Predictors of high platelet reactivity assessed by multiple electrode aggregometry in healthy individuals ‒ the role of leukocyte count

Platelets ◽  
2021 ◽  
pp. 1-2
Author(s):  
Patrycja Szymanska ◽  
Magdalena Boncler ◽  
Jacek Golanski
Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 5362-5362 ◽  
Author(s):  
Michael Spannagl ◽  
Csilla Jambor

Abstract Background: Platelet inhibition by clopidogrel is often determined using ADP induced aggregometry. TRAP-6 stimulates platelets via the PAR receptors and is influenced to a much lesser extend by aspirin or clopidogrel. The value of the determination of TRAP-6 induced aggregometry in patients treated with clopidogrel is unknown. We evaluated the relation of clopidogrel non-responsiveness as determined by multiple electrode aggregometry (MEA) (1) vs. TRAP-6 induced aggregation. MEA provides a measurement of platelet aggregation in whole blood by monitoring changes in electrical impedance via disposable test cells each containing two pairs of electrodes (1). Methods: Following IRB approval hirudin-anticoagulated blood (Dynabyte, Munich, Germany) was sampled from 993 patients. Aggregation induced by arachidonic acid (0.5 mM), ADP (6.4 μM) or TRAP-6 (32μM) was determined in whole blood using a new generation impedance aggregometer. The device is called Multiplate analyzer (Dynabyte, Munich, Germany), indicating the multiplicity of channels and sensors per channel of the device. After dilution (1:2 with 0.9% NaCl solution) of hirudin-anticoagulated whole blood and stirring for three minutes in the test cuvettes at 37°C, the activator was added and aggregation was continuously recorded for six minutes. The increase of impedance due to the attachment of platelets to the electrodes is detected for each sensor unit separately and transformed to arbitrary aggregation units. The aggregation is quantified as area under the curve (AUC). Results: 618 patients were on chronic therapy with 100 mg aspirin/d, 295 patients on clopidogrel 75 mg/d (237 on dual therapy). Aspirin therapy had no influence on TRAP-6- induced aggregation (112+−260 vs. 110+−25; mean +− sd; aspirin vs. no aspirin, p> 0.05 Mann-Whitney U-test). In contrast clopidogrel induced a minor but significant reduction of TRAP6-induced aggregation (107+− 277 vs. 113+−246; p<0.05). Patients on clopidogrel had a significantly lower ADP induced aggregation (41+−30 vs. 86 +−33) compared to controls (p<0.05), and patients on aspirin had a significantly lower arachidonic acid induced aggregation compared to controls (23+−28 vs. 94 +− 35, p<0.05). 89 of 295 patients (30%) were stratified as clopidogrel non-responders based on the cut-off presented in (2). Patients were divided into 4 quartiles (q1-4) depending on their TRAP-6 induced aggregation. The rate of non-responsiveness in Q1 was 8.1%, in Q2 20%, in Q3 38% and 54% in Q4. ADPinduced aggregation was significantly higher in Q4 than in any other quartile (p<0.05). Conclusion: A high TRAP-6 induced aggregation is associated with an increased rate of clopidogrel non-responsiveness as determined by multiple electrode aggregometry. TRAP-6 induced aggregometry seems to indicate the global platelet potential and might allow a prediction of clopidogrel responsiveness before the induction of therapy.


2011 ◽  
Vol 105 (06) ◽  
pp. 1110-1111
Author(s):  
Lukas Strohmeier ◽  
Franz Quehenberger ◽  
Manfred Neubauer ◽  
Mariana Stettin ◽  
Franz Rainer ◽  
...  

2009 ◽  
Vol 102 (08) ◽  
pp. 397-403 ◽  
Author(s):  
Jolanta Siller-Matula ◽  
Ghazaleh Gouya ◽  
Michael Wolzt ◽  
Bernd Jilma

SummarySeveral test systems exist for assessment of platelet function in patients under clopidogrel or aspirin therapy. The objective was to cross-validate the Multiple Electrode Aggregometry (MEA) with three other methods used for determining platelet reactivity under treatment with clopidogrel and aspirin. Platelet function was assessed by the MEA, Vasodilator Stimulated Phosphoprotein (VASP) phosphorylation assay, Platelet Function Analyzer-100 (PFA-100) and the Cone and Platelet Analyzer. Measurements were performed in blood from nine healthy volunteers at baseline, 2, 4, 6 and 72 hours after clopidogrel and aspirin loading. The apparent effect size for clopidogrel and aspirin was greatest for the MEA: treatment induced a 19-fold difference in the arachidonic acid-induced platelet aggregation and an 11-fold difference in the adenosine diphosphate-induced platelet aggregation before/after treatment. For comparison, aspirin and clopidogrel induced only 2.0– to 2.6 -fold changes in other tests (VASP assay, Cone and Platelet Analyzer and PFA-100). Maximal effects were seen 2 hours after aspirin loading and shorter than 72 hours after clopidogrel loading. In conclusion, aspirin and clopidogrel produce stronger signals in the MEA compared to several other methods.


