How should we implement current evidence on ACE-inhibition in the treatment of patients surviving a myocardial infarction?

initially described as an endocrine system regulating salt and water balance by its actions on the kidneys. We know now that it is an important endocrine as well as an autocrine / paracrine system influencing most, if not all organs in our body, especially the heart and vasculature. Clinical trials with ACE-inhibitors have documented that treatment does not only reduce blood pressure, but also reduces mortality and morbidity in patients with heart failure (1, 2), as well as in patients surviving acute myocardial infraction (AMI) (3–6). Moreover, several trials have indicated a reduction in coronary artery disease and ischemic events with ACE-inhibitors (7, 8). The HOPE trial was also able to demonstrate a reduction in morbidity and mortality with ACE-inhibition in high risk patients without left ventricular (LV) dysfunction (9). If all this evidence is interpreted at face-value, then ACE-inhibitors should be compulsory treatment in all patients who have had a myocardial infarction. Patients with preserved LV function after AMI may not have long-term activation of the RAAS. It is only during chronic activation that the RAAS has a deleterious effect in cardiovascular disease. It may be difficult to justify the use of ACE-inhibitors in patients surviving an AMI, without any signs and symptoms of cardiovascular de-compensation. It is, therefore, important for clinicians to scrutinize available data conservatively and to identify and treat those patients who may benefit most from ACE inhibitors and refrain from treating patients who have minimal or no effect. There is no doubt that all patients with heart failure or asymptomatic LV dysfunction need ACE-inhibitors (1, 2). Patients intolerant to ACE-inhibitors may alternatively be treated with angiotensin receptor (AT2) blockers (10, 11). Strong evidence also exists supporting ACE inhibition in patients with heart failure or LV dysfunction following AMI (3, 4) but evidence for treating an unselected group of post AMI patients is weak (5, 6), and data on long-term treatment is absent. Cardio-specific troponins, which are highly sensitive and specific markers of myocardial necrosis, have improved the diagnosis of AMI. These markers have resulted in the detection of very small infarctions, not necessarily in need of secondary prevention with ACEinhibitors. Moreover, improved detection of acute coronary syndromes has lead to early catheterization in many cases and a high rate of revascularization with stent implantation. There are controversial reports regarding the use of ACE-inhibitors in patients with coronary stents (12, 13). ACE inhibition may even augment in-stent re-stenosis (14). Secondary prevention with ACE-inhibitors to all patients surviving an AMI may, therefore, be unnecessary or even harmful. A proper assessment of clinical status, prognosis and LV function is necessary in order to initiate appropriate treatment after AMI. In this issue of the Scandinavian Cardiovascular Journal, Reikvam et al. (15) have reported how clinicians in some Norwegian hospitals assess patients following AMI, and to what extent they initiate ACE inhibitors post AMI. In their study, LV ejection fraction was assessed in 53% of the patients prior to discharge, either by echocardiography or with radionuclide ventriculography. Older patients were less likely to have their ejection fraction determined. Only 40% were discharged with an ACE inhibitor, of which 16% were already on such treatment prior to admission. The odds ratio of ACE-inhibitor treatment being