The potential long-term impact of danazol on coronary risk hinges on its effect on lipoprotein metabolism rather than its influence on total plasma lipids. Danazol may exert a regulatory influence on three key processes in lipoprotein metabolism: hepatic lipase activity; low-density lipoprotein receptor function; and lecithin:cholesterol acyl-transferase activity. Danazol decreases plasma fibrinogen and lipoprotein (a) levels, promotes fibrinolysis and causes a rise in plasminogen. Such changes are beneficial as they inhibit the process of thrombosis. Androgenic properties of danazol produce effects of plasma lipids and lipoproteins which oppose estrogen-induced changes. The usual recipients of danazol therapy are premenopausal females, in whom the absolute risk of ischemic heart disease is low. If the drug were shown to increase ischemic heart disease risk, detrimental factors must be weighted against its considerable and proven clinical benefits.