PLG and atherosclerosis: The basis of this theory was that (i) binding of plasminogen to fibrin or the cell surface is crucial for its activation to plasmin [44]; (ii) lipoprotein(a), a risk factor for cardiovascular diseases and atherosclerosis [45], competes with plasminogen for binding to fibrin and the cell surface [46]; and (iii) regulated fibrinolysis can occur without bleeding.