Experimental evidence suggests that ACE-inhibitors possess cardioprotective properties. Since ACE-inhibitors can prevent bradykinin breakdown and can stimulate prostaglandin production, it is thought that these cardioprotective effects are mediated by bradykinin and prostaglandins. This article summarizes the results indicating that bradykinin and prostaglandins, although not the only factors, do play an important role in cardioprotection by ACE-inhibitors. Special attention is paid to the presence of the sulphydryl moiety of certain ACE-inhibitors. Probably, these sulphydryl group-containing ACE-inhibitors have an additional protective effect through an interaction with bradykinin or through scavenging of free radicals. However, these cardioprotective effects have not yet been shown in patients with ischaemic heart disease, although some studies indicate that ACE-inhibitors are also able to cause anti-ischaemic effects in patients. Further studies are required to establish the clinical importance of cardioprotection by ACE-inhibitors in ischaemic heart disease.