scholarly journals Association between functional neurometry test results and blood biomarkers indicative of anaemia, subclinical inflammation, and endothelial dysfunction

2021 ◽  
Vol 14 (5) ◽  
pp. 225-233
Author(s):  
Renata de Melo Guerra Ribas ◽  
Valdenilson Ribeiro Ribas ◽  
Diélita Carla Lopes de Oliveira ◽  
Marcelo Tavares Viana ◽  
Joyce Gomes de Moraes ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Subclinical Inflammation ◽  
Test Results ◽  
Blood Biomarkers

Endothelial dysfunction is an independent factor responsible for vasospastic angina

2001 ◽  
Vol 101 (6) ◽  
pp. 707-713 ◽  
Author(s):  
Hiroki TERAGAWA ◽  
Masaya KATO ◽  
Junichi KUROKAWA ◽  
Togo YAMAGATA ◽  
Hideo MATSUURA ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Coronary Stenosis ◽  
Intima Media Thickness ◽  
Control Group ◽  
Test Results ◽  
Independent Factor ◽  
Atherosclerotic Changes ◽  
Significant Coronary Stenosis

In order to evaluate peripheral endothelial function in patients with vasospastic angina (VSA), we measured flow-mediated dilation (FMD) of the brachial artery in patients with VSA and compared it with FMD in patients without VSA. Endothelial dysfunction is considered one of the mechanisms underlying VSA. However, its exact role remains to be clarified. The study included 30 patients with positive spasm-provocational test results without evidence of significant coronary stenosis (VSA group) and 30 patients with negative spasm-provocational test results without evidence of significant coronary stenosis (control group). In each patient, brachial artery diameter responses to hyperemic flow and glyceryl trinitrate spray were measured using high-resolution ultrasound. The carotid intima-media thickness was also measured as a marker of systemic atherosclerosis. FMD was lower in the VSA group (4.8±0.5%) compared with the control group (9.4±0.7%, P < 0.0001). In the VSA group, FMD was not affected by coronary risk factors or the presence of atherosclerotic changes on coronary angiography. Glyceryl trinitrate-induced dilation did not differ between the two groups. The intima-media thickness was comparable between the VSA (0.85±0.04mm) and control groups (0.81±0.05mm). These findings indicated that peripheral endothelial function is impaired only in the VSA group, whereas the atherosclerotic changes were similar in the two groups. We conclude that endothelial dysfunction may be an independent factor responsible for the development of VSA.

scholarly journals Is endothelial dysfunction a driving force of COVID-19 induced coagulopathy?

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
O Dukhin ◽  
A Kalinskaya ◽  
I Molodtsov ◽  
A Maltseva ◽  
D Sokorev ◽  
...  
Keyword(s):  
Growth Rate ◽  
Platelet Aggregation ◽  
Endothelial Dysfunction ◽  
Endothelial Damage ◽  
Reference Ranges ◽  
Test Results ◽  
Plasma Coagulation ◽  
Funding Sources ◽  
Significant Difference ◽  
Induced Aggregation

Abstract Background/Introduction There are numerous reports regarding the direct endothelial damage by the SARS-CoV-2 that can lead to activation of both plasma hemostasis and platelet aggregation. However, the mechanism of interaction between endothelium and haemostasis in COVID-19 remains unclear. Purpose The aim of our study was to assess the relationship between each link of clot formation process (endothelial function, plasma coagulation, platelet aggregation) with the severity of the disease. Methods 58 COVID-19 patients were included in our study. Patients were divided into moderate (n=39) and severe (n=18) subgroups. All patients underwent a flow-mediated dilation (FMD) test, impedance aggregation, rotational thromboelastometry, thrombodynamics and von Willebrand factor antigen (vWF: Ag) quantification. All measurements were repeated on days 3 (point 2) and 9 (point 3) of hospitalization. Results COVID-19 patients demonstrated the enhanced plasma coagulation (clotting time, s 613,0 [480; 820], clot growth rate, μm/min 32,75 [29,3; 38,7]). At point 1 no significant difference in parameters of plasma coagulation between patients' subgroups was noted. At point 2 a significant decrease in the size (CS, μm 1278.0 [1216.5; 1356.5] vs 965.0 [659.8; 1098.0], p&lt;0,01) and clot growth rate (μm/min 32,4 [29,2; 35,0] vs 17,7 [10,3; 24,4], p&lt;0,01) under the influence of anticoagulants in the moderate subgroup compared with point 1 was observed. We didn't observe such phenomenon in severe subgroup. There was no significant difference in platelet aggregation between subgroups at point 1. During the course of the disease the patients in the moderate and severe subgroups demonstrated a significant increase in platelet aggregation induced by arachidonic acid and ADP (severe: AUC ARA 48,0 [25,0; 59,0] vs 77,5 [55,8; 92,7], p=0,04; AUC ADP 44,0 [41,0; 56,0] vs 58,0 [45,5; 69,0], p=0,04; moderate: AUC ARA 31,5 [19,8; 50,7] vs 56,0 [39,0; 76,0], p=0,01; AUC ADP 43,0 [20,0; 59,0] vs 56,6 [50,3; 70,5], p=0,04;), in moderate subgroup the significant increase in TRAP-induced aggregation was also noted (AUC TRAP 58,0 [41,0; 69,5] vs 76,0 [58,3; 81,5], p=0,048). There were no significant differences in the FMD-test results between the patient subgroups. FMD-test results were predominantly within the reference ranges (7,1 [4,0; 8,8]). Patients in the severe subgroup had significantly higher levels of vWF: Ag (228,0 [205,3; 240,7] vs 232,0 [226,0; 423,0], p=0,03). Conclusion SARS-CoV-2 infection was characterized by increased levels of vWF:Ag, that could represent the local endothelial damage, meanwhile there was no generalized endothelial dysfunction assessed via FMD-test in moderate to severe patients. At the same time the enhanced plasma coagulation in COVID-19 patients was observed. FUNDunding Acknowledgement Type of funding sources: None.

