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Neuroendocrine activation in acute myocardial infarction (AMI) may have important physiological consequences for myocardial perfusion and function. We measured plasma angiotensin II in 60 patients with AMI within 6 hours of pain and on days 1–3 and day 10. On admission, All was normal at 9.9 + 1.3 pmol/1 (normal range 2–12 pmol/1). At day 3. All rose markedly to 77.5 ± 25.0 in those with heart failure (group 1. n = 13); but All also rose in uncomplicated patients (group 2. n = 47) to 27.X + 4.0 (p< (0001). At day 10, levels of All remained high, especially in group 1 (50.5 + 22.2 vs. 6.1 + 1.5. p<0..005). Thus neuroendocrine activation, present early in AMI, is seen in both uncomplicated infarcts and in those developing heart failure. Angiotensin II mediated vasoconstriction perhaps enhanced by catecholamines could have deleterious effects on myocardial function and perfusion, and indicates the potential for angio-tensin-converting enzyme inhibitors in early AMI.