Pulmonary arterial hypertension (PAH) is characterized by endothelial dysfunction and microthrombi formation. The role of anticoagulation remains controversial, with studies demonstrating inconsistent effects on PAH mortality. Clinical anticoagulation practices are currently heterogeneous, reflecting physician preference. This study uses thrombelastography (TEG) and hematology markers to evaluate whether clot formation and fibrinolysis are abnormal in PAH patients. Venous blood was collected from healthy volunteers (n=20) and patients with PAH (n=20) on stable medical therapy for TEG analysis. Individual TEG parameters and a calculated coagulation index were used for comparison. In addition, hematologic markers, including fibrinogen, factor VIII activity, von Willebrand factor (vWF) activity, vWF antigen, and alpha2-antiplasmin, were measured in PAH patients and compared to healthy volunteers. Between group differences were analyzed using t tests and linear mixed models, accounting for repeated measures when applicable. Although the degree of fibrinolysis (LY30) was significantly lower in PAH patients compared to healthy volunteers (0.3%±0.6 versus 1.3%±1.1, p=0.04), all values were within the normal reference range (0-8). All other TEG parameters were not significantly different between PAH patients and healthy volunteers (pâ¥0.15 for all). Similarly, alpha2-antiplasmin activity levels were higher in PAH patients compared to healthy volunteers (103.7%±13.6 versus 82.6%±9.5, p<0.0001), but all individual values were within the normal range (75-132%). There were no other significant differences in hematologic markers between PAH patients and healthy volunteers (pâ¥0.07 for all). Sub-group analysis comparing TEG results in patients treated with or without prostacyclin-pathway targeted therapies were also non-significant. In conclusion, treated PAH patients do not demonstrate abnormal clotting kinetics or fibrinolysis by TEG.â