Neuroendocrine activation in acute myocardial infarction.
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, AII was normal at 9.9 + 1.3 pmol/l (normal range 2-12 pmol/l). At day 3, AII rose markedly to 77.5 + 25.0 in those with heart failure (group 1, n = 13); but AII also rose in uncomplicated patients (group 2, n = 47) to 27.8 + 4.0 (p less than 0.001). At day 10, levels of AII remained high, especially in group 1 (50.5 + 22.2 vs 6.1 + 1.5, p less than 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 angiotensin-converting enzyme inhibitors in early AMI.
D000368:Aged; D000804:Angiotensin II / Q000096:biosynthesis / Q000097:blood; D006333:Heart Failure / Q000097:blood; D006439:Hemodynamics; D006801:Humans; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D009490:Neurosecretory Systems / Q000503:physiopathology*; D012084:Renin-Angiotensin System
D000804:Angiotensin II