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1 l in the general population of patients with primary pulmonary hypertension.
2 as improved survival in patients with severe primary pulmonary hypertension.
3 ated in the study; four had CDH, and one had primary pulmonary hypertension.
4 rotein (BMPR-II) have been shown to underlie primary pulmonary hypertension.
5 ated in tumorigenesis and in the etiology of primary pulmonary hypertension.
6 small pulmonary arteries that is typical of primary pulmonary hypertension.
7 nary hypertension may actually have familial primary pulmonary hypertension.
8 gic features indistinguishable from those of primary pulmonary hypertension.
9 registry of 67 families affected by familial primary pulmonary hypertension.
10 ch has recently been found to cause familial primary pulmonary hypertension.
11 virus HHV-8 may have a pathogenetic role in primary pulmonary hypertension.
12 nol (prostacyclin) in patients with advanced primary pulmonary hypertension.
13 ascular remodeling that is characteristic of primary pulmonary hypertension.
14 oncern are changes in brain biochemistry and primary pulmonary hypertension.
15 mportant cause of morbidity and mortality in primary pulmonary hypertension.
16 In lung tissue from 10 of 16 patients with primary pulmonary hypertension (62 percent), cells withi
17 old) and diseased lung specimens (emphysema, primary pulmonary hypertension) additional HOX genes fro
18 issue samples from 16 patients with sporadic primary pulmonary hypertension and 14 patients with seco
20 naling pathway is defective in patients with primary pulmonary hypertension and may implicate the pat
21 ive properties is an effective treatment for primary pulmonary hypertension and pulmonary arterial hy
22 rs as an idiopathic disease (formerly called primary pulmonary hypertension) and as a consequence of
23 nitrogen load, concurrent medical stressors, primary pulmonary hypertension, and hepatic glutamine sy
24 the DiGeorge, Holt-Oram, Alagille, familial primary pulmonary hypertension, and Noonan syndromes.
26 dilators, many of which have been studied in primary pulmonary hypertension, are now undergoing study
27 ied by chronic pulmonary thromboembolism and primary pulmonary hypertension, are relatively cryptic i
28 been used successfully to palliate endstage primary pulmonary hypertension but has not been attempte
30 prostenol improves survival in patients with Primary Pulmonary Hypertension compared with that predic
42 ality of life, and survival in patients with primary pulmonary hypertension, its use in patients with
43 As previously demonstrated in patients with primary pulmonary hypertension, long-term PGI2 may have
45 e transcriptase-polymerase chain reaction in primary pulmonary hypertension lung specimens when compa
46 that many patients with apparently sporadic primary pulmonary hypertension may actually have familia
48 nal therapy alone in 81 patients with severe primary pulmonary hypertension (New York Heart Associati
49 broplasia [valvular heart disease (VHD)] and primary pulmonary hypertension observed in patients taki
51 rganization (WHO) functional class II or III primary pulmonary hypertension or PAH related to either
53 on (P < 0.001), and lung transplantation for primary pulmonary hypertension (P = 0.045) were associat
54 gh HIV-associated pulmonary hypertension and primary pulmonary hypertension (PPH) are clinically and
55 he pathogenesis is unknown and any link with primary pulmonary hypertension (PPH) has been speculativ
57 study was to determine whether patients with primary pulmonary hypertension (PPH) have an immunogenet
73 , and subjects with moderate RV failure from primary pulmonary hypertension (PPH) or idiopathic dilat
74 o investigate the responses of patients with primary pulmonary hypertension (PPH) to constant work ra
75 twentieth century, the published reports on primary pulmonary hypertension (PPH) were confined to cl
76 prostacyclin dose reduction in patients with primary pulmonary hypertension (PPH) who developed high
77 lantation) from eight patients with Stage IV primary pulmonary hypertension (PPH) with the reactivity
79 nesis of the vascular lesions characterizing primary pulmonary hypertension (PPH), an often fatal pul
80 4 idiopathic dilated cardiomyopathy (IDC), 8 primary pulmonary hypertension (PPH), and 13 nonfailing
81 ilated cardiomyopathy (IDC), 8 subjects with primary pulmonary hypertension (PPH), and 32 organ donor
82 f prostacyclin is an effective treatment for primary pulmonary hypertension (PPH), and has recently b
84 de effects, such as cardiac valvulopathy and primary pulmonary hypertension (PPH), limits the clinica
85 lmonary vascular resistance in patients with primary pulmonary hypertension (PPH), right atrial press
86 he lung tissue obtained from 6 patients with primary pulmonary hypertension (PPH)-including 2 patient
98 cases of moderate to severe PH (15 cases of primary pulmonary hypertension [PPH], eight cases of Eis
100 ary hypertension occurs in 3 distinct forms: primary pulmonary hypertension, pulmonary hypertension o
101 e echocardiographic manifestations of severe primary pulmonary hypertension reflect abnormalities in
102 pproximately 6% of cases recorded in the NIH Primary Pulmonary Hypertension Registry are inherited in
103 edicted by the National Institutes of Health Primary Pulmonary Hypertension Registry's survival equat
106 Treatment with infusion of prostacyclin for primary pulmonary hypertension was approved, paving the
107 nt of persons carrying the gene for familial primary pulmonary hypertension, we hypothesized that man
108 lung disease that is indistinguishable from primary pulmonary hypertension, we investigated the gene
110 heart disease and cardiac cirrhosis (1), and primary pulmonary hypertension with primary biliary cirr
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