Copeptin as a Diagnostic and Prognostic Biomarker in Cardiovascular Diseases

Mu, Danni; Cheng, Jin; Qiu, Ling; Cheng, Xinqi

doi:10.3389/fcvm.2022.901990

Cited by 20 publications

(14 citation statements)

References 241 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Copeptin is a C-terminal fragment of the precursor pre-pro-vasopressin and a surrogate marker of vasopressin [17]. In contrast to vasopressin, copeptin is very stable in plasma at room temperature and easy and robust to measure.…”

Section: Medicine and Dentistrymentioning

confidence: 99%

ST2 and copeptine – modern biomarkers for monitoring the effectiveness of treatment of decompensated heart failure in patients after acute myocardial infarction

2022

View full text Add to dashboard Cite

The aim of the study was to increase the efficiency of diagnostic methods to find means to improve the treatment of patients with decompensated heart failure in the post-infarction period. Materials and methods. This study is based on an examination of 120 patients with decompensated HF (60 patients with STEMI and 60 with non-STEMI). Patients with previous STEMI complicated by decompensated heart failure were divided into groups, depending on their treatment. The studied groups were homogeneous in terms of age, sex, the severity of the course of the disease, duration of the post-infarction period, and the presence of clinical manifestations of decompensation. The patients were observed on the first day after hospitalization, after 1 and 2 months after treatment. Copeptin serum levels were assayed using the EK 065-32, EIA Copeptine kit (RayBiotech, Inc., USA). ST-2 in blood serum was determined with the help of the Presage ST-2 kit (Critical Diagnostics, USA). The level of ST2 was determined in ng/ml. Results. We analysed the effect of therapy on the level of ST2 in the blood serum of examined patients with STEMI and non-STEMI complicated by decompensated heart failure. All the treatment regimens we proposed led to a significant decrease in the level of this peptide in blood serum after the end of the treatment. In patients of group I who received basic therapy drugs, the average ST2 concentration was (49.47±1.77) ng/ml before treatment. After 1 and 2 months of therapy, it was (44.92±1.22) ng/ml and (41.67±1.18) ng/ml, respectively (p˂0.05). The patients with decompensated heart failure after non-STEMI from group I had a copeptin level of (18.13±0.10) pg/ml before treatment and probably decreased to levels of (16.29±0.15) pg/ml and (15.09±0.14) pg/ml after 1 and 2 months under the influence standard therapy. Conclusions. We found the dependence of copeptin and ST2 levels on decompensated HF in the early and late post-infarction periods. It was established that the use of the therapy with a combination of the studied drugs led to a more intense decrease in serum copeptin, compared to therapy with succinic acid, arginine drugs, and standard therapy (p˂0.05). Using a differentiated treatment algorithm for patients with decompensated heart failure in the post-infarction period, copeptin and ST2 in blood serum increases the effectiveness of treatment and prevents complications.

show abstract

Section: Medicine and Dentistrymentioning

confidence: 99%

ST2 and copeptine – modern biomarkers for monitoring the effectiveness of treatment of decompensated heart failure in patients after acute myocardial infarction

2022

View full text Add to dashboard Cite

show abstract

“…Copeptin level at the hospital admission for AMI has a good predictive value for progression to chronic heart failure and one-year mortality [ 9 , 10 ]. Copeptin is a diagnostic and prognostic biomarker of cardiovascular diseases, including the rapid detection of acute myocardial infarction (AMI) and stroke, and the prediction of mortality in heart failure (HF) [ 11 ]. Elevated copeptin levels traducing vasopressin level increase are reported in the setting of AMI and shock [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Involvement of Vasopressin in Tissue Hypoperfusion during Cardiogenic Shock Complicating Acute Myocardial Infarction in Rats

