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Published on: October 1, 2019
C-type natriuretic peptide plasma levels increase in patients with chronic heart failure as a function of clinical
Silvia Del Ry1, Claudio Passino, Maristella Maltinti
1Institute of Clinical Physiology, National Research Council, Pisa, Italy.
Insights
Plasma levels of C-type natriuretic peptide (CNP) increase with chronic heart failure (CHF) severity. Elevated CNP suggests a role in endothelial dysfunction in CHF patients.
Area of Science:
- Cardiology
- Endocrinology
- Vascular Biology
Background:
- C-type natriuretic peptide (CNP) is structurally related to other natriuretic peptides but its role in chronic heart failure (CHF) remains controversial.
- CNP is secreted by the endothelium and heart, suggesting potential involvement in cardiovascular regulation.
Purpose of the Study:
- To investigate the role of CNP in CHF by measuring plasma CNP levels.
- To assess the relationship between plasma CNP levels and the clinical severity and functional status of CHF patients.
Main Methods:
- Prospective study of 133 CHF patients and 21 age-matched healthy controls.
- Plasma CNP levels were measured using radioimmunoassay after solid-phase extraction.
- Clinical severity was assessed using NYHA functional classification, and left ventricular ejection fraction (EF) was determined.
Main Results:
- Plasma CNP levels were significantly elevated in CHF patients compared to healthy controls.
- CNP levels increased progressively with worsening NYHA class (I to IV), indicating a correlation with clinical severity.
- A significant positive correlation was observed between plasma CNP levels and left ventricular ejection fraction (EF).
Conclusions:
- Elevated plasma CNP is associated with increased clinical and functional severity in CHF.
- These findings suggest a pathophysiological role for CNP in CHF, potentially influencing endothelial vasomotor function due to its vasorelaxing properties.
Background:
[corrected] C-type natriuretic peptide (CNP), secreted by the endothelium and the heart, is structurally related to atrial and brain natriuretic peptides, but its clinical significance in chronic heart failure (CHF) is controversial.
Aim:
To investigate the role of CNP in CHF, plasma CNP levels were determined in a prospective series of 133 patients with CHF (age 64 +/- 1 years, left ventricular ejection fraction (EF), 31.5 +/- 0.7%, mean +/-S.E.M.) and in 21 age-matched healthy subjects.
Methods And Results:
CNP was measured by a radioimmunoassay (sensitivity: 0.41+/-0.009 pg/tube) after a preliminary solid-phase extraction. Plasma level of CNP in healthy subjects was 2.7 +/- 0.2 pg/ml and significantly increased in CHF, as a function of clinical severity: 4.9 +/- 0.7 pg/ml in NYHA class I; 7.0 +/- 0.4 pg/ml in class II (p < 0.001 vs. controls); 9.6 +/- 0.7 pg/ml in class III (p < 0.001 vs. controls and class I and II), and 11.8 +/- 2.0 pg/ml in class IV (p < 0.001 vs. controls, class I and II; Fisher's test after ANOVA). A significant relation was also found between CNP plasma levels and EF (R = 0.40, p < 0.001).
Conclusion:
Plasma CNP elevation is related to clinical and functional disease severity. These findings suggest a pathophysiological role for this peptide that, for its vasorelaxing activity, could influence the endothelial vasomotor response in CHF.
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