PMID- 24015338
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130909
LR  - 20220129
IS  - 2045-8932 (Print)
IS  - 2045-8940 (Electronic)
IS  - 2045-8932 (Linking)
VI  - 3
IP  - 2
DP  - 2013 Apr
TI  - Circulating angiogenic modulatory factors predict survival and functional class 
      in pulmonary arterial hypertension.
PG  - 369-80
LID - 10.4103/2045-8932.110445 [doi]
AB  - The diagnosis of pulmonary arterial hypertension (PAH) is frequently delayed. We 
      hypothesized that circulating angiogenic modulatory protein levels might 
      correspond with vascular remodeling activity and serve as sensitive biomarkers of 
      PAH. Levels of soluble endoglin (sEng), soluble vascular endothelial growth 
      factor receptor-1 (sVEGFR1), N-terminal brain natriuretic peptide (NT-proBNP), 
      C-reactive protein (CRP), and other biomarkers were measured in peripheral blood 
      from 97 PAH patients, 16 first-degree relatives of idiopathic or heritable 
      pulmonary arterial hypertension (HPAH) patients, and 56 controls, and correlated 
      with disease, functional class, hemodynamic parameters, exercise capacity, and 
      transplant-free survival. Endoglin expression was analyzed in lung tissues of six 
      individuals with idiopathic or HPAH and four individuals without PAH. Levels of 
      sEng, sVEGFR1, CRP, and NT-proBNP were elevated in Group I PAH of diverse 
      etiologies, with sEng performing better than NT-proBNP in detecting PAH (receiver 
      operator characteristic-area-under-the curve [ROC-AUC] of 0.82 +/- 0.03 vs. 0.71 +/- 
      0.05, P = 0.016). While sEng, sVEGFR1, and NT-proBNP correlated with New York 
      Heart Association (NYHA) class, sEng levels were more sensitive than NT-proBNP in 
      detecting NYHA Class I-II disease (ROC-AUC of 0.88 +/- 0.05 vs. 0.67 +/- 0.08, P = 
      0.028). sEng, sVEGFR1, CRP, and NT-proBNP predicted transplant-free survival by 
      univariate Cox regression. After adjusting for NT-proBNP levels, each of the 
      other three markers predicted transplant-free survival. In multivariate analysis, 
      sEng and CRP were independent predictors of survival. Endoglin expression was 
      markedly enhanced in the microvascular endothelium and endovascular lesions of 
      PAH versus control lung tissues. Circulating angiogenic proteins sEng and sVEGFR1 
      are sensitive markers of prognosis and function in Group I PAH, including mildly 
      symptomatic disease, and may provide unique noninvasive data reflecting 
      underlying remodeling activity.
FAU - Malhotra, Rajeev
AU  - Malhotra R
AD  - Department of Medicine, Cardiovascular Research Center, Cardiology Division, 
      Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, 
      USA.
FAU - Paskin-Flerlage, Samuel
AU  - Paskin-Flerlage S
FAU - Zamanian, Roham T
AU  - Zamanian RT
FAU - Zimmerman, Patrick
AU  - Zimmerman P
FAU - Schmidt, Jonathan W
AU  - Schmidt JW
FAU - Deng, Donna Y
AU  - Deng DY
FAU - Southwood, Mark
AU  - Southwood M
FAU - Spencer, Robert
AU  - Spencer R
FAU - Lai, Carol S
AU  - Lai CS
FAU - Parker, William
AU  - Parker W
FAU - Channick, Richard N
AU  - Channick RN
FAU - Morrell, Nicholas W
AU  - Morrell NW
FAU - Elliott, C Gregory
AU  - Elliott CG
FAU - Yu, Paul B
AU  - Yu PB
LA  - eng
GR  - R01 AR057374/AR/NIAMS NIH HHS/United States
GR  - T32 HL007208/HL/NHLBI NIH HHS/United States
GR  - K08 HL079943/HL/NHLBI NIH HHS/United States
GR  - RG/13/4/30107/BHF_/British Heart Foundation/United Kingdom
GR  - HCS/P10/011/DH_/Department of Health/United Kingdom
PT  - Journal Article
PL  - United States
TA  - Pulm Circ
JT  - Pulmonary circulation
JID - 101557243
PMC - PMC3757832
OTO - NOTNLM
OT  - VEGF receptor-1
OT  - angiogenesis
OT  - biomarkers
OT  - endoglin
OT  - pulmonary arterial hypertension
COIS- Conflict of Interest: None declared.
EDAT- 2013/09/10 06:00
MHDA- 2013/09/10 06:01
PMCR- 2013/04/01
CRDT- 2013/09/10 06:00
PHST- 2013/09/10 06:00 [entrez]
PHST- 2013/09/10 06:00 [pubmed]
PHST- 2013/09/10 06:01 [medline]
PHST- 2013/04/01 00:00 [pmc-release]
AID - PC-3-369 [pii]
AID - 10.4103/2045-8932.110445 [doi]
PST - ppublish
SO  - Pulm Circ. 2013 Apr;3(2):369-80. doi: 10.4103/2045-8932.110445.