Pulmonary Vascular Disease: Pulmonary Vascular Disease: PAH |

The Role of Mononuclear Cell TF and Inflammatory Cytokines in Patients With Chronic Thromboembolic Pulmonary Hypertension FREE TO VIEW

Minxia Yang; Chaosheng Deng; Dawen Wu; Zhanghua Zhong; Xiaoting Lv; Zhihua Huang; Ningfang Lian; Kaixiong Liu
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First Affiliated Hospital of Fujian Medical University, Fuzhou, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A508. doi:10.1016/j.chest.2016.02.530
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SESSION TITLE: Pulmonary Vascular Disease: PAH

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Thrombosis and inflammation are two major factors underlying chronic thromboembolic pulmonary hypertension (CTEPH). TF, CRP, TNF-α and MCP-1 may play critical roles in the process of CTEPH thrombosis and pulmonary vascular remodeling.

METHODS: Ten patients with a confirmed diagnosis of CTEPH, 20 patients with PTE and 15 patients with other types of PH were enrolled in this study, along with 20 healthy subjects as the control group. The immunoturbidimetric method was used to determine the plasma content of CRP. The plasma levels of TNF-α, MCP-1, and TF antigen were measured by an enzyme-linked immunosorbent assay (ELISA), and TF activity was measured by the chromogenic substrate method. Percoll density gradient centrifugation was used to separate peripheral blood mononuclear cells from plasma. The level of monocyte TF mRNA was examined by RT-PCR. The correlations between all indices described above were analyzed.

RESULTS: In CTEPH patients, the expression of CRP, TNF-α, and MCP-1 was significantly higher than that in controls. The levels of TF activity, TF antigen, and TF mRNA in monocyte cells were increased in CTEPH patients when compared with control subjects, but only the TF antigen and TF mRNA levels were significantly different. In CTEPH patients, levels of CRP, MCP-1, and TNF-α significantly correlated with the level of TF antigen in plasma.

CONCLUSIONS: TF gene expression was increased in patients with CTEPH, suggesting that blood-borne TF mainly comes from mononuclear cells. TF expression significantly correlated with levels of CRP, TNF-α and MCP-1. These factors may play an important role in the development of CTEPH via the inflammation-coagulation-thrombosis cycle.

CLINICAL IMPLICATIONS: TF expression was increased in the plasma of patients with CTEPH, partly due to an increase in monocyte TF mRNA levels. Monocyte TF plays a key role during the CTEPH thrombotic process. At the same time, the inflammatory factors CRP, TNF-α and MCP-1 increased in the plasma of patients with CTEPH and correlated with mPAP, indicating that they are involved in the pathogenesis of CTEPH and determine disease severity. Moreover, high expression of TF correlated with expression of the inflammatory factors CRP, TNF-α and MCP-1 in patients with CTEPH. TF, CRP, TNF-α, and MCP-1 may not be attractive molecules to test for screening of CTEPH but may have value in determination of prognosis, which was not evaluated in our study.

DISCLOSURE: The following authors have nothing to disclose: Minxia Yang, Chaosheng Deng, Dawen Wu, Zhanghua Zhong, Xiaoting Lv, Zhihua Huang, Ningfang Lian, Kaixiong Liu

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