Background: Differentiation of pulmonary arterial hypertension (PAH) and pulmonary venous hypertension (PVH) often requires right heart catheterization (RHC). We sought to determine whether a combination of clinical and echocardiographic variables could predict the pulmonary diastolic to wedge (PAd-PWP) gradient and thus differentiate patients with PAH and PVH.
Methods: We prospectively enrolled 108 patients presenting for PH evaluation. We developed a multivariate model to predict PAd-PWP gradient and validated this model using bootstrapping technique.
Results: PAH patients had worse hemodynamics and were more likely to have evidence of right ventricular dilation and dysfunction whereas patients with PVH were older and more likely to have features of the metabolic syndrome. PAd-PWP gradient of ≥ 6 mm Hg accurately discriminated patients with PAH compared to PVH. Our model including clinical and echocardiographic variables was highly accurate for the prediction of PAd-PWP gradient with a slope 0.89 (slope of 1 represents perfect prediction).
Conclusions: In this prospective study of patients referred for PH evaluation, a model of readily available clinical parameters and simple echocardiographic measurements accurately predicted the PAd-PWP gradient, allowing discrimination of patients with PAH and PVH. This model requires validation in a larger cohort, but may afford clinicians more parsimony with referral for invasive testing in the evaluation of PH.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0076461 | PLOS |
PLoS One
May 2014
Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.
Background: Differentiation of pulmonary arterial hypertension (PAH) and pulmonary venous hypertension (PVH) often requires right heart catheterization (RHC). We sought to determine whether a combination of clinical and echocardiographic variables could predict the pulmonary diastolic to wedge (PAd-PWP) gradient and thus differentiate patients with PAH and PVH.
Methods: We prospectively enrolled 108 patients presenting for PH evaluation.
Anesthesiology
March 2005
Department of Anesthesiology, New York Medical College, Valhalla, USA.
Background: Pulmonary artery diastolic (PAD)-pulmonary wedge pressure (PWP) gradient has been shown to be increased in sepsis and acute respiratory distress syndrome (ARDS). Because pulmonary venous vasoconstriction induced by endotoxemia in sepsis or postcapillary leukocyte aggregation in ARDS or both can increase pulmonary venous resistance (Rpv), it is possible that the elevated Rpv increases PAD-PWP. The authors examined this possibility by assessing the correlation between Rpv and PAD-PWP gradient in patients with ARDS.
View Article and Find Full Text PDFChest
January 1991
Cardiopulmonary Service Instituto Nacional de Cardiologia Ignacio Chavez, Mexico City, Mexico.
We studied the hemodynamic behavior of the pulmonary circulation at rest and during exercise in six patients with MTB. As a group, in contrast to advanced fibrocaseous tuberculosis, these patients exhibited normal pulmonary hemodynamics at rest and during exercise. Only minor abnormalities in pulmonary vascular resistance at exercise (increased PAd-PWP gradient) were noted in two of the patients.
View Article and Find Full Text PDFAn initially widened pulmonary artery diastolic-pulmonary wedge pressure (PAD-PWP) gradient greater than 5 mm Hg has been reported to be associated with an 83% mortality rate in septic patients. To confirm and extend these observations, we retrospectively reviewed the charts of 47 septic patients. The patients were divided into 2 groups: group 1-12 patients who never had an abnormal gradient during their hospital course, and group 2-35 patients who had an abnormal gradient sometimes during their course.
View Article and Find Full Text PDFThe experience we describe derives from the short-term administration of isoproterenol in 15 patients with ventricular septal defect (VSD) and severe pulmonary artery hypertension (PAH). For the whole study group, mean pulmonary artery pressure (PAP) was 68.5 +/- 2.
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