title: Increased [18F]fluorodeoxyglucose accumulation in right ventricular free wall in patients with pulmonary hypertension and the effect of epoprostenol.
abstract: OBJECTIVE
  We examined whether right ventricular (RV) [(18)F]fluorodeoxyglucose (FDG) accumulation is increased in patients with pulmonary hypertension using gated positron emission tomography (PET) and whether RV FDG accumulation changes after therapy with epoprostenol.
  
  
  BACKGROUND
  Myocardial glucose utilization is increased in animal models with ventricular pressure overload.
  
  
  METHODS
  We performed gated FDG-PET in 24 patients with pulmonary hypertension. The RV standardized uptake value (SUV) of FDG was corrected for the partial volume effect based on the wall thickness measured by electron-beam computed tomography or magnetic resonance imaging.
  
  
  RESULTS
  The corrected RV SUV of FDG was significantly correlated with the pulmonary vascular resistance, mean pulmonary artery pressure, right atrial pressure, RV wall stress, and plasma brain natriuretic peptide levels, but not with the RV wall thickness and mass. After pulmonary vasodilator therapy with epoprostenol for three months, the corrected RV SUV of FDG significantly decreased in the responders, but not in the non-responders, and the percentage change of the corrected RV SUV of FDG was significantly correlated with the percentage change of the pulmonary vascular resistance (r = 0.78; p < 0.01) and RV systolic wall stress (r = 0.76; p < 0.05).
  
  
  CONCLUSIONS
  The RV FDG accumulation corrected for the partial volume effect was significantly increased in accordance with the severity of the RV pressure overload (i.e., the RV peak-systolic wall stress) in patients with pulmonary hypertension. Furthermore, the corrected RV FDG accumulation was decreased after the treatment with epoprostenol in accordance with the degree of reduction in the pulmonary vascular resistance and RV peak-systolic wall stress.
authors.affiliation: Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
authors.forename: Minako
authors.initials: M
authors.lastname: Oikawa
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kagaya
authors.forename: Hiroki
authors.initials: H
authors.lastname: Otani
authors.forename: Masahito
authors.initials: M
authors.lastname: Sakuma
authors.forename: Jun
authors.initials: J
authors.lastname: Demachi
authors.forename: Jun
authors.initials: J
authors.lastname: Suzuki
authors.forename: Tohru
authors.initials: T
authors.lastname: Takahashi
authors.forename: Jun
authors.initials: J
authors.lastname: Nawata
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Ido
authors.forename: Jun
authors.initials: J
authors.lastname: Watanabe
authors.forename: Kunio
authors.initials: K
authors.lastname: Shirato
mesh_terms: D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D011464:Epoprostenol / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000378:metabolism*; D006352:Heart Ventricles / Q000378:metabolism*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography; D013318:Stroke Volume; D014655:Vascular Resistance / Q000187:drug effects; D017725:Ventricular Pressure
chemical_list: D000959:Antihypertensive Agents; D019788:Fluorodeoxyglucose F18; D011464:Epoprostenol