“…Exogenous androgens in high dosages and/or prolonged administration have been shown to be atherogenic, by inducing ample changes in the lipid profile (increasing low-density lipoprotein-LDL cholesterol, triglycerides and apolipoprotein-B, and decreasing high-density lipoprotein-HDL cholesterol and apolipoprotein-A 1 ) [ 5 , 105 , 106 , 107 , 108 , 109 ], by increasing plasma homocysteine level [ 110 , 111 ], and by enhancing inflammation and oxidative stress at the endothelial level, with a consecutive reduction in NO synthesis [ 111 , 112 , 113 , 114 ]. AAS have also been shown to elevate blood pressure [ 111 , 112 , 115 ] and to induce hemorheological effects, through impairing vascular reactivity [ 105 , 111 ] and triggering a polycythemia-induced hyperviscosity syndrome (an intrinsic anabolic effect) [ 16 , 36 , 105 ]. Since the abovementioned altered parameters have been independently linked to various coagulation abnormalities (they lead to enhanced platelet adhesion and aggregation, activation of the coagulation cascade, and suppression of fibrinolysis [ 116 , 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 ]), it may be assumed that AAS abuse is prone to produce atherothrombotic phenomena also by influencing these cardiovascular risk markers.…”