Is Copeptin Level Associated With 1-Year Mortality After Out-of-Hospital Cardiac Arrest? Insights From the Paris Registry*
Guillaume GériFlorence DumasCamille Chenevier‐GobeauxAdrien BougléFabrice DaviaudTristan Morichau-BeauchantXavier JouvenJean-Paul MiraFrédéric PèneJean‐Philippe EmpanaAlain Cariou
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The availability of circulating biomarkers that helps to identify early out-of-hospital cardiac arrest survivors who are at increased risk of long-term mortality remains challenging. Our aim was to prospectively study the association between copeptin and 1-year mortality in patients with out-of-hospital cardiac arrest admitted in a tertiary cardiac arrest center.Retrospective monocenter study.Tertiary cardiac arrest center in Paris, France.Copeptin was assessed at admission and day 3. Pre- and intrahospital factors associated with 1-year mortality were analyzed by multivariate Cox proportional analysis.None.Two hundred ninety-eight consecutive out-of-hospital cardiac arrest patients (70.3% male; median age, 60.2 yr [49.9-71.4]) were admitted in a tertiary cardiac arrest center in Paris (France). After multivariate analysis, higher admission copeptin was associated with 1-year mortality with a threshold effect (hazard ratio(5th vs 1st quintile) = 1.64; 95% CI, 1.05-2.58; p = 0.03). Day 3 copeptin was associated with 1-year mortality in a dose-dependent manner (hazard ratio(2nd vs 1st quintile) = 1.87; 95% CI, 1.00-3.49; p = 0.05; hazard ratio(3rd vs 1st quintile) = 1.92; 95% CI, 1.02-3.64; p = 0.04; hazard ratio(4th vs 1st quintile) = 2.12; 95% CI, 1.14-3.93; p = 0.02; and hazard ratio(5th vs 1st quintile) = 2.75; 95% CI, 1.47-5.15; p < 0.01; p for trend < 0.01). For both admission and day 3 copeptin, association with 1-year mortality existed for out-of-hospital cardiac arrest of cardiac origin only (p for interaction = 0.05 and < 0.01, respectively). When admission and day 3 copeptin were mutually adjusted, only day 3 copeptin remained associated with 1-year mortality in a dose-dependent manner (p for trend = 0.01).High levels of copeptin were associated with 1-year mortality independently from prehospital and intrahospital risk factors, especially in out-of-hospital cardiac arrest of cardiac origin. Day 3 copeptin was superior to admission copeptin: this could permit identification of out-of-hospital cardiac arrest survivors at increased risk of mortality and allow for close observation of such patients.Keywords:
Copeptin
Increased neurohormonal activation is a key feature of heart failure (HF). Copeptin is a surrogate marker for proarginine vasopressin and the prognostic value of copeptin has been reported for multiple disease states of both nonvascular and cardiovascular etiology. Elevated plasma copeptin in HF has been associated with adverse outcomes such as increased mortality, risk of hospitalization and correlates with the severity of HF. Copeptin may add prognostic information to already established predictors such as clinical variables and natriuretic peptides in HF. In addition, copeptin has been found to be a superior marker when compared with BNP and NT-proBNP in HF patients discharged after hospitalization caused by HF or myocardial infarction (MI). The optimal use of copeptin in HF remains unresolved and future appropriately sized and randomized trials must determine the role of copeptin in HF as a marker of adverse outcomes, risk stratification or as a target in biomarker-guided therapy with arginine vasopressin-antagonists in individualized patient treatment and everyday clinical practice.
