There is a strong relationship between cigarette smoking and haemostatic parameters to increase the risk of cardiovascular events. Smoking influences negatively coagulation-fibrinolysis cascade at any level, although it acts primarily on those pathways that are most important for an effective clot formation: endothelium, platelets, and fibrinogen. Endothelial dysfunction is a main consequence of smoke compounds with significant changes in initiating physiologic coagulation process; platelet adhesiveness and aggregation increases as a result of smoking; finally, fibrinogen/fibrin framework strengthens clot thickness. Therefore, the whole coagulation cascade activates the thrombi formation pathway under smoking action. The risk of thrombotic cardiovascular events increases its frequency with more severe atherosclerotic alterations if compared to similar events in nonsmokers. Changes in haemostatic factors produced by smoking appear to be related to female sex, especially for those women who use oral contraceptives. Thrombosis of coronary and cerebral arteries are found with a major incidence in young women who are users. In conclusion, cigarette smoking modifies haemostatic parameters via thrombosis with consequently more rate of cardiovascular events.