (T.V., M.V.-C., P.E.B., E.M., E.H., V.R.T., M.S., H.S., R.Y.K., S.D., M.F.D.C., R.B.), Department of Radiology (T.V., M.V.-C., P.E.B., E.M., E.H., V.R.T., M.S., H.S., R.Y.K., S.D., M.F.D.C., R.B.), Division of Nuclear Medicine and Molecular Imaging, Department of Radiology (M.A., S.D., M.F.D.C., R.B.), Division of Thoracic Radiology, Department of Radiology (R.M.), and Cardiovascular Division (H.S., R.Y.K., G.S., M.F.D.C., R.B.), Brigham and Women's Hospital, Boston, MA; Division of Cardiology, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD (D.R.O.); Division of Medicine, Cardiology Service, Walter Reed National Military Medical Center, Bethesda, MD (E.H.); and Uniformed Services University of Health Sciences, Bethesda, MD (E.H.). rblankstein@bwh.harvard.edu.
Abstract
BACKGROUND: Although cardiac magnetic resonance (CMR) and positron emission tomography (PET) detect different pathological attributes of cardiac sarcoidosis (CS), the complementary value of these tests has not been evaluated. Our objective was to determine the value of combining CMR and PET in assessing the likelihood of CS and guiding patient management. METHODS AND RESULTS: In this retrospective study, we included 107 consecutive patients referred for evaluation of CS by both CMR and PET. Two experienced readers blinded to all clinical data reviewed CMR and PET images and categorized the likelihood of CS as no (<10%), possible (10%-50%), probable (50%-90%), or highly probable(>90%) based on predefined criteria. Patient management after imaging was assessed for all patients and across categories of increasing CS likelihood. A final clinical diagnosis for each patient was assigned based on a subsequent review of all available imaging, clinical, and pathological data. Among 107 patients (age, 55±11 years; left ventricular ejection fraction, 43±16%), 91 (85%) had late gadolinium enhancement, whereas 82 (76%) had abnormal F18-fluorodeoxyglucose uptake on PET, suggesting active inflammation. Among the 91 patients with positive late gadolinium enhancement, 60 (66%) had abnormal F18-fluorodeoxyglucose uptake. When PET data were added to CMR, 48 (45%) patients were reclassified as having a higher or lower likelihood of CS, most of them (80%) being correctly reclassified when compared with the final diagnosis. Changes in immunosuppressive therapies were significantly more likely among patients with highly probable CS. CONCLUSIONS: Among patients with suspected CS, combining CMR and PET provides complementary value for estimating the likelihood of CS and guiding patient management.
BACKGROUND: Although cardiac magnetic resonance (CMR) and positron emission tomography (PET) detect different pathological attributes of cardiac sarcoidosis (CS), the complementary value of these tests has not been evaluated. Our objective was to determine the value of combining CMR and PET in assessing the likelihood of CS and guiding patient management. METHODS AND RESULTS: In this retrospective study, we included 107 consecutive patients referred for evaluation of CS by both CMR and PET. Two experienced readers blinded to all clinical data reviewed CMR and PET images and categorized the likelihood of CS as no (<10%), possible (10%-50%), probable (50%-90%), or highly probable(>90%) based on predefined criteria. Patient management after imaging was assessed for all patients and across categories of increasing CS likelihood. A final clinical diagnosis for each patient was assigned based on a subsequent review of all available imaging, clinical, and pathological data. Among 107 patients (age, 55±11 years; left ventricular ejection fraction, 43±16%), 91 (85%) had late gadolinium enhancement, whereas 82 (76%) had abnormal F18-fluorodeoxyglucose uptake on PET, suggesting active inflammation. Among the 91 patients with positive late gadolinium enhancement, 60 (66%) had abnormal F18-fluorodeoxyglucose uptake. When PET data were added to CMR, 48 (45%) patients were reclassified as having a higher or lower likelihood of CS, most of them (80%) being correctly reclassified when compared with the final diagnosis. Changes in immunosuppressive therapies were significantly more likely among patients with highly probable CS. CONCLUSIONS: Among patients with suspected CS, combining CMR and PET provides complementary value for estimating the likelihood of CS and guiding patient management.
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