Gaudard

David

Bideaux

et al. 2023

IJMS

View full text Add to dashboard Cite

Acute heart failure (AHF) due to acute myocardial infarction (AMI) is likely to involve cardiogenic shock (CS), with neuro-hormonal activation. A relationship between AHF, CS and vasopressin response is suspected. This study aimed to investigate the implication of vasopressin on hemodynamic parameters and tissue perfusion at the early phase of CS complicating AMI. Experiments were performed on male Wistar rats submitted or not to left coronary artery ligation (AMI and Sham). Six groups were studied Sham and AMI treated or not with either a vasopressin antagonist SR-49059 (Sham-SR, AMI-SR) or agonist terlipressin (Sham-TLP, AMI-TLP). Animals were sacrificed one day after surgery (D1) and after hemodynamic parameters determination. Vascular responses to vasopressin were evaluated, ex vivo, on aorta. AHF was defined by a left ventricular ejection fraction below 40%. CS was defined by AHF plus tissue hypoperfusion evidenced by elevated serum lactate level or low mesenteric oxygen saturation (SmO2) at D1. Mortality rates were 40% in AMI, 0% in AMI-SR and 33% in AMI-TLP. Immediately after surgery, a sharp decrease in SmO2 was observed in all groups. At D1, SmO2 recovered in Sham and in SR-treated animals while it remained low in AMI and further decreased in TLP-treated groups. The incidence of CS among AHF animals was 72% in AMI or AMI-TLP while it was reduced to 25% in AMI-SR. Plasma copeptin level was increased by AMI. Maximal contractile response to vasopressin was decreased in AMI (32%) as in TLP- and SR- treated groups regardless of ligation. Increased vasopressin secretion occurring in the early phase of AMI may be responsible of mesenteric hypoperfusion resulting in tissue hypoxia. Treatment with a vasopressin antagonist enhanced mesenteric perfusion and improve survival. This could be an interesting therapeutic strategy to prevent progression to cardiogenic shock.

show abstract

“…The role of copeptin as a biomarker has been examined in a variety of cardiovascular, kidney and metabolic disorders. 21–23 …”

Section: Introductionmentioning

confidence: 99%

Copeptin as a Biomarker of Microcirculation Alterations in Systemic Sclerosis

Maciejewska¹,

Stec²,

Zaremba³

et al. 2023

CCID

View full text Add to dashboard Cite

Background Systemic sclerosis is a connective tissue disease characterized by vasculopathy and progressive fibrosis, leading to multiorgan dysfunction. Given the complex and not fully elucidated pathogenesis, biomarkers of rapid disease progression and therapeutic response are lacking. Copeptin, which reflects vasopressin activity in serum, is used in diagnosing or prognosing different cardiometabolic conditions. Objective The aim of study was to investigate the concentration of copeptin in patients with systemic sclerosis and correlate it with specific clinical symptoms. Patients and Methods Serum copeptin was measured in patients with systemic sclerosis (34 women and 3 men; mean age 57.6 years) and in healthy individuals (n=30) using commercially available ELISA kits. According to the criteria of LeRoy our systemic sclerosis cohort consisted of 17 patients with limited cutaneous systemic sclerosis (45.9%) and 20 diffuse cutaneous systemic sclerosis patients (54.1%). According to the criteria of LeRoy our systemic sclerosis cohort consisted of 17 patients with limited cutaneous systemic sclerosis (45.9%) and 20 diffuse cutaneous systemic sclerosis patients (54.1%). The median duration of the disease was 10 [4–14] years. Results We found significantly higher copeptin concentration in patients with systemic sclerosis (4.21 pmol/L [3.04–5.42]) in comparison to control group (3.40 pmol/L [2.38–3.76], p<0.01). Copeptin significantly correlated with Raynaud’s condition score (r=0.801, p<0.05). Patients with “late” capillaroscopic patterns had higher copeptin concentrations (5.37 pmol/L [4.29–8.06]) than patients with “early” (2.43 pmol/L [2.25–3.20], p<0.05) and “active” patterns (3.93 pmol/L [2.92–5.16], p<0.05]). Copeptin was found to be significantly higher in SSc patients with DUs (5.71 pmol/L [IQR 4.85–8.06]) when compared to SSc patients without DUs (3.31 pmol/L, [2.28–4.30], p<0.05). Additionally, copeptin concentration had good diagnostic accuracy in discriminating between patients with and without digital ulcers (AUC=0.863). Alprostadil decreased copeptin concentration from 4.96 [4.02–6.01] to 3.86 pmol/L [3.17–4.63] (p<0.01) after 4–6 cycles of administration. Conclusion Our findings suggest that copeptin may be a promising biomarker of microcirculation alterations in systemic sclerosis.

show abstract

Copeptin as a Diagnostic and Prognostic Biomarker in Cardiovascular Diseases

Cited by 20 publications

References 241 publications

ST2 and copeptine – modern biomarkers for monitoring the effectiveness of treatment of decompensated heart failure in patients after acute myocardial infarction

ST2 and copeptine – modern biomarkers for monitoring the effectiveness of treatment of decompensated heart failure in patients after acute myocardial infarction

Involvement of Vasopressin in Tissue Hypoperfusion during Cardiogenic Shock Complicating Acute Myocardial Infarction in Rats

Copeptin as a Biomarker of Microcirculation Alterations in Systemic Sclerosis

Contact Info

Product

Resources

About