scholarly journals PROGNOSTIC SIGNIFICANCE OF ENDOTHELIAL DYSFUNCTION MARKERS IN ARTERIAL HYPERTENSION

Author(s):  
V. I. Podzolkov ◽  
A. E. Bragina ◽  
N. A. Bragina

Aim. Assessment of prognostic significance of endothelial dysfunction markers: stable metabolites of nitric oxide (NOx), von Willebrand factor (vWF), endothelin-1 (E1), homocysteine and tissue plasminogen activator (tPA) in essential hypertension (EAH) patients not taking antihypertension therapy systematically.Material  and  methods. Totally, 12 EAH patients investigated (45 males, 79 females) (mean age 51,4±6,5 y. o., mean duration of AH 7,9±7,3 y.). Concentration of NOx in plasma was measured by spectrophotometry, and of vWF, homocysteine, E1 and tPA — by immune enzyme assay.Results. By the increase of SCORE risk level, there was significant increase of concentrations of NOx, E1, homocysteine and vWF in EAH patients (p<0,05), there were no changes in tPA levels (p>0,05). In 8 (8±1,1) years after baseline assessment, 115 patients were assessed second time. Of those 13 (11,3%) had cardiovascular events (CVE) and 5 (4,3%) died. By single factorial regression, the rate of CVE in EAH patients relate to homocystein level (р=0,01), NOx (р=0,001) and vWF (р=0,001). By multifactorial analysis, prognostic statistical significance is found for NOx (relative risk (RR) =3,8, р=0,006) and vWF (RR =3,5, р=0,005). In ROC-analysis there were found threshold levels of NOx (>46,6 mcM/L, AUC =0,863) and vWF (>1,68 mg/dL, AUC =0,738), the increase of which is followed by CVE development risk for the levels of NOx >46,6 mcM/L 3,8 times (sensitivity 81,9% and specificity 65,8%), vWF >1,68 mg/dL — 3,5 times (sensitivity 74,3% and specificity 62,7%). Combination of the parameters point on the risk increase up to 6,5 times (р=0,00007).Conclusion. NOx with the threshold of >46,6 mcM/L (RR =3,8) and vWF >1,68 mg/dL (RR =3,5) do show independent prognostic value for 5-year CVE risk assessment in EAH patients that can be applied as an additional method for risk stratification to estimate a group for more aggressive therapy and CVE prevention.

Blood ◽  
2016 ◽  
Vol 128 (3) ◽  
pp. 405-409 ◽  
Author(s):  
Efstathios Kastritis ◽  
Ioannis Papassotiriou ◽  
Evangelos Terpos ◽  
Maria Roussou ◽  
Maria Gavriatopoulou ◽  
...  

Key Points Serum levels of VWF antigen are elevated in AL amyloidosis, reflecting endothelial dysfunction. High VWF levels predict for poor outcome in patients with cardiac involvement and discriminate high-risk patients even within stage IIIB.


2020 ◽  
Vol 19 (3) ◽  
pp. 243-249 ◽  
Author(s):  
Sevket Balta

: Vascular diseases are the main reason for morbidity and mortality worldwide. As we know, the earlier phase of vascular diseases is endothelial dysfunction in humans, the endothelial tissues play an important role in inflammation, coagulation, and angiogenesis, via organizing ligand-receptor associations and the various mediators’ secretion. We can use many inflammatory non-invasive tests (flowmediated dilatation, epicedial fat thickness, carotid-intima media thickness, arterial stiffness and anklebrachial index) for assessing the endothelial function. In addition, many biomarkers (ischemia modified albumin, pentraxin-3, E-selectin, angiopoietin, endothelial cell specific molecule 1, asymmetrical dimethylarginine, von Willebrand factor, endothelial microparticles and endothelial progenitor cells) can be used to evaluate endothelial dysfunction. We have focused on the relationship between endothelial dysfunction and inflammatory markers of vascular disease in this review.


Author(s):  
Ferdows Atiq ◽  
Jens van de Wouw ◽  
Oana Sorop ◽  
Ilkka Heinonen ◽  
Moniek P. M. de Maat ◽  
...  

AbstractIt is well known that high von Willebrand factor (VWF) and factor VIII (FVIII) levels are associated with an increased risk of cardiovascular disease. It is still debated whether VWF and FVIII are biomarkers of endothelial dysfunction and atherosclerosis or whether they have a direct causative role. Therefore, we aimed to unravel the pathophysiological pathways of increased VWF and FVIII levels associated with cardiovascular risk factors. First, we performed a randomized controlled trial in 34 Göttingen miniswine. Diabetes mellitus (DM) was induced with streptozotocin and hypercholesterolemia (HC) via a high-fat diet in 18 swine (DM + HC), while 16 healthy swine served as controls. After 5 months of follow-up, FVIII activity (FVIII:C) was significantly higher in DM + HC swine (5.85 IU/mL [5.00–6.81]) compared with controls (4.57 [3.76–5.40], p = 0.010), whereas VWF antigen (VWF:Ag) was similar (respectively 0.34 IU/mL [0.28–0.39] vs. 0.34 [0.31–0.38], p = 0.644). DM + HC swine had no endothelial dysfunction or atherosclerosis during this short-term follow-up. Subsequently, we performed a long-term (15 months) longitudinal cohort study in 10 Landrace–Yorkshire swine, in five of which HC and in five combined DM + HC were induced. VWF:Ag was higher at 15 months compared with 9 months in HC (0.37 [0.32–0.42] vs. 0.27 [0.23–0.40], p = 0.042) and DM + HC (0.33 [0.32–0.37] vs. 0.25 [0.24–0.33], p = 0.042). Both long-term groups had endothelial dysfunction compared with controls and atherosclerosis after 15 months. In conclusion, short-term hyperglycemia and dyslipidemia increase FVIII, independent of VWF. Long-term DM and HC increase VWF via endothelial dysfunction and atherosclerosis. Therefore, VWF seems to be a biomarker for advanced cardiovascular disease.


