Incremental Prognostic Value of Global Longitudinal Strain and 18F-Fludeoxyglucose Positron Emission Tomography in Patients With Systemic Sarcoidosis.
In independent studies, abnormal global longitudinal strain (GLS) and myocardial inflammation or scar detected by 18F-fludeoxyglucose positron emission tomography (FDG-PET) are associated with poor prognosis among patients with high likelihood for cardiac sarcoidosis. However, commonly used imaging modalities have not been evaluated in the same population. Our goals were to examine the relation between GLS and FDG-PET, and to evaluate the incremental prognostic value of these imaging techniques for predicting major adverse cardiac events (MACE) in patients suspected to have cardiac sarcoidosis. We identified patients with systemic sarcoidosis who underwent an echocardiogram and FDG-PET within 60 days. Regional strain (average of base, mid, and apical segmental strains from each of 6 wall regions) was calculated and compared with regional FDG-PET findings. The associations among GLS, FDG-PET findings, and MACE (defined as death, ventricular tachycardia, heart failure hospitalization, or transplantation) were evaluated using a Cox model. Of 84 patients, 51 had abnormal FDG-PET. GLS was impaired in patients with abnormal versus normal FDG-PET (-14.2 ± 4.7% vs -17.9 ± 3.5%, p <0.01). After adjusting for clinical risk factors, both GLS and the number of segments with abnormal perfusion and metabolism on FDG-PET were associated with adverse cardiac events (p <0.01 for both). In conclusion, GLS and regional LS are impaired in patients with abnormal perfusion and metabolism detected using FDG-PET. Additionally, both GLS and abnormal FDG-PET have incremental prognostic value for predicting MACE in patients with systemic sarcoidosis.
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Brett W
BW
Sperry
Department of Cardiothoracic Surgery, Cleveland Clinic, Cleveland, Ohio.
Ahmed
A
Ibrahim
Menzies Research Institute Tasmania, Hobart, Tasmania, Australia.
Kazuaki
K
Negishi
Menzies Research Institute Tasmania, Hobart, Tasmania, Australia.
Tomoko
T
Negishi
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Parag
P
Patel
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Zoran B
ZB
Popović
Department of Pulmonary and Critical Care, Cleveland Clinic, Cleveland, Ohio.
Daniel
D
Culver
Department of Nuclear Medicine, Cleveland Clinic, Cleveland, Ohio.
Richard
R
Brunken
Menzies Research Institute Tasmania, Hobart, Tasmania, Australia; Baker-IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
Thomas H
TH
Marwick
Cedars-Sinai Heart Institute, Los Angeles, California. Electronic address: balaji.tamarappoo@cshs.org.
Balaji
B
Tamarappoo
D000328:Adult; D009202:Cardiomyopathies / Q000175:diagnosis* / Q000503:physiopathology; D004452:Echocardiography; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000494:pharmacology*; D005500:Follow-Up Studies; D006352:Heart Ventricles / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D049268:Positron-Emission Tomography / Q000379:methods*; D011237:Predictive Value of Tests; D011379:Prognosis; D019275:Radiopharmaceuticals / Q000494:pharmacology; D012189:Retrospective Studies; D012507:Sarcoidosis / Q000175:diagnosis*; D016277:Ventricular Function, Left / Q000502:physiology*
D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18