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Neurohumoral changes in patients with left ventricular dysfunction following acute myocardial infarction and the
Erik Tingberg1, Anders Roijer, Ulf Thilen
1Department of Cardiology, University Hospital, Lund, Sweden. erik.tingberg@skane.se
Insights
Long-term nitrate therapy in heart failure patients did not significantly alter neurohormonal status, except for a decrease in atrial natriuretic peptide (ANP). Hormone levels showed distinct associations with systolic and diastolic dysfunction post-myocardial infarction.
Area of Science:
- Cardiology
- Pharmacology
- Neuroendocrinology
Background:
- Cardiovascular regulation involves neurohumoral mechanisms, especially in heart failure.
- Limited data exists on long-term nitrate therapy's impact on these mechanisms.
Purpose of the Study:
- To investigate the effect of chronic isosorbide-5-mononitrate (IS-5-MN) on neurohumoral markers in patients with left ventricular (LV) dysfunction post-acute myocardial infarction (AMI).
Main Methods:
- Double-blind, randomized trial comparing IS-5-MN (60 mg daily for 11 months) with placebo in 47 patients with LV dysfunction post-AMI.
- Patients also received ramipril.
- Measured plasma levels of natriuretic peptides (ANP, BNP), catecholamines (epinephrine, norepinephrine), ADH, aldosterone, renin activity, and other neuropeptides.
Main Results:
- Chronic nitrate therapy resulted in a significant decrease in ANP levels.
- No significant changes were observed in other neurohormonal markers.
- Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) correlated with diastolic dysfunction, while renin activity (PRA), norepinephrine (NEPI), and aldosterone (Aldo) correlated with systolic dysfunction.
Conclusions:
- Chronic nitrate therapy minimally impacts the neurohumoral profile in LV dysfunction post-AMI, primarily decreasing ANP.
- A temporal dissociation exists between hormones related to diastolic (ANP, BNP) and systolic (PRA, NEPI, Aldo) dysfunction one year post-infarction.
- Brain natriuretic peptide (BNP) alone may not fully capture heart failure pathophysiology; exploring other neurohormonal factors for monitoring therapy is recommended.
Background:
Several neurohumoral mechanisms involved in cardiovascular regulation are activated in the failing heart, but only limited information is available regarding the influence of long-term nitrate therapy.
Materials And Methods:
This was a double-blind, randomized comparison of isosorbide-5-mononitrate (IS-5-MN), 60 mg given orally, once daily for 11 months to patients (n = 47) with left ventricular (LV) dysfunction following acute myocardial infarction (AMI). Forty-five patients received placebo. All patients received ramipril.Plasma natriuretic peptides (atrial [ANP] and brain [BNP] natriuretic peptide), epinephrine, norepinephrine (NEPI), antidiuretic hormone, aldosterone (Aldo), renin activity (PRA), substance P, neuropeptide Y-like immunoreactivity, calcitonin gene-related peptide, and vasoactive intestinal peptide were measured at baseline and at the end of the treatment period. Clinical, echocardiographic, and hemodynamic data were also obtained.
Results And Conclusions:
Chronic nitrate therapy does not significantly affect the neurohumoral status in patients with LV dysfunction after AMI, apart from a decrease in ANP. Some hormones are more closely associated with diastolic dysfunction/increased volume load (ANP and BNP) and others are more closely associated with systolic dysfunction (PRA, NEPI, Aldo). There is a temporal dissociation of these 2 groups of hormones 1 year post infarction: ANP and BNP decrease, whereas NEPI and Aldo show a slight increase. BNP levels do not reflect all important pathophysiologic mechanisms in heart failure. Consequently, the use of other neurohormonal factors than BNP for monitoring of heart failure therapy should be explored.
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