Neuroendocrine changes in acute myocardial infarction.

Acute myocardial infarction is associated with complex neuroendocrine changes, including release of arginine vasopressin, norepinephrine, and epinephrine, and activation of the renin-angiotensin system. Arginine vasopressin levels are maximal on admission, and subsequently fall even in patients in whom left ventricular failure develops. Plasma levels of norepinephrine and epinephrine are at their highest on admission and return to the normal range in patients with uncomplicated infarction, but they remain significantly elevated in patients in whom left ventricular failure or late ventricular arrhythmias develop. In contrast to catecholamines and arginine vasopressin, plasma renin and angiotensin levels are within normal limits on admission in patients without complications but increase by the third day. Patients with left ventricular failure already have increased plasma levels of renin and angiotensin on admission, but further marked and persistent increases occur over the following days. All of the aforementioned hormones may interact to cause systemic or coronary vasoconstriction, which may have short-term adverse hemodynamic consequences. Furthermore, increased afterload may result in infarct expansion and left ventricular dilatation, which will impair left ventricular function still further. Interruption of the cycle of vasoconstriction and worsening left ventricular failure by angiotensin converting enzyme inhibitors may reduce the incidence of heart failure after myocardial infarction.