[Thrombotic, fibrinolytic and proliferative activities of pulmonary vascular bed in secondary pulmonary hypertension].
OBJECTIVE
To determine whether pulmonary vascular bed contributes to the development of in situ thrombosis and vascular remodelling in secondary pulmonary hypertension (SPH) via changes in its local secretory activities.


METHODS
Seventy-one patients with the diagnosis of secondary pulmonary hypertension (38 females, mean age 40.36+/-1.05 years) were included in the study. Selective right and left heart catheterization was performed to each patient for diagnostic purposes. Blood samples obtained from left ventricle (LV) and pulmonary artery (PA) of each patient were analyzed for levels of plasminogen activator inhibitor-1 (PAI-1), platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), D-dimer, von Willebrand factor (vWF), protein-C, antithrombin-III, fibrinogen, and plasminogen. Results were compared between LV and PA. Correlation analysis between each parameter and mean pulmonary artery pressure (MPAP) was performed.


RESULTS
Although mean level of VEGF in LV and PA were found to be in normal range, it was significantly higher in LV than in PA (p<0.001). Mean PDGF and D-dimer levels, which remained in normal range were also higher in LV (p<0.001 and p<0.001, respectively) than in PA;.vWF showed similar degree of elevation in both LV and PA. Only one parameter, PAI-1, was found to be significantly higher in PA than in LV (p=0.012). Antithrombin-III, protein C, plasminogen, and fibrinogen levels showed no significant differences between two chambers. They also remained in normal range, except for fibrinogen, which was slightly elevated in both LV and PA. Correlation analysis revealed strong positive correlation between D-dimer level in both LV and PA and MPAP (r=0.775, p<0.001 and r=0.649, p<0.001, respectively).


CONCLUSIONS
In SPH, pulmonary vascular bed shows increased thrombotic, hypofibrinolytic, and proliferative activities, which are partially related to the severity of illness.
Ergün
Kumral
K
Department of Cardiology, Türkiye Yüksek Ihtisas Hospital, Ankara, Turkey. kumralcagli@yahoo.com
Balbay
Yücel
Y
Cihan
Gökhan
G
Aras
Dursun
D
Cağli
Kerim
K
Ayaz
Selime
S
Bilgiç
Filiz
F
Balbay
Oner A
OA
Saşmaz
Hatice
H
Korkmaz
Sule
S
D000328:Adult; D000990:Antithrombin III / Q000378:metabolism; D006328:Cardiac Catheterization; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000503:physiopathology*; D008297:Male; D010958:Plasminogen / Q000378:metabolism; D015849:Plasminogen Inactivators / Q000097:blood; D010982:Platelet-Derived Growth Factor / Q000378:metabolism; D011486:Protein C / Q000378:metabolism; D011652:Pulmonary Circulation; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
D015849:Plasminogen Inactivators; D010982:Platelet-Derived Growth Factor; D011486:Protein C; D042461:Vascular Endothelial Growth Factor A; D014841:von Willebrand Factor; D000990:Antithrombin III; D005340:Fibrinogen; D010958:Plasminogen