Background: Pulmonary arterial hypertension (PAH) is a chronic progressive disease characterized by persistent elevation of pulmonary artery pressure. Regardless of the initial trigger, the elevated pulmonary arterial pressure and vascular resistance in patients with PAH are primarily caused by remodeling and thrombosis of small- and medium-sized pulmonary arteries and arterioles, as well as sustained vasoconstriction. Recent studies have emphasized the relevance of several biomarkers of hemostasis in the PAH progression. However, there is no agreement whether hemostatic indices are indeed distinguishing PAH patients from controls. Methods: Plasma fibrinogen, D-dimer, platelet count, and mean platelet volume, and platelet aggregation induced by ADP and collagen were serially measured in 34 patients with PAH, and 34 matched by age and sex normal volunteers. Results: Hemostatic indices were significantly higher for fibrinogen (p = 0.0001), D-dimer (p = 0.001), mean platelet volume (p = 0.001), and platelet aggregation induced by ADP-, and collagen (p = 0.0001 for both) in PAH pstients when compared to healthy controls. In contrast, platelet counts were almost identical between both groups. Conclusions: Patients with PAH exhibit activation of hemostatic indices compared to healthy controls. These data support previous observations that hemostatic abnormalities including platelet activation may directly impact pathogenesis of PAH, and need to be confirmed in larger randomized studies with more comprehensive assessment of hemostatic indices for justification of antithrombotic strategies.
- Pulmonary Arterial Hypertension
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