Background-C-type natriuretic peptide (CNP) is a vasodilator produced by the vascular endothelium. It shares structural and physiological properties with the cardiac hormones atrial natriuretic peptide and brain natriuretic peptide (BNP), but little is known about its pathophysiological role in chronic heart failure (CHF). We assessed the hypothesis that CNP is produced by the heart in patients with CHF. Methods and Results-Myocardial CNP production was determined (difference in plasma levels between the aortic root and coronary sinus [CS]) in 9 patients undergoing right and left heart catheterization as part of their CHF assessment (all male, age 59Ϯ9 years; New York Heart Association class 2.2Ϯ0.1; left ventricular ejection fraction 29Ϯ5%; creatinine 105Ϯ8 mol/L [all values meanϮSEM]). BNP, established as originating from myocardium, was assessed from the same samples as a positive control. Analyses were performed by a blinded operator using a standard competitive radioimmunoassay kit (Peninsula Laboratories, Bachem Ltd UK). A step-up (29%) in plasma CNP concentration was found from the aorta to the CS (3.55Ϯ1.53 versus 4.59Ϯ1.54 pg/mL, respectively; Pϭ0.035). The mean increase in CNP was 0.90Ϯ0.35 pg/mL (range 0.05 to 2.80 pg/mL). BNP levels increased by 57% from aorta to CS (86.0Ϯ20.5 versus 135.0Ϯ42.2 pg/mL; Pϭ0.01). CS CNP levels correlated with mean pulmonary capillary wedge pressure (rϭ0.82, Pϭ0.007). Conclusions-We have shown that CNP is produced by the heart in patients with CHF. Although further evaluation is required to define its full pathophysiological role in this condition, CNP may represent an important new local mediator in the heart. (Circulation. 2003;107:571-573.)

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Btype natriuretic peptide (BNP) and its pro-peptide N terminal fragment (NTproBNP) are raised in conditions associated with abnormal ventricular structure and function and are independent predictors of survival in diverse clinical settings. Patients without raised baseline plasma BNP demonstrate an early, transient increase in concentrations following percutaneous coronary intervention (PCI), 1 but longer term effects are unknown. Potential benefits of PCI on ventricular remodelling are likely to be greatest in patients with raised baseline plasma BNP concentrations, reflecting increased wall stress or ongoing ischaemia. We hypothesised that in patients with stable coronary disease and an elevated baseline NTproBNP, successful PCI would result in a significant reduction in the plasma concentration. METHODSThe study population was recruited from a larger prospective study of risk factors for coronary in-stent restenosis.2 To define an elevated baseline value, NTproBNP was measured in a group of 30 healthy volunteers of similar age and sex distribution (mean age 50 years, 83% male) to the patient group who had no history or clinical signs of cardiovascular disease, and underwent comprehensive non-invasive testing to exclude cardiac pathology. The 90th centile was selected as the cut-off value to define raised NTproBNP, corresponding to an NT proBNP concentration of .75 fmol/ml. Local ethics committee approval was obtained and all subjects gave written informed consent.Twenty eight patients with stable angina and raised baseline NTproBNP, undergoing elective, single native vessel stenting to de novo lesions, were included in the PCI group. Blood was drawn before intervention, and then 1, 6, and 24 hours after the procedure. A final sample was obtained at six months follow up. The control group consisted of 13 patients with stable angina and elevated baseline plasma NTproBNP who underwent coronary angiography without subsequent PCI. In these patients bloods were drawn at baseline, 1, 6, and 24 hours, and 7 days post-angiography. Data were also available on a further 19 patients undergoing elective stenting in whom baseline NTproBNP was not raised (that is ( 75 fmol/ml).NTproBNP was analysed by immunoluminometric assay. NTproBNP concentrations are presented as median and interquartile ranges, and were log transformed for analysis. RESULTSClinical characteristics were similar in the PCI and control groups (table 1). Ventricular function at baseline was assessed in 32 of the 41 patients and clinical heart failure was an exclusion criterion for the main study; 17/32 had normal function, 12/32 had moderate dysfunction, and 3/32 had severe dysfunction. NTproBNP concentrations did not vary according to category of left ventricular function.Baseline NTproBNP concentration was 257 (170-771) fmol/ml in the PCI group and 188 (106-550) fmol/l in the control group (p = 0.5). In the PCI group plasma NTproBNP concentrations decreased over time (analysis of variance (ANOVA) p , 0.0001). Concentrations at 1 hour (281 (192-721) fmol...

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