Abstract

Pulmonary arterial hypertension (PAH; WHO group 1) is a progressive disease characterized by profound vascular remodeling of the media with proliferation of smooth muscle cells in pulmonary arteries and arterioles. In contrast, pulmonary hypertension (PH) associated with left heart disease (WHO group 2) is caused largely by passive transmission of elevated pulmonary venous pressures into the lung arterial system. Recent studies showed increased glucose metabolism in the lung parenchyma in animal models or small PAH patient cohorts, and may reflect underlying metabolic abnormalities in the remodeled pulmonary vasculature. However, there is no study to compare lung FDG uptake in patients with PAH with those with PH due to left heart disease (group 2 PH), in which the same metabolic abnormalities may not be evident. The aim of this study was to compare lung FDG uptake among three groups including PAH groups, group 2 PH and control subjects. Twenty-two patients with PAH (13 patients with idiopathic PAH and 9 patients with connective tissue disease), 8 patients with group 2 PH, as well as 14 control subjects (no lung disease, no uncontrolled diabetes or PH) were included. There were no significant differences in the mean age between cohorts (PAH 55.6±14.0 vs control 55.9±17.1 vs group 2 PH 59.4±14.5 yrs, p=0.83). Mean pulmonary arterial pressure (mPAP) was assessed with right heart catheterization and was not significantly different between PAH and group 2 PH (45.0±12.1 vs 42.1 mmHg, p=0.56). All subjects underwent FDG-PET/CT imaging. Regions of interest (ROIs) were drawn manually to include the lateral one-third of the lungs on the sagittal images to avoid including obvious pulmonary vessels or non-specific fibrosis. The mean standard uptake value (SUV g/cc) of FDG in each lung was obtained and average values of both lungs were calculated as mean lung FDG SUV. The correlation between mPAP and mean lung FDG SUV was also analyzed in PAH and group 2 PH. PAH patients demonstrated significantly increased mean lung FDG SUV compared with control subjects and group 2 PH (PAH: 0.79±0.27 vs control: 0.53±0.19 vs group 2 PH: 0.35±0.20, p<0.0001). The mean lung FDG SUV did not correlate with mPAP either in PAH or group 2 PH. PAH is associated with increased pulmonary FDG uptake indicating increased glucose metabolism in the lung. This may represent active inflammation and requires further study.

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