Polycystic Ovarian Syndrome (PCOS) affects as many as 20% of reproductive-aged women. PCOS presents with reproductive and metabolic features, endothelial dysfunction and potential aberrant coagulation and fibrinolysis. Altered haemostasis risks also noted in current management strategies may significantly increase cardiovascular disease (CVD) risks in this patient group. We aimed to comprehensively assess haemostasis and fibrinolysis in PCOS versus controls; 107 lean, overweight and obese women with and 67 women without PCOS were assessed for prothrombin fragments 1 and 2 (PF1 and 2), plasminogen, tissue plasminogen activator (tPA), thrombin activatable fibrinolysis inhibitor (TAFI) and thrombin generation (TG). We had previously measured plasminogen activator inhibitor 1 (PAI-1) and asymmetric dimethylarginine (ADMA) as well as the hormonal and metabolic markers for these participants. Significantly higher levels of ADMA (0.70 vs 0.39 µmol/L, p<0.0001), increased PAI-1 (4.80 vs 3.66 U/mL, p<0.0001) and increased plasminogen (118.39 vs 108.46%, p<0.0001) were seen in PCOS versus controls even after adjustment for age and BMI (p<0.0001, p=0.005, p=0.024, respectively). A significantly lower difference was noted between PCOS and controls in PF1&2 (180.0 vs 236.0 pmol/L, p=0.028) and higher for tPA (11.35 vs 9.20 ng/mL, p=0.025), however when adjusted for age and BMI these differences became borderline for the former (p=0.05) and insignificant for the latter (p=0.545). No difference was noted between the two groups for TAFI and TG. Results from this study suggest that the aberrant haemostasis observed in women with PCOS is mainly due to a hypofibrinolytic state. With increased activity of inhibitor of fibrinolysis, PAI-1 and increased plasminogen, a hypofibrinolytic state occurs. These changes may be related to an abnormal endothelial function, to hormonal and metabolic abnormalities or to other mechanism of action in PCOS. A hypofibrinolytic state serves as a further CV risk factor and risk marker in PCOS, which may contribute to CVD development.