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Derivation of mean pulmonary artery pressure from noninvasive parameters.
BACKGROUND: The assessment of pulmonary pressure is important for the diagnosis and management of patients with pulmonary hypertension. Mean pulmonary artery pressure (MPAP) has been used in the current definition of pulmonary hypertension. However, invasive derivation by Doppler echocardiography provides the peak pulmonary artery systolic pressure (PASP). The aim of this study was to derive a method to predict MPAP from PASP.
METHODS: Invasive hemodynamic pressures in 307 patients who underwent right heart catheterization were examined. Simple regression techniques were used to determine the relationship between MPAP and PASP in a derivation cohort (n = 198) and a validation sample (n = 109). Bland-Altman analysis was performed to examine predicted versus observed values of MPAP.
RESULTS: MPAP and PASP at catheterization were strongly related over a range of pressures (R(2) = 0.89, n = 198; SE, 4.04; P < .0001). The relation of MPAP to PASP in the derivation cohort (MPAP = 0.61 × PASP + 1.95 mm Hg) was validated in the test sample, with an R(2) value of 0.94 for predicted versus observed MPAP (SE, 2.87; P < .0001). The relationship of predicted versus observed MPAP was constant across different degrees of pressure elevation, as well as different etiologies of pulmonary hypertension. Applying the equation to Doppler-derived pulmonary pressures, there was excellent correlation of predicted MPAP from echocardiography and invasively measured MPAP (R(2) = 0.78, P < .0001).
CONCLUSIONS: MPAP can be accurately predicted from PASP over a wide pressure range for different etiologies of pulmonary hypertension. This finding may help define MPAP noninvasively.
METHODS: Invasive hemodynamic pressures in 307 patients who underwent right heart catheterization were examined. Simple regression techniques were used to determine the relationship between MPAP and PASP in a derivation cohort (n = 198) and a validation sample (n = 109). Bland-Altman analysis was performed to examine predicted versus observed values of MPAP.
RESULTS: MPAP and PASP at catheterization were strongly related over a range of pressures (R(2) = 0.89, n = 198; SE, 4.04; P < .0001). The relation of MPAP to PASP in the derivation cohort (MPAP = 0.61 × PASP + 1.95 mm Hg) was validated in the test sample, with an R(2) value of 0.94 for predicted versus observed MPAP (SE, 2.87; P < .0001). The relationship of predicted versus observed MPAP was constant across different degrees of pressure elevation, as well as different etiologies of pulmonary hypertension. Applying the equation to Doppler-derived pulmonary pressures, there was excellent correlation of predicted MPAP from echocardiography and invasively measured MPAP (R(2) = 0.78, P < .0001).
CONCLUSIONS: MPAP can be accurately predicted from PASP over a wide pressure range for different etiologies of pulmonary hypertension. This finding may help define MPAP noninvasively.
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