Copeptin, a fragment of the vasopressin precursor, as a novel predictor of outcome in heart failure

Stoiser, Brigitte; Mörtl, Deddo; Hülsmann, Martin; Berger, Rudolf; Struck, Joachim; Morgenthaler, N. G.; Bergmann, Andreas; Pacher, Richard

doi:10.1111/j.1365-2362.2006.01724.x

Cited by 196 publications

(146 citation statements)

References 29 publications

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“…It is well known that certain diseases such as heart failure, acute myocardial infarction, hemorrhage and sepsis result in marked elevation of copeptin [31][32][33][34], but, in the general population, the most likely cause of having elevated copeptin is a low water intake. Given the multiple reports on an independent relationship between high copeptin and risk of cardiometabolic diseases, the potential of using increased hydration as a preventive tool for these diseases has acquired increasing interest.…”

Section: Discussionmentioning

confidence: 99%

Effects of hydration on plasma copeptin, glycemia and gluco-regulatory hormones: a water intervention in humans

et al. 2017

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Purpose High plasma copeptin, a marker of vasopressin, predicts diabetes mellitus. We tested if copeptin could be suppressed by increased water intake in healthy individuals, and if a water-induced change in copeptin was accompanied by altered concentrations of glucose, insulin or glucagon. Methods Thirty-nine healthy individuals underwent, in random order, 1 week of high water intake (3 L/day on top of habitual intake) and 1 week of normal (habitual) fluid intake (control). Fasting plasma concentrations of copeptin, glucose, insulin and glucagon were compared between the ends of both periods. Furthermore, acute copeptin kinetics were mapped for 4 h after ingestion of 1 L of water. Results After acute intake of 1 L water, copeptin was significantly reduced within 30 min, and reached maximum reduction within 90 min with on average 39% reduction (95% confidence interval (95 CI) 34-45) (p < 0.001) and remained low the entire test period (4 h). One week of increased water intake led to a 15% reduction (95 CI 5-25) (p = 0.003) of copeptin compared to control week. The greatest reduction occurred among subjects with habitually high copeptin and concentrated urine ("water-responders"). Water-responders had significant water-induced reduction of glucagon, but glucose and insulin were unaffected. Conclusions Both acute and 1 week extra water intake potently reduced copeptin concentration. In those with the greatest decline (water-responders), who are typically low drinkers with high baseline copeptin, water induced a reduction in fasting glucagon. Long-term trials assessing the effect of water on glucometabolic traits should focus on low-water drinkers with high copeptin concentration.

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Section: Discussionmentioning

confidence: 99%

Effects of hydration on plasma copeptin, glycemia and gluco-regulatory hormones: a water intervention in humans

et al. 2017

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“…Copeptin is also associated with ventricular remodeling because of changes in LV ejection fraction (LVEF) and volumes (6) . It was found to be the strongest predictor of mortality especially in patients NYHA classes II and III (1,2,4,7) . Although vasopressin has beneficial effects in short term in CHF, it may have deleterious effects in the long term owing to vasoconstriction, decrease in cardiac output and contractility (8) .…”

Section: Introductionmentioning

confidence: 99%

“…V 2 receptor is responsible for the antidiuretic effect of vasopressin, which leads to increased preload and consequently, increased left ventricular (LV) filling (2,3) . Vasopressin also promotes myocardial fibrosis by stimulating cardiac fibroblasts (2)(3)(4) . Vasopressin concentration cannot be determined readily because of it is unstable and rapidly cleared feature (4) .…”

Section: Introductionmentioning

confidence: 99%

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Copeptin in Severe Mitral Regurgitation Caused by Degenerative Mitral Disease

