PMID- 27221958
OWN - NLM
STAT- MEDLINE
DCOM- 20170428
LR  - 20170817
IS  - 1897-4279 (Electronic)
IS  - 0022-9032 (Linking)
VI  - 74
IP  - 11
DP  - 2016
TI  - Plasma concentrations of tissue factor and its inhibitor in chronic 
      thromboembolic pulmonary hypertension: a step closer to explanation of the 
      disease aetiology?
PG  - 1332-1338
LID - 10.5603/KP.a2016.0088 [doi]
AB  - BACKGROUND: The aetiology of chronic thromboembolic pulmonary hypertension 
      (CTEPH) is not clearly understood. In some patients, the disease is preceded by 
      acute pulmonary embolism (APE), and is characterised by intravascular thrombosis, 
      vasoconstriction, inflammation and remodelling of pulmonary arteries. Ensuing 
      pulmonary hypertension leads to potentially fatal chronic right ventricle 
      failure. Both inborn and acquired risk factors were identified. Pathogenesis of 
      haemostatic disorders is not completely explained, and extrinsic coagulation 
      pathway disorders may play a role in CTEPH aetiology. AIM: To evaluate levels of 
      tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in CETPH, and to 
      delineate their role in the disease pathogenesis. METHODS: Plasma concentrations 
      of TF and TFPI were evaluated in 21 CTEPH patients, in 12 patients with pulmonary 
      arterial hypertension (PAH), in 55 APE survivors without persistent pulmonary 
      hypertension after at least 6 months from the acute episode, and in 53 healthy 
      volunteers (control group C). Most patients were treated with vitamin K 
      antagonists (VKA), and some with unfractionated or low molecular weight heparin. 
      Exclusion criteria included malignancy, inflammation, and recent operation. 
      RESULTS: Tissue factor concentration was lower in CTEPH and in post-APE patients, 
      not stratified by anticoagulation modality, as compared to control group (p = 
      0.042; p = 0.011) and PAH group (p = 0.024, p = 0.014). Patients with CTEPH and 
      post-APE on adequate VKA-anticoagulation had similar TF concentration to group C. 
      TFPI concentration was similar in CETPH and post-APE patients irrespective of 
      anticoagulation, and higher as compared to group C (respectively, p = 0.012; p = 
      0.024; p = 0.004). TFPI concentration was similar in patients with CETPH and in 
      post-APE group, both on adequate VKA-anticoagulation when compared to group C. In 
      the post-APE group, there was no significant difference in TFPI concentration 
      between patients receiving adequate and subjects without anticoagulation. Group C 
      was significantly (p = 0.000) younger than any other group, and showed 
      correlation (r = 0.31) between age and TFPI concentration. CONCLUSIONS: In CTEPH 
      there is a high consumption of TF, leading to reduction in plasma concentration 
      of TF and increase in TFPI. Adequate VKA-anticoagulation normalises TF and TFPI 
      plasma concentrations, as is the case of APE survivors.
FAU - Cisowska-Czajka, Marta E
AU  - Cisowska-Czajka ME
AD  - Centra Medyczne Luxmed-Medycyna Rodzinna we Wroclawiu, Wojewowdzki Szpital 
      Specjalistyczny we Wroclawiu - Osrodek Badawczo-Rozwojowy. martacisowska1@wp.pl.
FAU - Mazij, Mariusz P
AU  - Mazij MP
FAU - Kotschy, Maria H
AU  - Kotschy MH
FAU - Lewczuk, Jerzy
AU  - Lewczuk J
LA  - eng
PT  - Journal Article
DEP - 20160525
PL  - Poland
TA  - Kardiol Pol
JT  - Kardiologia polska
JID - 0376352
RN  - 0 (Anticoagulants)
RN  - 0 (Lipoproteins)
RN  - 0 (lipoprotein-associated coagulation inhibitor)
RN  - 12001-79-5 (Vitamin K)
RN  - 9035-58-9 (Thromboplastin)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Anticoagulants/pharmacology/therapeutic use
MH  - Humans
MH  - Hypertension, Pulmonary/*blood/drug therapy/etiology
MH  - Lipoproteins/*blood
MH  - Middle Aged
MH  - Pulmonary Embolism/blood
MH  - Thromboplastin/*analysis
MH  - Vitamin K/antagonists & inhibitors
MH  - Young Adult
OTO - NOTNLM
OT  - anticoagulation
OT  - chronic thromboembolic pulmonary hypertension (CTEPH)
OT  - tissue factor (TF)
OT  - tissue factor pathway inhibitor (TFPI)
EDAT- 2016/05/26 06:00
MHDA- 2017/04/30 06:00
CRDT- 2016/05/26 06:00
PHST- 2015/10/28 00:00 [received]
PHST- 2016/04/18 00:00 [accepted]
PHST- 2016/04/04 00:00 [revised]
PHST- 2016/05/26 06:00 [pubmed]
PHST- 2017/04/30 06:00 [medline]
PHST- 2016/05/26 06:00 [entrez]
AID - VM/OJS/KP/10180 [pii]
AID - 10.5603/KP.a2016.0088 [doi]
PST - ppublish
SO  - Kardiol Pol. 2016;74(11):1332-1338. doi: 10.5603/KP.a2016.0088. Epub 2016 May 25.