2Ankara Türkiye Yüksek İhtisas Hastanesi, Kardiyoloji Bölümü, Ankara, Türkiye
3Department of Cardiology, Yüksek Ihtisas Heart-Education and Research Hospital, Ankara, Turkey
4Türkiye Yüksek İhtisas Eğitim ve Araştırma Hastanesi, Kardiyoloji Kliniği, Ankara
5Türkiye Yüksek İhtisas Hastanesi, Kalp ve Damar Cerrahisi Kliniği, Ankara
6Ankara Türkiye Yüksek İhtisas Hastanesi, Hematoloji ve Bölümü Ankara, Türkiye
7Abant İzzet Baysal Üniversitesi, Göğüs Hastalıkları Bölümü, Bolu, Türkiye
8Ankara Türkiye Yüksek İhtisas Hastanesi, Göğüs Hastalıkları Bölümü, Ankara, Türkiye
9Clinic of Cardiology, Türkiye Yüksek İhtisas Hospital, Ankara
10Department of Cardiology, Yüksek İhtisas Heart-Education and Research Hospital, Ankara, Turkey
Abstract
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). Conclusion: In SPH, pulmonary vascular bed shows increased thrombotic, hypofibrinolytic, and proliferative activities which are partially related to the severity of illness.