2017 ◽  
Vol 117 (05) ◽  
pp. 923-933 ◽  
Author(s):  
Liana Iliev ◽  
Veronika Bruno ◽  
Miklos Rohla ◽  
Florian Egger ◽  
Thomas Weiss ◽  
...  

SummaryElevated platelet turnover contributes to high platelet reactivity. High platelet reactivity after percutaneous coronary intervention (PCI) is associated with major adverse cardiovascular events (MACE). The purpose of this study was to determine the prognostic value of platelet turnover and function with regard to MACE after PCI with stent implantation. In this prospective observational study, 486 consecutive patients after PCI on aspirin and clopidogrel were included to determine platelet turnover (mean platelet volume (MPV), reticulated platelet fraction (RPF)) and platelet function (multiple electrode aggregometry (MEA), vasodilator-stimulated phosphoprotein-phosphorylation (VASP-P) assay). At six-months follow-up, MACE occurred in 10.7 % of patients. RPF (odds ratio [OR]=1.173 (95% confidence interval [CI 95 %] 1.040–1.324), p=0.009) and MPV (OR=1.459 (CI 95 % 1.059–2.008), p=0.021) were univariable predictors of MACE, whereas VASP-P (OR=1.016 (CI 95 % 1.000–1.032), p=0.052) and MEA (OR=0.999 (CI 95 % 0.980–1.017), p=0.895) failed to predict MACE. RPF remained the only platelet variable independently associated with MACE. The best model to predict MACE included: troponin I (OR=1.007 (CI 95 % 1.002–1.012), p=0.009), RPF (OR=1.136 (CI 95 % 1.001–1.288), p=0.048), CRP (OR=1.008 (CI 95 % 1.001–1.014), p=0.023) and history of myocardial infarction (OR=2.039 (CI 95 % 1.093–3.806), p=0.025). RPF (OR=1.211 (CI 95 % 1.042–1.406), p=0.012) was also independently associated with in-hospital bleedings. In conclusion, RPF as index of platelet turnover is an independent predictor of MACE and bleeding events in PCI patients on dual antiplatelet therapy. Since RPF can reliably be quantified along with routine haemograms, RPF might easily be applied in the setting of cardiovascular risk prediction.


2020 ◽  
Vol 11 (SPL1) ◽  
pp. 1396-1399
Author(s):  
Disha Bhatero ◽  
Punam Sawarkar ◽  
Gaurav Sawarkar

Covid-19 is an infectious disease caused by novel Coronavirus. The overall prevalence rate of Covid-19 in Worldwide ( 9.94M )& it is (529 K) & (153 K) in India and Maharashtra. This situation can be considered under JanapadodhwansaVyadhi in Ayurveda. The primary purpose of Ayurveda  is the prevention of the disease in healthy individuals and eradication of disease, which are curable. Immunity comes under the Vyadhikshamatva. Further, Covid-19 infection is correlated with Vataj-Kaphaj Jwara. In Ayurveda Rasayana therapy to boost up immunity (Bala  & Vyadhikshamatva). The present study aimed to explore the concept of infectious disease and its prevention through different lifestyles described in Ayurveda. The above need-based information is collected from various Ayurvedicliterature (Laghutrayee, Bruhatryayi) along with numerous research articles from databases, such as PubMed, Google Scholar. All collected data were depicted in narrative form and tabular manner under different heads. Considering the above aspect in the prevention of Covid-19, the role of Ayurveda intervention may be proved more beneficial in Covid-19. Further, adoption of code of conduct may efficiently overcome the current pandemic situation by maintaining good immunity & implementation of Ahar, Vihar Vidhis, Dincharya, and Rutucharya& Sadvritta  for improving disease resistance.


2020 ◽  
Vol 18 (3) ◽  
pp. 204-214 ◽  
Author(s):  
Aida Habib ◽  
Giovanna Petrucci ◽  
Bianca Rocca

<P>Under physiological conditions, peripheral arteries release endogenous vascular-protective and antithrombotic agents. Endothelial cells actively synthesize vasoactive mediators, which regulate vascular tone and platelet reactivity thus preventing thrombosis. Atherosclerosis disrupts homeostasis and favours thrombosis by triggering pro-thrombotic responses in the vessels, platelet activation, aggregation as well as vasoconstriction, phenomena that ultimately lead to symptomatic lumen restriction or complete occlusion. <P> In the present review, we will discuss the homeostatic role of arterial vessels in releasing vascular-protective agents, such as nitric oxide and prostacyclin, the role of pro- and anti-thrombotic vascular receptors as well as the contribution of circulating platelets and coagulation factors in triggering the pro-thrombotic response(s). We will discuss the pathological consequences of disrupting the protective pathways in the arteries and the pharmacological interventions along these pathways.</P>


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1437.2-1438
Author(s):  
T. Kvlividze ◽  
V. Polyakov ◽  
В. Zavodovsky ◽  
Y. Polyakova ◽  
L. Seewordova ◽  
...  