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Copeptin is a novel neuroendocrine peptide recently introduced to the field of acute medicine biomarkers. It is 39 amino acids glycopeptide cosynthesized with arginine vasopressin (AVP) and released together i n stoichiometric pattern from the hypothalamus upon stimulation of AVP release. Due to difficulties of AVP assay, copeptin largely replaced it in clinical assay as surrogate biomarker because copeptin has easier and more valid measurement methods. In acutestress condition, copeptin rises and reflects stress level exactly like AVP which was largely known as mediator of non -specific stress conditions beside its prominent role in water homeostasis. Acute myocardial infarction (AMI) is an acute stress state in which plasma copeptin rises. Early identification of AMI is a problem due to the delayed appearance of the cardiospecific troponins which start to rise within 6 -9 hours from the onset of chest pain. In the recent years many studies concluded that, when copeptin is combined with cardiac troponins in diagnosis of patients presenting with acute chest pain in early hours, it accelerates early rule in of AMI and rule out of non -MI patients. This review article discusses the biochemical and physiological basics of copeptin beside its clinical diagnostic value in AMI according to results and conclusions of some studies carried out on copeptin in AMI diagnostic field.
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ABSTRACT Copeptin, a surrogate marker for vasopressin, is increased immediately following an acute myocardial infarction (AMI). In several studies, using a single multi-marker strategy, copeptin in combination with either conventional or high-sensitive troponin drawn at presentation of patients with AMI was able to rule out AMI with high negative predictive value (NPV). Copeptin is also reviewed as a prognostic marker for predicting mortality and morbidity in AMI and allows risk stratification of patients into low, moderate and high risk patients. This review looked at past researches conducted on copeptin as either a diagnostic marker for those presenting to emergency department with chest pain, or its prognostic value. Keywords: acute myocardial infarction, copeptin, troponin, diagnostic, prognostic
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Copeptin is stable and detectable,so it could be an alternative of arginine vasopressin.Copeptin combined with troponin T (TnT) contributes to the diagnosis of coronary syndrome.Copeptin is an independent predictor in adverse events of non-ST segment elevation acute myocardial infarction.Combined detection of copeptin and brain natriuretic peptide(BNP) can predict the prognosis of heart failure.
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Background Although most people with relapsing onset multiple sclerosis (R-MS) eventually transition to secondary progressive multiple sclerosis (SPMS), little is known about disability progression in SPMS. Methods All R-MS patients in the Cardiff MS registry were included. Cox proportional hazards regression was used to examine a) hazard of converting to SPMS and b) hazard of attaining EDSS 6.0 and 8.0 in SPMS. Results 1611 R-MS patients were included. Older age at MS onset (hazard ratio [HR] 1.02, 95%CI 1.01–1.03), male sex (HR 1.71, 95%CI 1.41–2.08), and residual disability after onset (HR 1.38, 95%CI 1.11–1.71) were asso- ciated with increased hazard of SPMS. Male sex (EDSS 6.0 HR 1.41 [1.04–1.90], EDSS 8.0 HR 1.75 [1.14–2.69]) and higher EDSS at SPMS onset (EDSS 6.0 HR 1.31 [1.17–1.46]; EDSS 8.0 HR 1.38 [1.19–1.61]) were associated with increased hazard of reaching disability milestones, while older age at SPMS was associated with a lower hazard of progression (EDSS 6.0 HR 0.94 [0.92–0.96]; EDSS 8.0: HR 0.92 [0.90–0.95]). Conclusions Different factors are associated with hazard of SPMS compared to hazard of disability progres- sion after SPMS onset. These data may be used to plan services, and provide a baseline for comparison for future interventional studies and has relevance for new treatments for SPMS RobertsonNP@cardiff.ac.uk
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Vasopressin and its receptors play a key role in maintaining homeostasis in physiological and pathophysiological conditions. As a result, the vasopressin system has become an important target for both diagnostic and therapeutic use in a number of diseases. Kopeptin, C-terminal part of vasopressin prohormone. Copeptin has come to be seen as an important marker for identifying high-risk patients and predicting outcomes for various diseases. This improves the clinical value of commonly used biomarkers and risk stratification tools. The area that could benefit most from the introduction of the copeptin measurement in practice is cardiovascular disease. Determination of the level of copeptin becomes a fast and reliable method of differential diagnosis, especially in acute coronary syndromes. A special role in the diagnosis of acute myocardial infarction (AMI) is given to the combination of copeptin and troponin. According to available sources, such a combination eliminates AMI with very high sensitivity and negative predictive value. Moreover, elevated levels of copeptin correlate with poorer prognosis, and a higher risk of side effects after AMI, especially in patients with heart failure.