Significant hemostasis and endothelial dysfunction blood biomarkers of unstable atherosclerotic plaques in coronary arteries

2018 ◽  
Vol 275 ◽  
pp. e146
Author(s):  
E. Striukova ◽  
E. Kashtanova ◽  
Y.A. Polonskaya ◽  
E. Stakhneva ◽  
A. Chernyavskii ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Coronary Arteries ◽  
Atherosclerotic Plaques ◽  
Blood Biomarkers

scholarly journals Dyslipidemia, subclinical inflammation, hepatic cholestasis and endothelial dysfunction in schoolchildren with excess fat: A study from the United Arab Emirates

PLoS ONE ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. e0210316 ◽  
Author(s):  
Elhadi H. Aburawi ◽  
Sania Al Hamad ◽  
Javed Yasin ◽  
Lolowa A. Almekhaini ◽  
Abdul-Kader Souid
Keyword(s):  
Endothelial Dysfunction ◽  
United Arab Emirates ◽  
Subclinical Inflammation

scholarly journals Subclinical Inflammation and Endothelial Dysfunction in Young Patients with Diabetes: A Study from United Arab Emirates

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0159808 ◽  
Author(s):  
Elhadi H. Aburawi ◽  
Juma AlKaabi ◽  
Taoufik Zoubeidi ◽  
Abdullah Shehab ◽  
Nader Lessan ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
United Arab Emirates ◽  
Young Patients ◽  
Subclinical Inflammation ◽  
Patients With Diabetes

scholarly journals Subclinical Inflammation and Endothelial Dysfunction in Patients with Chronic Pancreatitis and Newly Diagnosed Pancreatic Cancer

2015 ◽  
Vol 61 (4) ◽  
pp. 1121-1129 ◽  
Author(s):  
A. Gasiorowska ◽  
R. Talar-Wojnarowska ◽  
A. Kaczka ◽  
A. Borkowska ◽  
L. Czupryniak ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Chronic Pancreatitis ◽  
Endothelial Dysfunction ◽  
Subclinical Inflammation ◽  
Newly Diagnosed

scholarly journals Adipocytokines in metabolically healthy obesity

2019 ◽  
Vol 13 (3) ◽  
pp. 169-175
Author(s):  
Sofia G. Shulkina ◽  
Elena N. Smirnova ◽  
Maxim I. Yudin ◽  
Mikhail A. Osadchuk ◽  
Maxim V. Trushin
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Metabolic Disorders ◽  
International Diabetes Federation ◽  
Resistance Index ◽  
High Density Lipoproteins ◽  
Control Group ◽  
Subclinical Inflammation ◽  
Tnf Α

The aim of the investigation was to study the relationship among adipokines, markers of subclinical inflammation and endothelial dysfunction in patients with metabolic healthy obesity (MHO). The study included 50 persons aged 25-50 years with obesity in the absence of metabolic disorders (International Diabetes Federation criteria, 2005, marked as MHO), the control group consisted of 50 healthy respondents without obesity. We studied clinical and biochemical parameters, insulin resistance index (HOMA-IR), levels of leptin, soluble leptin receptors (sLR), resistin, adiponectin, C-reactive protein (CRP-hs), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), endothelin-1 (ET-1), von Willebrand factor, free leptin index was calculated in a formula (FLI = leptin × 100 / sLR). In MHO patients, independently of HOMA-IR index, there was an increase in leptin, FLI, resistin, VEGF, and IL-6 parameters. The concentration of CRP-hs and TNF-α in MHO group with HOMA-IR ≥2.7 was increased. Systolic blood pressure correlated with leptin level (r=0.43, P<0.05), FLI (r=0.54; P=0.01), TNF-α (r=0.44; P<0.05) and IL-6 (r=0.33; P<0.05); diastolic blood pressure - with leptin level (r=0.35, P<0.05). Links between high density lipoproteins and leptin (r=–0.55 and r=–0.60; P<0.01), resistin (r=0.32; P<0.05 and r=0.60; P<0.01) and VEGF (r=–0.70, P<0.01) were established. The VEGF level correlated with HOMA-IR (r=0.62; P<0.01), leptin (r=0.29; P<0.05), FLI (r=0.50; P<0.05), resistin (r=0.70; P<0.01), IL-6 (r=0.74, P<0.01) and ET-1 (r=0.29; P<0.05). Obese patients without metabolic disorders, having normotension and normal insulin sensitivity, are less influenced to adverse cardiovascular risks due to less expressed hormonal and inflammatory activation of adipose tissue and, as a result, less pronounced endothelial dysfunction. While insulin resistance develops, cardiovascular risk increases due to activation of subclinical inflammation, angiogenic endothelial dysfunction and leptin resistance.

scholarly journals Subclinical Inflammation, Endothelial Progenitor Cell Depletion, and Endothelial Dysfunction in Adolescents with Obesity

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Hong Huang ◽  
Judith A. Groner ◽  
Jennifer Kuck ◽  
Lisa Nicholson ◽  
Robert Murray ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Cell Depletion ◽  
Subclinical Inflammation ◽  
Endothelial Progenitor
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