Role of left ventricular dysfunction in selective neurohumoral activation in the recovery phase of anterior wall acute myocardial infarction.

Neurohumoral activation is readily apparent in patients with symptomatic congestive heart failure (CHF) and in the acute phase after acute myocardial infarction. In this study, the neurohumoral profiles of 36 asymptomatic patients in the early convalescent phase after acute myocardial infarction were examined. All patients in the study had a radionuclide ejection fraction less than or equal to 45% and underwent cardiac catheterization 11 to 30 days after infarction. Venous blood samples were obtained in the supine state for the measurement of norepinephrine, angiotensin II, plasma renin activity and aldosterone in all patients. Despite the reduced ejection fraction and extensive wall motion abnormalities, plasma norepinephrine was not elevated and did not correlate with any measured hemodynamic, angiographic or clinical variables. The renin-angiotensin II aldosterone system was activated, as expected, in the 9 study patients receiving loop diuretics. However, even in the 27 patients not taking diuretics, plasma angiotensin II and renin activity levels were increased in relation to Killip classification, the presence of a left ventricular (LV) aneurysm and LV ejection fraction. Activation of the renin-angiotensin-aldosterone system can be identified in hemodynamically compensated postinfarction patients not taking diuretics and appears to be related to the extent of LV dysfunction.