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The hazard ratio and median survival time are the routine indicators in survival analysis. We briefly introduced the relationship between hazard ratio and median survival time and the role of proportional hazard assumption. We compared 110 pairs of hazard ratio and median survival time ratio in 58 articles and demonstrated the reasons for the difference by examples. The results showed that the hazard ratio estimated by the Cox regression model is unreasonable and not equivalent to median survival time ratio when the proportional hazard assumption is not met. Therefore, before performing the Cox regression model, the proportional hazard assumption should be tested first. If proportional hazard assumption is met, Cox regression model can be used; if proportional hazard assumption is not met, restricted mean survival times is suggested.风险比（hazard ratio，HR）和中位生存时间是生存分析时的常规分析和报告指标。本文简要介绍了HR和中位生存时间的关系以及比例风险假定在这两者之间的作用，分析了检索出的58篇文献中的110对风险比和中位生存时间比的差异，并通过实例阐明了产生这种差异的原因。结果表明，在不满足比例风险假定时，Cox回归模型计算得到的风险比是不合理的，且与中位生存时间之比不等价。因此，在使用Cox回归模型前，应先进行比例风险假定的检验，只有符合比例风险假定时才能使用该模型；当不符合比例风险假定时，建议使用限制性平均生存时间。.
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Copeptin, the C-terminal part of the prohormone of vasopressin (AVP), is released together with AVP in stoichiometric concentrations reflecting an individual's stress level. Copeptin has come to be regarded as an important marker for identifying high-risk patients and predicting outcomes in a variety of diseases. It improves the clinical value of commonly used biomarkers and the tools of risk stratification. Elevated AVP activation and higher copeptin concentrations have been previously described in acute systemic disorders. However, the field that could benefit the most from the introduction of copeptin measurements into practice is that of cardiovascular disease. Determination of copeptin level emerges as a fast and reliable method for differential diagnosis, especially in acute coronary syndromes. A particular role in the diagnosis of acute myocardial infarction (AMI) is attributed to the combination of copeptin and troponin. According to available sources, such a combination allows AMI to be ruled out with very high sensitivity and negative predictive value. Moreover, elevated copeptin levels correlate with a worse prognosis and a higher risk of adverse events after AMI, especially in patients who develop heart failure. Some authors suggest that copeptin might be valuable in defining the moment of the introduction of treatment and its monitoring in high-risk patients. The introduction of copeptin into clinical practice might also provide a benefit on a larger scale by suggesting changes in the allocation of financial resources within the health system. Although very promising, further larger trials are required in order to assess the clinical benefits of copeptin in everyday practice and patient care.
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Elevated levels of arginine vasopressin (AVP) have been reported to be involved in the pathogenesis of heart failure (HF). Recent evidence has shown the role of copeptin, the C-terminal fragment of pro-AVP, as a biomarker in patients with HF. However, the relevant information is still limited. Therefore, we evaluated 39 Japanese patients admitted for HF between 2013 and 2015 (23 males and 16 females with an average age of 79.2 years). They were treated according to the Japanese acute HF guideline. Plasma copeptin levels were measured on admission and about 1 week later. The median plasma copeptin levels on admission were 0.5 (0.1-50.6) pmol/L, higher than the normal values (0.24 ± 0.06 pmol/L). Despite the similar clinical severity on admission, the patients showed great variability in plasma copeptin levels. They were divided into three groups (13 patients/group) according to plasma copeptin levels on admission: highest (> 30.8 pmol/L), midrange, and lowest (< 0.2 pmol/L) groups. Initial treatment improved HF symptoms in 37 of 39 patients, with the two unresponsive patients in the lowest group. Notably, plasma copeptin responses to initial treatment were different, depending on admission copeptin levels. The initial treatment significantly decreased copeptin levels in the highest group, but increased copeptin levels in the lowest group. By contrast, patients in the midrange group showed no significant changes. Thus, the treatment appears to restore the plasma copeptin levels. In conclusion, HF is a complex syndrome with the differential integration of stimulatory and inhibitory inputs to the AVP/copeptin secretory system.
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