Neuroendocrine activation after acute myocardial infarction.
Neuroendocrine response after acute myocardial infarction (MI) results in activation of the sympathetic nervous system, the renin-angiotensin system, and vasopressin and atrial natriuretic peptide release. The net effect of this response is vasoconstriction, cardiac stimulation and regional flow redistribution that may have a favorable effect in some situations and a deleterious effect in others. The possible adverse effects of vasoconstriction were studied in a Veterans Administration Cooperative Study that evaluated a 48-hour infusion of sodium nitroprusside in the setting of acute MI. In the presence of mild, probably primarily diastolic left ventricular dysfunction, nitroprusside appeared to have an adverse effect on long-term survival. However, in the presence of more severe, probably predominantly systolic dysfunction, nitroprusside had a favorable effect on the prognosis. Therefore, the decision of whether to accept or inhibit neuroendocrine activation in acute MI probably depends on the severity of the disease and the timing of the therapeutic intervals.
Cohn
J N
JN
Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.
D009320:Atrial Natriuretic Factor / Q000378:metabolism; D006801:Humans; D008297:Male; D015337:Multicenter Studies as Topic; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism*; D009490:Neurosecretory Systems / Q000378:metabolism*; D009599:Nitroprusside / Q000627:therapeutic use; D011897:Random Allocation; D012084:Renin-Angiotensin System / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects; D014667:Vasopressins / Q000378:metabolism
D014667:Vasopressins; D009599:Nitroprusside; D009320:Atrial Natriuretic Factor