Background:Interest in highly specialized tissue cytokines contributed to the discovery of new biologically active molecules. Nesfatin-1 (NF) - discovered in 2006 as an anorexigenic factor. NF-1 is believed to be involved in the regulation of energy homeostasis by regulating appetite and water intake. The role of NF-1 in the pathogenesis of inflammatory diseases is poorly understood. Recently, studies have found a relationship between an increased level of NF-1 and inflammatory markers in various pathologies.Objectives:Study of the level of nesfatin-1 in the blood serum of healthy people, determination of the correlation between the level of NF-1 with the severity of clinical symptoms and classic markers of inflammation in patients with RA.Methods:120 persons were examined: 90 patients with RA and 30 healthy people. All patients underwent a complete clinical and laboratory examination. Plasma NF-1 levels were determined using commercial test systems (RaiBiotech, cat # EIA-NESF) according to the manufacturer’s instructions. Patients with various forms of RA were comparable in age to the group of healthy individuals. Statistical processing of clinical examination data was carried out using the “STATISTICA 10.0 for Windows” software package. Quantitative data were processed statistically using the parametric Student’s t-test, qualitative data using the non-parametric chi-square test. The significance of differences between groups was determined using analysis of variance. The results were considered statistically significant at p <0.05.Results:The average level of NF-1 in blood serum in healthy individuals was 31.79 ± 3.21 ng / ml (M ± σ). The level of normal NF-1 values in healthy individuals, defined as M ± 2σ, ranged from 25.3 to 37.83 ng / ml. There was no significant difference in the levels of circulating NF-1 and BMI in healthy individuals and patients with RA (p> 0.05). The inverse relationship of a lower level of NF-1 with an increase in BMI was not significant.Group 1 (66 patients with RA) with increased serum NF-1 levels (> 37.83 ng / ml), and group 2 (44 patients) with normal values (<37.83 ng / ml). A high level of NF-1 was characteristic for patients with high activity according to DAS28, RF seropositive, ACCP-positive, with extra-articular manifestations, who had been ill for 10 years or more. A reliable relationship between the level of NF-1 in the blood serum and laboratory parameters of RA activity - ESR, CRP, was shown, and secondary synovitis was more common. Our data show a direct correlation between the NF-1 level of the pro-inflammatory markers of RA.Conclusion:The positive correlation between the level of NF-1 and classical markers of inflammation, such as CRP and ESR, confirms the involvement of NF-1 in the pathophysiology of inflammation in RA. This is also evidenced by the correlation of a high level of NF-1 in the blood serum with a more severe clinical picture of RA. It is known that NF-1 can promote the release of pro-inflammatory cytokines such as interleukin-8 (IL-8), interleukin-6 (IL-6), and macrophage inflammatory protein-1a (MIP-1a) in the chondrocytes of RA patients.It is necessary to further study the role of NF-1 in the pathogenesis of systemic inflammatory reactions and the possibility of targeting pro-inflammatory cytokines, the possibility of regulating the level of NF-1 by drugs.References:[1]Kvlividze T.Z., Zavodovsky B.V., Akhverdyan Yu.R. Kvlividze T.Z., Zavodovsky B.V., Akhverdyan Yu.R., Polyakova Yu.V., Sivordova L.E., Yakovlev A.T., Zborovskaya I.A. Serum nesfatin -1 as a marker of systemic inflammation in rheumatoid arthritis. Klinicheskaya Laboratornaya Diagnostika (Russian Clinical Laboratory Diagnostics). 2019; 64 (1): 53-56 (in Russ.).Disclosure of Interests:None declared


Lupus ◽  
2021 ◽  
pp. 096120332110103
Author(s):  
Anna Truszewska ◽  
Agnieszka Wirkowska ◽  
Kamila Gala ◽  
Piotr Truszewski ◽  
Łucja Krzemień-Ojak ◽  
...  

Background For long Epstein–Barr virus (EBV) has been suspected to be involved in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to verify the association between EBV, cell-free DNA (cfDNA) and kidney disease in SLE. Methods Blood samples were obtained from 43 SLE patients and 50 healthy individuals. EBV load was measured via real-time PCR assay. Sizing and quantification of plasma cfDNA was performed on Bioanalyzer. We proposed that the uniformity of cfDNA fragmentation can be described using cfDNA fragmentation index. Results SLE patients with chronic kidney disease (CKD +) had higher EBV load compared to CKD(–) patients (P = 0.042). Patients with high cfDNA level had higher EBV load (P = 0.041) and higher cfDNA fragmentation index (P < 0.001) compared to patients with low cfDNA level. Among patients with high cfDNA level, EBV load was higher in CKD(+) group compared to CKD(–) group (P = 0.035). EBV load was positively correlated with the fragmentation index in all SLE patients (P = 0.028, R2 = 0.13), and the correlation was even more pronounced in CKD (+) patients (P < 0.001, R2 = 0.20). Conclusions We showed that EBV load was associated with non-uniform cfDNA fragmentation, higher cfDNA levels, and kidney disease in SLE patients. Although the causality of this relationship could not be determined with the current study, it brings rationale for further investigations on the role of EBV and cfDNA interplay in SLE pathogenesis.


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