There is a strong relationship between cigarette smoking and 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 endothelium, platelets, and fibronogen. Moreover, coronary circulation is the target organ of the damage due to smoking esposure. 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 non-smokers. Therefore, the knowledge of the characteristic alterations of the coronary circulation typically due to smoking and its comparison with those observed in similar people who are not smoking is basic to better understand the problems related to the subject.