TY - JOUR
T1 - Role of left ventricular dysfunction in neurohumoral activation in the recovery phase of anterior wall acute myocardial infarction
AU - Vaughan, Douglas E.
AU - Lamas, Gervasio A.
AU - Pfeffer, Marc A.
N1 - Funding Information:
From the Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts. This study was supported in part by a grant from E.R. Squibb & Sons and by Clinical Research Center Grant RR-02635 from the National Institutes of Health, Betheada, Maryland. During the period of the study, Dr. Pfeffer was the recipient of an Established Investigator Award from the American Heart Association, Dallas, Texas. Dr. Lamas was recipient of training grant HL-07049 from the National Institutes of Health. Dr. Vaughan is the recipient of a Clinical Scientist Award from the American Heart Association. Manuscript received December 27, 1989; revised manuscript received and accepted April 27,199O. Address for reprints: Douglas E. Vaughan, MD, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115.
PY - 1990/9/1
Y1 - 1990/9/1
N2 - 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 ≤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, angtotensin 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.
AB - 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 ≤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, angtotensin 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.
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U2 - 10.1016/0002-9149(90)90476-H
DO - 10.1016/0002-9149(90)90476-H
M3 - Article
C2 - 1975472
AN - SCOPUS:0024997401
SN - 0002-9149
VL - 66
SP - 529
EP - 532
JO - The American journal of cardiology
JF - The American journal of cardiology
IS - 5
ER -