PURPOSE: To evaluate quantitative differences in central pulmonary artery (PA) and pulmonary global and regional enhancement in patients with and without pulmonary hypertension (PH) using dual-energy computed tomography (DECT). MATERIALS AND METHODS: We retrospectively studied 391 thoracic DECT studies and identified 89 patients with PA pressure (PAP) data and a pulmonary angiogram. PH was defined as a mean PAP of ≥25 mm Hg on right heart catheterization (RHC) (n=19) or a systolic PAP of ≥40 mm Hg on echocardiography (n=20). PH absence was defined by entirely normal echocardiography or RHC (n=50). PA enhancement (PAenh) was calculated from DECT iodine images. Volumetric enhancement of each whole lung (WLenh), 6 standard lung regions (RLenh), and 24 two-dimensional standardized regions of interest (ROIenh) was performed in each patient using pulmonary blood volume analysis. RESULTS: Mean PAenh was greater in PH patients compared with controls (272 vs. 252 HU, P<0.05), with a reciprocal reduction in mean WLenh (27 vs. 32 HU, P<0.01). Mean ROIenh (n=2058) confirmed lower parenchymal enhancement in PH (27 vs. 32 HU, P<0.001), with greater mean ROIenh standard deviation (10.5 vs. 9.3, P<0.001). Mean intrapatient pulmonary enhancement variability was greater in PH patients than in controls for 6 RLenh (variance 37 vs. 22, P=0.02) and 24 ROIenh measures (variance 188 vs. 130, P=0.04). RLenh and ROIenh variance correlated with RHC pulmonary vascular resistance (PVR) (r=0.44, 0.48; P=0.04, 0.03, respectively). A ratio of PAenh/WLenh distinguished PH from non-PH patients (10.9 vs. 8.4, P<0.001) and correlated best with PVR (r=0.59, P=0.004). CONCLUSIONS: PH patients demonstrate increased PAenh with a reciprocal reduction and greater variation in parenchymal enhancement; a DECT ratio of central to parenchymal enhancement correlates with PVR and may help identify PH.
PURPOSE: To evaluate quantitative differences in central pulmonary artery (PA) and pulmonary global and regional enhancement in patients with and without pulmonary hypertension (PH) using dual-energy computed tomography (DECT). MATERIALS AND METHODS: We retrospectively studied 391 thoracic DECT studies and identified 89 patients with PA pressure (PAP) data and a pulmonary angiogram. PH was defined as a mean PAP of ≥25 mm Hg on right heart catheterization (RHC) (n=19) or a systolic PAP of ≥40 mm Hg on echocardiography (n=20). PH absence was defined by entirely normal echocardiography or RHC (n=50). PA enhancement (PAenh) was calculated from DECT iodine images. Volumetric enhancement of each whole lung (WLenh), 6 standard lung regions (RLenh), and 24 two-dimensional standardized regions of interest (ROIenh) was performed in each patient using pulmonary blood volume analysis. RESULTS: Mean PAenh was greater in PH patients compared with controls (272 vs. 252 HU, P<0.05), with a reciprocal reduction in mean WLenh (27 vs. 32 HU, P<0.01). Mean ROIenh (n=2058) confirmed lower parenchymal enhancement in PH (27 vs. 32 HU, P<0.001), with greater mean ROIenh standard deviation (10.5 vs. 9.3, P<0.001). Mean intrapatient pulmonary enhancement variability was greater in PH patients than in controls for 6 RLenh (variance 37 vs. 22, P=0.02) and 24 ROIenh measures (variance 188 vs. 130, P=0.04). RLenh and ROIenh variance correlated with RHC pulmonary vascular resistance (PVR) (r=0.44, 0.48; P=0.04, 0.03, respectively). A ratio of PAenh/WLenh distinguished PH from non-PH patients (10.9 vs. 8.4, P<0.001) and correlated best with PVR (r=0.59, P=0.004). CONCLUSIONS: PH patients demonstrate increased PAenh with a reciprocal reduction and greater variation in parenchymal enhancement; a DECT ratio of central to parenchymal enhancement correlates with PVR and may help identify PH.
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