Regular ArticleCalibrated automated thrombography demonstrates hypercoagulability in patients with idiopathic pulmonary arterial hypertension
Section snippets
Patients
This prospective study included consecutive patients with iPAH without any comorbidity. All clinical data and plasma samples were collected at diagnosis when patients were not yet on oral anticoagulant treatment. Patients were referred for diagnosis at the Department of Respiratory Diseases at the Nancy University Hospital. All patients were investigated to identify an underlying cause of pulmonary hypertension, following the guidelines [3]. The procedure of haemodynamic measurements was part
Patients and controls
Patients’ characteristics are displayed in Table 1. Sixteen patients (6 females), aged 57 ± 4, were studied. Three patients were in the New York Heart Association (NYHA) functional class II, 9 in class III and 4 in class IV. Twenty-nine healthy subjects (12 females) aged 58 ± 3 (range 17 to 82) were also studied as controls.
Standard laboratory data
The mean PT was 1.1 (range 0.99 to 1.3). The mean of plasma fibrinogen level was 3.8 g/l (range 2.2 to 6). The mean of plasma CRP was 6.2 mg/l (< 5 mg/l).
CAT and biomarkers of the in vivo activation of coagulation
All CAT parameters are
Discussion
To our knowledge, the present study is the first to demonstrate a hypercoagulable phenotype using CAT in iPAH patients. This method assesses thrombin generation taken into account all coagulation proteins in the plasma. Thereby, we have shown that iPAH patients have some degree of hypercoagulability in a population, which was similar in terms of age and pulmonary haemodynamics to the one of the French registry [31].
Our team has been involved in the development and the standardization of the CAT
Conflict of interest statement
No authors have any conflict of interest to declare.
Acknowledgments
Supported grants from the Conseil Régional de Lorraine, Association Régionale d'Aide aux Insuffisants Respiratoires de Lorraine, Glaxo Smith Kline, Bayer and Association des Chefs de Service du CHU de Nancy. Study sponsors had no involvement in the study design, in the collection, analysis and interpretation of data nor in the writing of the manuscript.
The authors thank Pr Athanase Benetos for his help for the recruitment of controls and acknowledge controls, and patients for their agreement to
References (43)
- et al.
Updated clinical classification of pulmonary hypertension
J Am Coll Cardiol
(2009) - et al.
Pathobiology of pulmonary hypertension. The role of platelets and thrombosis
Clin Chest Med
(2001) - et al.
Coagulation and fibrinolytic profiles in patients with severe pulmonary hypertension
Chest
(1996) - et al.
Abnormalities in circulating von Willebrand factor and survival in pulmonary hypertension
Am J Med
(1998) - et al.
Endothelial cell dysfunction correlates differentially with survival in primary and secondary pulmonary hypertension
Am Heart J
(2000) - et al.
Abnormal multimeric and oligomeric composition is associated with enhanced endothelial expression of von Willebrand factor in pulmonary hypertension
Chest
(1993) von Willebrand factor, endothelial dysfunction, and cardiovascular disease
J Thromb Haemost
(2006)- et al.
Platelet activation and fibrinopeptide formation in pulmonary hypertension
Chest
(1993) - et al.
Significance of a plasma D-dimer test in patients with primary pulmonary hypertension
Chest
(2002) - et al.
Plasma levels of thrombomodulin in pulmonary hypertension
Am J Med
(1996)