Abstract

Background: We have previously demonstrated that [18F]fluorodeoxyglucose (FDG) accumulation evaluated by ECG gated positron emission tomography (PET) is increased in the right ventricular (RV) free wall of patients with pulmonary hypertension (PH) and that this accumulation is ameliorated after medical therapy associated with hemodynamic improvement. However, it remains to be examined whether RV FDG accumulation has a prognostic significance in patients with PH. Methods and results: From March 2001 to June 2004, we performed gated FDG-PET in 27 patients with PH, including 18 with pulmonary arterial hypertension and 9 with chronic thromboembolic pulmonary hypertension. We examined baseline clinical parameters, invasive hemodynamic data, imaging data with cardiac MR, electron beam CT and FDG-PET quantified by calculating standardized uptake value (SUV) and corrected for partial volume effect based on the RV free wall thickness, the composite primary endpoint defined as all-cause mortality, lung transplantation, hospitalization for progression of PH and deterioration of NYHA functional class and/or >15% reduction in 6-min walk distance (6MWD) from baseline, and all-cause mortality as the second endpoint. During the mean follow-up period of 66 months, 15 patients reached the composite primary endpoint, including all-cause mortality in 4, lung transplantation in 1, hospitalization for PH progression in 9, deterioration of NYHA functional class and/or >15% reduction in 6MWD from baseline in 1 and death in 11 (41%). In FDG-PET measurements, corrected RV free wall SUV was significantly increased in the endpoint group compared with the no endpoint group (10.1±2.7 vs. 7.6±2.2, P=0.02). Univariate COX hazard analysis showed that the corrected RV SUV of FDG was significantly correlated with the composite endpoint (hazard ratio 1.25, 95% confidence interval 1.04-1.51, P=0.04). This relationship remained significant even after adjustment for NYHA functional class or 6MWD. In Kaplan-Meier analysis for the composite primary endpoint, patients with a corrected RV SUV of FDGSUV ≥8.5 had a significantly poor prognosis compared with those with <8.5 (log-rank P=0.005 for the composite endpoint, P=0.07 for all-cause mortality). Furthermore, the corrected RV SUV of FDG at 3months after epoprostenol treatment could predict survival in patients with PAH better than the reduction in pulmonary vascular resistance by ≥30% (log-rank P=0.02, P=0.34, respectively). Conclusions: These results indicate that enhanced FDG accumulation in the RV is a useful prognostic factor in patients with PH.

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