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• W2051255785 abstract "Background Plasma von Willebrand factor antigen (vWF:Ag) has been used as a marker of endothelial perturbation in a number of vascular disorders. In this study, vWF:Ag was determined as an attempt to evaluate the severity of endothelial cell dysfunction in primary pulmonary hypertension (PPH) and congenital heart disease-associated pulmonary hypertension (CHD-PH) comparatively and to determine its impact on short-term survival. Methods and Results Clinical, hemodynamic, and biochemical data were obtained from 11 patients with PPH and 24 with CHD-PH. Patient groups were similar in terms of age and pulmonary artery pressure. vWF:Ag was measured by electroimmunodiffusion. Patients were followed up for 1 year and at that time, data collected at the beginning of the study were subjected to univariate and multivariate analyses. vWF:Ag was increased in patients (normal reference value 87% ± 23% activity, mean ± SD), with higher levels in the PPH group (231% ± 89%) in comparison with the CHD-PH group (127% ± 68%) (P < .001). Multivariate analysis showed that survival was influenced by the underlying cause of pulmonary hypertension and vWF:Ag levels but not by patient age, sex, or pulmonary artery pressure. Seven of 10 nonsurvivors but only 4 of 25 survivors had PPH (P = .007). vWF:Ag was 255 ± 90% in the nonsurvivor group and 121% ± 54% in the survivors (P < .001). Conclusions Our findings suggest that short-term survival is related to the severity of endothelial cell dysfunction in pulmonary hypertension. In addition, exceedingly high vWF:Ag levels in PPH might reflect a particular pattern of endothelial cell dysfunction that could be associated with decreased short-term life expectancy in this disorder compared with secondary forms of pulmonary hypertension." @default.
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• W2051255785 date "2000-04-01" @default.
• W2051255785 modified "2023-09-29" @default.
• W2051255785 title "Endothelial cell dysfunction correlates differentially with survival in primary and secondary pulmonary hypertension" @default.
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• W2051255785 doi "https://doi.org/10.1016/s0002-8703(00)90038-3" @default.
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