Related Experiment Video
Updated: Aug 24, 2026

Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System
Published on: June 11, 2020
Activation of neurohumoral systems following acute myocardial infarction
J L Rouleau1, L A Moyé, J de Champlain
1Cardiology Department, CHUS, Sherbrooke, Quebec, Canada.
Insights
Following a heart attack, persistent neurohumoral activation is common in patients with left ventricular dysfunction, even without overt heart failure. Measuring these neurohormone levels before hospital discharge may identify high-risk patients for targeted interventions.
Area of Science:
- Cardiology
- Neuroendocrinology
- Internal Medicine
Background:
- Patients with acute myocardial infarction (AMI) typically show neurohumoral system activation upon hospital admission.
- This activation usually normalizes within 72 hours, except in cases of left ventricular dysfunction with or without heart failure.
Purpose of the Study:
- To investigate persistent neurohumoral activation in patients post-myocardial infarction with left ventricular dysfunction but no overt heart failure at hospital discharge.
Main Methods:
- The Survival and Ventricular Enlargement (SAVE) study measured plasma neurohormone levels (plasma renin activity, norepinephrine, arginine vasopressin, atrial natriuretic peptide) in 522 patients 12 days post-infarction.
- All participants had left ventricular ejection fraction ≤40% but no overt heart failure.
Main Results:
- Patients without overt heart failure but with left ventricular dysfunction exhibited elevated levels of all measured neurohormones compared to controls.
- This indicates a subgroup with persistent neurohumoral activation at hospital discharge post-infarction.
Conclusions:
- Persistent neurohumoral activation involves multiple systems in a significant subgroup of post-MI patients with left ventricular dysfunction.
- Predischarge measurement of these neurohormonal levels could identify patients at higher risk for complications and potential beneficiaries of specific pharmacologic interventions.
Abstract:
Previous 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 less than or equal to 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 subgroup 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.
Related Concept Videos
Sympathetic Signaling
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...
Sympathetic Activation
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Regulation of Heart Rates
The SNS increases heart rate through the release of norepinephrine and epinephrine, which act on beta-1 adrenergic receptors in the heart. This action increases the rate of depolarization in the sinoatrial (SA) node, the heart's...
Myocarditis I: Introduction
Heart Failure II: Pathophysiology

