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Published on: April 30, 2020
Possible Enzymatic Downregulation of the Natriuretic Peptide System in Patients with Reduced Systolic Function and
Syed S Zaidi1, Ryan D Ward1, Kodangudi Ramanathan1,2
1Department of Medicine, University of Tennessee Health Science Center, College of Medicine, 956 Court Ave, Memphis, TN 38163, USA.
Insights
Natriuretic peptide system enzymes corin and neprilysin are altered in systolic dysfunction. Corin levels decrease, while neprilysin, ANP, BNP, and cGMP increase, suggesting impaired natriuretic peptide activity in heart failure.
Area of Science:
- Cardiology
- Biochemistry
- Molecular Biology
Background:
- The natriuretic peptide system is crucial in heart failure (HF) progression.
- Expression of corin (activating enzyme) and neprilysin (degrading enzyme) in HF is not well understood.
Purpose of the Study:
- To compare plasma levels of corin, neprilysin, ANP, BNP, and cGMP.
- To investigate enzyme expression in patients with reduced systolic function and decompensated heart failure (dHF).
Main Methods:
- Pilot study with 48 participants.
- Compared plasma levels in controls (normal ejection fraction) versus patients with systolic dysfunction (with and without dHF).
- Measurements included corin, neprilysin, ANP, BNP, and cGMP.
Main Results:
- Corin levels were significantly lower in systolic dysfunction patients compared to controls.
- Neprilysin, cGMP, and ANP levels were higher in systolic dysfunction patients and highest in dHF patients.
- Corin levels were not affected by decompensated HF status.
Conclusions:
- Reduced systolic function is associated with decreased corin and increased neprilysin, ANP, BNP, and cGMP.
- This pattern suggests enzymatic downregulation of natriuretic peptide activity in reduced ejection fraction.
- Findings may have diagnostic and prognostic implications for heart failure management.
Background:
In patients with reduced systolic function, the natriuretic peptide system affects heart failure (HF) progression, but the expression of key activating (corin) and degrading enzymes (neprilysin) is not well understood.
Methods And Results:
This pilot study (n=48) compared plasma levels of corin, neprilysin, ANP, BNP, and cGMP in control patients with normal ejection fractions (mean EF 63 ± 3%) versus patients with systolic dysfunction, with (EF 24 ± 8%) and without (EF 27 ± 7%) decompensated HF (dHF), as defined by Framingham and BNP criteria. Mean ages, use of beta blockers, and ACE-inhibitors-angiotensin receptor blockers were similar between the groups. Corin levels were depressed in systolic dysfunction patients (797 ± 346 pg/ml) versus controls (1188 ± 549, p<0.02), but levels were not affected by dHF (p=0.77). In contrast, levels of neprilysin (p<0.01), cGMP (p<0.001), and ANP (p<0.001) were higher in systolic dysfunction patients than controls and were the highest in patients with dHF.
Conclusions:
Levels of neprilysin, ANP, BNP, and cGMP increased in patients with reduced systolic function and were the highest in dHF patients. Conversely, corin levels were low in patients with reduced EF with or without dHF. This pattern suggests possible enzymatic downregulation of natriuretic peptide activity in patients with reduced EF, which may have diagnostic and prognostic implications.
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