Kılıçgedik¹,

Gürbüz²,

Efe³

et al. 2017

Kosuyolu Heart Journal

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Introduction: Copeptin is known to be increased in cardiac heart failure. The role of copeptin in patients with severe mitral regurgitation has not been assessed in patients with preserved ejection fraction. The objective of this study is to evaluate the role of severe mitral regurgitation caused by degenerative mitral disease in copeptin release. Patients and Methods:39 patients with degenerative mitral regurgitation (DMR group) and 30 control subjects (control group) were included in the study. The clinical and echocardiographic findings were recorded. Blood samples were obtained in 15 min before echocardiographic examination for determination of plasma copeptin. Global left ventricular longitudinal and circumferential strains were evaluated by applying 2D speckle-tracking imaging.Results: There was no statistical difference among copeptin levels of all groups (median values are for DMR:10.7 (9.0-17.1); control group:13.2 (10.6-20.7; p= 0.42). GCSTR and GLSTR were significantly lower in the DMR group (-19.2 ± 5.5 vs. -23.8 ± 5.3; p= 0.002 and -17.1 ± 4.3 vs. -19.9 ± 2.4 p= 0.002 respectively). LAV (83.7 ± 38.8 vs. 34.1 ± 7.5 p= 0.0001), E/e' (9.6 ± 4.0 vs. 6.0 ± 1.4; p= 0.0001), and E/A (1.79 ± 0.5 vs. 0.9 ± 0.24 p= 0.0001) ratios were significantly higher in the DMR group. Conclusion:Our study demonstrated that there is no significant change in serum copeptin concentrations in severe mitral regurgitation due to degenerative mitral disease. This can be attached to the filling changes of left atrium, atrial stretch receptors, and increased stroke volume. Key Words: Copeptin; mitral regurgitation Dejeneratif Mitral Hastalığa Bağlı İleri Mitral Yetersizliğinde Kopeptin ÖZETGiriş: Kopeptinin kalp yetersizliğinde yükseldiği bilinmektedir. Korunmuş ejeksiyon fraksiyonlu ileri mitral yetersizliği olan hastalarda kopeptinin rolü bilinmemektedir. Bu çalışmanın amacı kopeptin salınımında dejeneratif mitral hastalığa bağlı ileri mitral yetersizlikliğinin rolünü değerlendirmektir. Hastalar ve Yöntem:Dejeneratif ileri mitral yetersizliği olan 39 hasta (DMR grubu) ve 30 kontrol deneği (kontrol grubu) çalışmaya alındı. Klinik ve ekokardiyografik bulgular kayıt altına alındı. Plasma kopeptin düzeyini belirlemek için ekokardiyografik incelemeden 15 dakika önce kan örnekleri alındı. Global sol ventriküler longitudinal ve sirkumferensiyal değerlendirme 2D specle tracking görüntüleme ile yapıldı. Bulgular: Gruplar arasında kopeptin düzeyleri açısından anlamlı fark yoktu (median değerleri DMR: 10.7 (9.0-17.1); kontrol grup:13.2 (10.6-20.7) (p= 0.42)). GCSTR ve GLSTR değerleri DMR grubunda control grubuna göre daha düşüktü ( -19.2 ± 5.5 vs. -23.8 ± 5.3; p= 0.002 ve -17.1 ± 4.3 vs. -19.9 ± 2.4 p= 0.002 sırasıyla). LAV (83.7 ± 38.8 vs. 34.1 ± 7.5 p= 0.0001), E/e' (9.6 ± 4.0 vs. 6.0 ± 1.4; p= 0.0001) ve E/A (1.79 ± 0.5 vs. 0.9 ± 0.24 p= 0.0001) oranları DMR grubunda anlamlı olarak yüksekti.Sonuç: Bizim çalışmamız; dejeneratif mitral hastalığa bağlı ileri mitral yetersizliğinde kontrol grubuna göre kopeptin düzeylerinde anlamlı...

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“…Copeptin is a glycosylated peptide with a 39 amino acid structure secreted in equimolar concentrations with arginine vasopressin (AVP) from the hypothalamus [55]. Studies have shown that due to limited availability, and rapid clearance from the circulation, measuring AVP in the plasma is difficult [56,57].…”

Section: Copeptinmentioning

confidence: 99%

Biomarkers for Diagnosis and Prognosis of Acute Heart Failure

Choudhary

Somma

Maisel

2013

Curr Emerg Hosp Med Rep

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High mortality, morbility and hospitalization as a result of acute heart failure (AHF) represents an increasing public health dilemma. A prompt and appropriate therapeutic approach in the management of AHF has been demonstrated to be of great importance in reducing patient mortality and in-hospital length of stay. As consequence, at the moment of patient presentation, it is of great importance to make a fast and accurate diagnosis and risk stratification. Although an global clinical evaluation is mandatory, in some cases the signs and instrumental findings are not sufficient for a complete patient's diagnosis and risk stratifications. Multiple studies demonstrated that biomarkers assessment plus clinical judgement provide additional diagnostic and prognostic value in AHF patients. Moreover, data from the literature demonstrated the utility of a multimarkers approach in patients with heart failure in order to ameliorate diagnostic and prognostic accuracy. This paper is dedicated to addressing the actual state of the art on the utility in the management of acute heart failure of the following biomarkers: natriuretic peptides, procalcitonin, MRproADM, copeptine, neutrophil gelatinase associated lipocalin and galectin 3.

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Copeptin, a fragment of the vasopressin precursor, as a novel predictor of outcome in heart failure

Cited by 196 publications

References 29 publications

Effects of hydration on plasma copeptin, glycemia and gluco-regulatory hormones: a water intervention in humans

Effects of hydration on plasma copeptin, glycemia and gluco-regulatory hormones: a water intervention in humans

Copeptin in Severe Mitral Regurgitation Caused by Degenerative Mitral Disease

Biomarkers for Diagnosis and Prognosis of Acute Heart Failure

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