Key result
No evidence of net myocardial secretion of proCCK was found in patients with failing (TC proCCK 0.05 pmol/l, p=0.365) or structurally normal hearts, questioning its role as a cardiac biomarker.
Why the study?
Although the CCK gene is expressed in the mammalian heart, it was unknown whether cardiac gene expression leads to proCCK secretion in humans.
Observational (n=115)
p-value: p=0.365
There is no evidence of net myocardial secretion of proCCK in humans with or without heart failure, questioning its utility as a cardiac biomarker.
No net myocardial proCCK secretion detected in HFrEF or nonfailing hearts; challenges its proposed role as cardiac biomarker and leaves plasma source open.
Cholecystokinin (CCK) is secreted from the intestines in response to food intake. We previously reported that the CCK gene is also expressed in the mammalian heart, and it has been hypothesized that proCCK could be a novel cardiac biomarker. However, it is not known whether cardiac gene expression leads to secretion in humans. To investigate myocardial secretion of proCCK in patients with heart failure with reduced ejection fraction (HFrEF) or arrythmias. A total of 115 patients undergoing invasive cardiac procedures were included: 55 with HFrEF (67 years [interquartile range (IQR) 60–76], 72.7 % male, LVEF 30 % [IQR 20–35]), and 60 without HFrEF (26 with Wolff-Parkinson-White syndrome (WPW) (30 years [IQR 26–39], 61.5 % male), and 34 with atrial fibrillation (AFIB) (66 years [IQR 60–71], 61.8 % male)). Blood was collected from the coronary sinus (CS) as well as the left atrium or femoral artery (A) to determine the transcardiac concentration gradient (TC proCCK ) (CS proCCK concentration - A proCCK concentration). Radioimmunoassays were used for measurements of plasma hormones. TC proCCK across failing hearts was 0.05 pmol/l (IQR: −1.49–2.67) ( p = 0.365 ). In non-failing hearts, TC proCCK was 0.35 pmol/l (IQR: −1.57–1.29) ( p = 0.778 ) for WPW and 0.68 pmol/l (IQR: −1.58–3.28) ( p = 0.133 ) for AFIB. Transcardiac gradients for N-terminal pro B-type natriuretic peptide (NT-proBNP) were observed in all groups. No evidence of net myocardial secretion of proCCK was found in either failing or structurally normal hearts, questioning its proposed role as a cardiac biomarker. • The CCK gene is expressed in the mammalian heart but whether this leads to active secretion in humans is not known. • By analyzing transcardiac gradient from falling and structurally hearts, the myocardial secretion was evaluated in humans. • Our results question the role of proCCK as a cardiac biomarker.
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Deis et al. (2025) conducted an observational in Heart failure with reduced ejection fraction (HFrEF) and arrhythmias (n=115). Heart failure with reduced ejection fraction (HFrEF) vs. Structurally normal hearts (WPW or AFIB) was evaluated on Transcardiac concentration gradient of proCCK (TC proCCK) (p=0.365). No evidence of net myocardial secretion of proCCK was found in patients with failing (TC proCCK 0.05 pmol/l, p=0.365) or structurally normal hearts, questioning its role as a cardiac biomarker.
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