OBJECTIVE: To optimise an echocardiographic estimation of pulmonary vascular resistance (PVR(e)) for diagnosis and follow-up of pulmonary hypertension (PHT). DESIGN: Cross-sectional study. SETTING: Tertiary referral centre. PATIENTS: Patients undergoing right heart catheterisation and echocardiography for assessment of suspected PHT. METHODS: PVR(e) ([tricuspid regurgitation velocity ×10/(right ventricular outflow tract velocity-time integral+0.16) and invasive PVR(i) ((mean pulmonary artery systolic pressure-wedge pressure)/cardiac output) were compared in 72 patients. Other echo data included right ventricular systolic pressure (RVSP), estimated right atrial pressure, and E/e' ratio. Difference between PVR(e) and PVR(i) at various levels of PVR was sought using Bland-Altman analysis. Corrected PVR(c) ((RVSP-E/e')/RVOT(VTI)) (RVOT, RV outflow time; VTI, velocity time integral) was developed in the training group and tested in a separate validation group of 42 patients with established PHT. RESULTS: PVR(e)>2.0 had high sensitivity (93%) and specificity (91%) for recognition of PVR(i)>2.0, and PVR(c) provided similar sensitivities and specificities. PVR(e) and PVR(i) correlated well (r=0.77, p<0.01), but PVR(e) underestimated marked elevation of PVR(i)-a trend avoided by PVR(c). PVR(c) and PVR(e) were tested against PVR(i) in a separate validation group (n=42). The mean difference between PVR(e) and PVR(i) exceeded that between PVR(c) and PVR(i) (2.8±2.7 vs 0.8±3.0 Wood units; p<0.001). A drop in PVR(i) by at least one SD occurred in 10 patients over 6 months; this was detected in one patient by PVR(e) and eight patients by PVR(c) (p=0.002). CONCLUSION: PVR(e) distinguishes normal from abnormal PVR(i) but underestimates high PVR(i). PVR(c) identifies the severity of PHT and may be used to assess treatment response.
OBJECTIVE: To optimise an echocardiographic estimation of pulmonary vascular resistance (PVR(e)) for diagnosis and follow-up of pulmonary hypertension (PHT). DESIGN: Cross-sectional study. SETTING: Tertiary referral centre. PATIENTS: Patients undergoing right heart catheterisation and echocardiography for assessment of suspected PHT. METHODS: PVR(e) ([tricuspid regurgitation velocity ×10/(right ventricular outflow tract velocity-time integral+0.16) and invasive PVR(i) ((mean pulmonary artery systolic pressure-wedge pressure)/cardiac output) were compared in 72 patients. Other echo data included right ventricular systolic pressure (RVSP), estimated right atrial pressure, and E/e' ratio. Difference between PVR(e) and PVR(i) at various levels of PVR was sought using Bland-Altman analysis. Corrected PVR(c) ((RVSP-E/e')/RVOT(VTI)) (RVOT, RV outflow time; VTI, velocity time integral) was developed in the training group and tested in a separate validation group of 42 patients with established PHT. RESULTS: PVR(e)>2.0 had high sensitivity (93%) and specificity (91%) for recognition of PVR(i)>2.0, and PVR(c) provided similar sensitivities and specificities. PVR(e) and PVR(i) correlated well (r=0.77, p<0.01), but PVR(e) underestimated marked elevation of PVR(i)-a trend avoided by PVR(c). PVR(c) and PVR(e) were tested against PVR(i) in a separate validation group (n=42). The mean difference between PVR(e) and PVR(i) exceeded that between PVR(c) and PVR(i) (2.8±2.7 vs 0.8±3.0 Wood units; p<0.001). A drop in PVR(i) by at least one SD occurred in 10 patients over 6 months; this was detected in one patient by PVR(e) and eight patients by PVR(c) (p=0.002). CONCLUSION: PVR(e) distinguishes normal from abnormal PVR(i) but underestimates high PVR(i). PVR(c) identifies the severity of PHT and may be used to assess treatment response.
Authors: Antonella Meloni; Jon Detterich; Alessia Pepe; Paul Harmatz; Tom D Coates; John C Wood Journal: Blood Cells Mol Dis Date: 2014-11-24 Impact factor: 3.039
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