Hepatology ◽  
2013 ◽  
Vol 58 (3) ◽  
pp. 1189-1189 ◽  
Author(s):  
Chundamannil E. Eapen ◽  
Joshua E. Elias ◽  
Ian Mackie ◽  
Elwyn Elias

2021 ◽  
Vol 12 ◽  
Author(s):  
Antonela Lelas ◽  
Hildegard Theresia Greinix ◽  
Daniel Wolff ◽  
Günther Eissner ◽  
Steven Zivko Pavletic ◽  
...  

Chronic graft-versus-host disease (cGvHD) is an immune mediated late complication of allogeneic hematopoietic stem cell transplantation (alloHSCT). Discovery of adequate biomarkers could identify high-risk patients and provide an effective pre-emptive intervention or early modification of therapeutic strategy, thus reducing prevalence and severity of the disease among long-term survivors of alloHSCT. Inflammation, endothelial injury, and endothelial dysfunction are involved in cGvHD development. Altered levels of acute phase reactants have shown a strong correlation with the activity of several immune mediated disorders and are routinely used in clinical practice. Since elevated von Willebrand factor (VWF) and factor VIII (FVIII) levels have been described as acute phase reactants that may indicate endothelial dysfunction and inflammation in different settings, including chronic autoimmune diseases, they could serve as potential candidate biomarkers of cGvHD. In this review we focused on reported data regarding VWF and FVIII as well as other markers of inflammation and endothelial dysfunction, evaluating their potential role in cGvHD.


2020 ◽  
pp. 528-534
Author(s):  
A. M. SABUROVA ◽  
◽  
KH.R. NASYRDZHANOVA ◽  
KH.YO. SHARIPOVA ◽  
◽  
...  

Objective: Examination the relationship between the state of biomembranes and indicators of endothelial dysfunction in patients with chronic obstructive pulmonary disease (COPD). Methods: 40 patients with COPD at the age of 27-64 years were treated at the City Health Center № 2 named after academician K.T. Tadzhiev. There were 21 men (52.5%), and 19 women (47.5%). The control group is represented by 30 healthy persons, comparable by sex and age. The content of inflammatory markers of vascular endothelium – CRP, fibrinogen and von Willebrand factor (VWF) – was studied. The functional state of erythrocyte membranes was studied by determining of permeability of erythrocyte membranes (PEM) and sorption ability of erythrocytes (SAE). Results: Study of endothelial dysfunction in patients with COPD showed an increase in fibrinogen content by 71.15% (2.6±0.08 and 4.45±0.16 g/L), VWF by 35.4% (95.7±2.3 and 129.6±2.3%) and an increase in serum CRP by 15 times (2.09±0.1 and 32.2±0.1 mg/L). There was a change in PEM and an increase in SAE by 27.8% (39.5±0.5 and 50.5±0.6%, respectively) compared with the control group, that reflects damage of erythrocytes and is considered as a factor of endogenous intoxication. A significant direct relationship was established between SAE and indicators of vascular dysfunction: with VWF (r=0.34; p<0.05) and fibrinogen (r=0.47; p<0.05). Conclusions: The development and progression of COPD are accompanied by dysfunction of the vascular endothelium, the criteria for which are an increase in the level of CRP, fibrinogen and VWF. On the background of COPD, erythrocytes are involved in the pathological process, which is confirmed by an increase in PEM and SAE and with a significant relationship between SAE and endothelial dysfunction. Laboratory manifestations of endothelial dysfunction accompanied by functional impairment of biomembranes (increased PEM and increased SAE), can be considered as a factor of the poor prognosis of COPD. Keywords: COPD , biomembrane, endothelial dysfunction, CRP, fibrinogen, von Willebrand factor, permeability of erythrocyte membranes, sorption ability of erythrocytes.


2000 ◽  
Vol 84 (08) ◽  
pp. 195-203 ◽  
Author(s):  
Andrew Stewart ◽  
Fraser Witherow ◽  
Susan Grieve ◽  
Pamela Dawson ◽  
Keith Fox ◽  
...  

SummaryIntra-arterial desmopressin caused dose and time dependent increases (p <0.001 for all) in forearm blood flow (all doses) and plasma tissue plasminogen activator (t-PA) concentrations (desmopressin ≥70 ng/min). Although plasma t-PA concentrations rose in both forearms, there was a modest local release of t-PA in the infused forearm (14 ng/100 mL of tissue/min, p <0.05). At desmopressin doses ≥300 ng/min, plasma von Willebrand factor (vWf) and Factor VIII:C concentrations rose in both forearms (p <0.001) and correlated with the rise in interleukin-6 concentrations (r = 0.92, p <0.001; r = 0.85, p = 0.002 respectively). Neither desmopressin nor substance P caused t-PA, vWf or Factor VIII:C release in the patients, although desmopressin increased plasma interleukin-6 concentrations as in healthy volunteers. We conclude that desmopressin releases t-PA, vWf and Factor VIII:C predominantly via systemic mechanisms, possibly mediated by cytokine release. Patients with type 3 vWD appear to have a generalised failure to release t-PA acutely despite a normal interleukin-6 response to desmopressin infusion.


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