C-type Natriuretic Peptides in Coronary Disease
Pricket TCR et al. show in their publication “C-Type Natriuretic Peptides in Coronary Disease” that “in contrast to the close association of NT-proBNP with cardiac function, and predictive value for outcome after myocardial infarction, plasma NT-proCNP (T-terminal C-type Natriuretic Peptide) is highly correlated with renal function and is an independent predictor of mortality and cardiac readmission in individuals with unstable angina.”
C-type Natriuretic Peptides in Coronary Disease
C-Type Natriuretic Peptides in Coronary Disease
Prickett TCR et al., Clin Chem, 2017; 63(1):316-324
Biomedica recently launched a novel validated NT-proCNP ELISA assay to support clinical research:
- EXTENSIVELY VALIDATED for clinical samples
- RELIABLE – 7 human serum based standards and 2 controls for biologically reliable data
- Excellent stability in all matrices after sample collection
- EASY – conventional 96-well format
For detailed information please click corresponding links:
BI-20812 NT-proCNP ELISA IFU
BI-20812 NT-proCNP ELISA Validation Data
BI-20812 NT-proCNP ELISA MSDS
Related publications
Sangaralingham SJ, McKie PM, Ichiki T, Scott CG, Heublein DM, Chen HH, Bailey KR, Redfield MM, Rodeheffer RJ, Burnett JC Jr. Hypertension. 2015. 65(6):1187-94. PMID: 25895587.
Abstract
C-type natriuretic peptide (CNP) is an endothelium-derived peptide that is released as a protective mechanism in response cardiovascular injury or disease. However, no studies have investigated circulating CNP, identifying clinical factors that may influence CNP and its relationship to cardiovascular disease in the general population. We studied 1841 randomly selected subjects from Olmsted County, MN (mean age, 63±11 years; 48% men). Plasma CNP was measured by a well-established radioimmunoassay and echocardiography, clinical characterization, and detailed medical record review were performed. We report that CNP circulates at various concentrations (median, 13 pg/mL), was unaffected by sex, was weakly associated by age, and that highest quartile of CNP identified a high-risk phenotype. Subjects with CNP in the highest quartile were associated with increased risk of myocardial infarction (multivariable-adjusted hazard ratio, 1.51; 95% confidence interval, 1.09-2.09; P=0.01) but not heart failure, cerebrovascular accidents, or death during a follow-up of 12 years. Addition of the highest quartile of CNP to clinical variables led to a modest increase in the integrated discrimination improvement for risk of myocardial infarction. In a large community-based cohort, elevated circulating CNP identified a high-risk phenotype that included cardiovascular comorbidities and left ventricular dysfunction, and provided evidence that highest concentrations of CNP potentially has prognostic value in predicting future risk of myocardial infarction. Together, these data from the general population highlight the potential value of CNP and support the need for additional studies to evaluate whether mechanisms regulating CNP could improve outcomes.