Endothelial cell injury and dysfunction have been well documented in pulmonary hypertension. From the morphologic point of view, structural changes found using scanning and transmission electron microscopy have suggested a phase of enhanced metabolic function of endothelial cells. From the biochemical point of view, evidence for endothelial cell dysfunction in pulmonary hypertension comes from reports showing abnormal circulating levels of endothelin, thrombomodulin, and vWF that are associated with increased immunostaining of the pulmonary vascular endothelium for endothelin and vWF.> Reduction of endothelium-derived vasodilators has been reported as well. A possibility exists that the magnitude of endothelial cell dysfunction is correlated with the extent and severity of pulmonary microvascular damage in pulmonary hypertension more ventolin inhalers. If so, the assessment of endothelial cell function using biochemical markers might have prognostic implications. We therefore planned the present study to examine prospectively whether a correlation exists between circulating levels of vWF and short-term prognosis in patients with pulmonary hypertension. Other variables such as patient sex, age, mean pulmonary arterial pressure, and the etiology of pulmonary hypertension also were analyzed to determine their predictive value in identifying which patients would be unlikely to survive over the short term.
Materials and Methods
Patients and Study Protocol
This study involved 40 patients with precapillaiy pulmonary hypertension who were under medical treatment at the Heart Institute of the School of Medicine of the University of Sao Paulo, Brazil. Patients entered the study consecutively, and patients with primary and secondary pulmonary hypertension were included. Levels of mean pulmonary arterial pressure higher than 25 mm Hg at rest in the presence of normal pulmonary wedge pressure at routine cardiac catheterization were considered necessary for patient inclusion.
Category: Pulmonary Hypertension
Tags: endothelial cells, pulmonary hypertension, von Willebrand factor