Copeptin in acute coronary syndromes and heart failure management: State of the art and future directions

Schurtz, Guillaume; Lamblin, Nicolas; Bauters, Christophe; Goldstein, Patrick; Lemesle, Gilles

doi:10.1016/j.acvd.2015.04.002

Cited by 25 publications

(16 citation statements)

References 42 publications

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“…This can be explained by the fact that hyponatraemia in cancer patients may not only be caused by paraneoplastic AVP secretion, but by any other condition seen in noncancer patients: comorbidities, medication or symptoms as vomiting, nausea, dehydration or stress . Of note, irrespective of SIAD, copeptin is known to be elevated due to stress and acute conditions such a pneumonia, stroke or heart failure . The nonosmotic stress‐related copeptin stimulus in acute hospitalized hyponatraemic patients may, therefore, confound the osmotic or paraneoplastic impulse …”

Section: The Role Of Copeptin In the Diagnosis Of Siadmentioning

confidence: 99%

Copeptin and its role in the diagnosis of diabetes insipidus and the syndrome of inappropriate antidiuresis

Refardt

Winzeler

2019

Clinical Endocrinology

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Clinical Endocrinology. 2019;91:22-32. wileyonlinelibrary.com/journal/cen 1 | INTRODUC TI ON Arginine vasopressin (AVP) is the main regulating hormone of body fluid homeostasis. It is secreted from the posterior pituitary upon osmotic or nonosmotic stimuli, with the main osmotic stimulus being increased plasma osmolality and the main nonosmotic stimulus being hypovolaemia and promotes water reabsorption via V2 receptors in the kidney, thereby normalizing hypertonicity and vasomotor tone. Disorders of body fluid homeostasis are common and can be divided into hyper-and hypoosmolar circumstances: the classical AbstractCopeptin is secreted in an equimolar amount to arginine vasopressin (AVP) but can easily be measured in plasma or serum with a sandwich immunoassay. The main stimuli for copeptin are similar to AVP, that is an increase in osmolality and a decrease in arterial blood volume and pressure. A high correlation between copeptin and AVP has been shown. Accordingly, copeptin mirrors the amount of AVP in the circulation.Copeptin has, therefore, been evaluated as diagnostic biomarker in vasopressin-dependent disorders of body fluid homeostasis. Disorders of body fluid homeostasis are common and can be divided into hyper-and hypoosmolar circumstances: the classical hyperosmolar disorder is diabetes insipidus, while the most common hypoosmolar disorder is the syndrome of inappropriate antidiuresis (SIAD). Copeptin measurement has led to a "revival" of the direct test in the differential diagnosis of diabetes insipidus. Baseline copeptin levels, without prior thirsting, unequivocally identify patients with nephrogenic diabetes insipidus. In contrast, for the difficult differentiation between central diabetes insipidus and primary polydipsia, a stimulated copeptin level of 4.9 pmol/L upon hypertonic saline infusion differentiates these two entities with a high diagnostic accuracy and is clearly superior to the classical water deprivation test. On the contrary, in the SIAD, copeptin measurement is of only little diagnostic value. Copeptin levels widely overlap in patients with hyponatraemia and emphasize the heterogeneity of the disease. Additionally, a variety of factors lead to unspecific copeptin elevations in the acute setting further complicating its interpretation. The broad use of copeptin as diagnostic marker in hyponatraemia and specifically to detect cancer-related disease in SIADH patients can, therefore, not be recommended. K E Y W O R D Scopeptin, diabetes insipidus, diagnosis, hypernatremia, hyponatraemia, primary polydipsia, SIAD This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Section: The Role Of Copeptin In the Diagnosis Of Siadmentioning

confidence: 99%

Copeptin and its role in the diagnosis of diabetes insipidus and the syndrome of inappropriate antidiuresis

Refardt

Winzeler

2019

Clinical Endocrinology

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“…Vasopressin (AVP) is secreted into the circulation from the hypothalamic gland as a response to changes in plasma osmolarity, blood volume and reduced cardiac output [1][2][3] . Increased secretion of AVP is also seen as a response to trauma and oxidative stress 4,5 .…”

Section: Introductionmentioning

confidence: 99%

Copeptin Release in Cardiac Surgery–A New Biomarker to Identify Risk Patients?

Holm

Szabó

Alehagen

et al. 2018

Journal of Cardiothoracic and Vascular Anesthesia

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“…Vasopressin has three receptors V 1a , V 1b, and V 2 . Via V 1a receptors, vasopressin causes vasoconstriction and cardiac remodeling by increasing afterload, decreasing systemic vascular resistance, and increasing cardiac output (1) . 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) .…”

Section: Introductionmentioning

confidence: 99%

“…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%

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 in acute coronary syndromes and heart failure management: State of the art and future directions

Cited by 25 publications

References 42 publications

Copeptin and its role in the diagnosis of diabetes insipidus and the syndrome of inappropriate antidiuresis

Copeptin and its role in the diagnosis of diabetes insipidus and the syndrome of inappropriate antidiuresis

Copeptin Release in Cardiac Surgery–A New Biomarker to Identify Risk Patients?

Copeptin in Severe Mitral Regurgitation Caused by Degenerative Mitral Disease

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