TY - JOUR
T1 - Activation of neurohumoral systems following acute myocardial infarction
AU - Rouleau, Jean L.
AU - Moyé, Lemuel A.
AU - de Champlain, Jacques
AU - Klein, Marc
AU - Bichet, Daniel
AU - Packer, Milton
AU - Sussex, Bruce
AU - Arnold, J. Malcolm
AU - Sestier, François
AU - Parker, John O.
AU - McEwan, M. M Patricia
AU - Bernstein, Victoria
AU - Cuddy, Thomas E.
AU - Delage, François
AU - Nadeau, Claude
AU - Lamas, Gervasio A.
AU - Gottlieb, Stephen S.
AU - McCans, John
AU - Pfeffer, Marc A.
N1 - Funding Information:
From the University of Sherbrooke, Quebec; University of Texas Health Science Center at Houston, Houston, Texas; Hopital du Sacre-Coeur de Montreal Montreal, Quebec; Mount Sinai Medical Center, New York, New York; Institut de Cardiologie de Quebec, Quebec; Memorial University, St. John’s, Newfoundland; Victoria Hospital, London, Ontario; Hopital Notre-Dame de Montreal, Montreal, Quebec; Kingston General Hospital, Kingston, Ontario, Canada; The Wellesley Hospital, Toronto, Ontario; University of British Columbia, Vancouver, British Columbia; University of Manitoba, Winnipeg, Manitoba; Hotel-Dieu de Levis, Quebec; Hopital Enfant-Jesus, Quebec; Brigham and Women’s Hospital, Boston, Massachusetts; University of Maryland Hospital, Baltimore, Maryland; and Jewish General Hospital, Montreal, Quebec. This study was supported by the Medical Research Council of Canada and Bristol-Myers Squibb Canada.
PY - 1991/11/18
Y1 - 1991/11/18
N2 - studies have indicated that patients with an acute myocardial infarction have marked activation of all neurohumoral systems on admission to the hospital. This activation begins to subside within the first 72 hours so that by 7-10 days, all plasma neurohormones have returned to normal. The only documented exceptions were found to occur in patients with left ventricular dysfunction and overt heart failure, where both plasma renin activity and atrial natriuretic peptide were increased, and in patients with left ventricular dysfunction but no overt heart failure, where only atrial natriuretic peptide was increased. Although these studies suggest that neurohumoral activation rarely occurs at the time of hospital discharge, they were small and may have missed an important subgroup of patients with persistent neurohumoral activation. In the Survival and Ventricular Enlargement (SAVE) study, 522 patients had plasma neurohumoral levels measured at a mean of 12 days postinfarction. All SAVE patients had left ventricular dysfunction (left ventricular ejection fraction ≤40%), but no overt heart failure. In this group of patients, all neurohumoral levels (plasma renin activity, norepinephrine, arginine vasopressin, and atrial natriuretic peptide) were found to be increased compared with age-matched control subjects. These results indicate that, in fact, a sub-group of patients without overt heart failure has persistent neurohumoral activation at the time of hospital discharge postinfarction, and that this activation involves several neurohumoral systems. Since patients with persistent neurohumoral activation postinfarction are likely those most at risk of developing complications and the ones most likely to benefit from pharmacologic interventions blunting the effects of neurohumoral activation, measurement of predischarge neurohumoral levels may be useful.
AB - studies have indicated that patients with an acute myocardial infarction have marked activation of all neurohumoral systems on admission to the hospital. This activation begins to subside within the first 72 hours so that by 7-10 days, all plasma neurohormones have returned to normal. The only documented exceptions were found to occur in patients with left ventricular dysfunction and overt heart failure, where both plasma renin activity and atrial natriuretic peptide were increased, and in patients with left ventricular dysfunction but no overt heart failure, where only atrial natriuretic peptide was increased. Although these studies suggest that neurohumoral activation rarely occurs at the time of hospital discharge, they were small and may have missed an important subgroup of patients with persistent neurohumoral activation. In the Survival and Ventricular Enlargement (SAVE) study, 522 patients had plasma neurohumoral levels measured at a mean of 12 days postinfarction. All SAVE patients had left ventricular dysfunction (left ventricular ejection fraction ≤40%), but no overt heart failure. In this group of patients, all neurohumoral levels (plasma renin activity, norepinephrine, arginine vasopressin, and atrial natriuretic peptide) were found to be increased compared with age-matched control subjects. These results indicate that, in fact, a sub-group of patients without overt heart failure has persistent neurohumoral activation at the time of hospital discharge postinfarction, and that this activation involves several neurohumoral systems. Since patients with persistent neurohumoral activation postinfarction are likely those most at risk of developing complications and the ones most likely to benefit from pharmacologic interventions blunting the effects of neurohumoral activation, measurement of predischarge neurohumoral levels may be useful.
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U2 - 10.1016/0002-9149(91)90264-L
DO - 10.1016/0002-9149(91)90264-L
M3 - Article
C2 - 1684082
AN - SCOPUS:0026338444
SN - 0002-9149
VL - 68
SP - 80
EP - 86
JO - The American journal of cardiology
JF - The American journal of cardiology
IS - 14
ER -