scholarly journals Impact of electric cardioversion on platelet activation

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250353
Author(s):  
Harald Haidl ◽  
Johanna Gaugler ◽  
Gerhard Cvirn ◽  
Hildegard Jasser-Nitsche ◽  
Wolfgang Schwinger ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Adenosine Diphosphate ◽  
Serum Levels ◽  
Thrombin Receptor ◽  
Activation Markers ◽  
Platelet Factor ◽  
Geometric Means ◽  
Integrin Αiibβ3 ◽  
Before And After ◽  
Electric Cardioversion

Introduction Atrial fibrillation (AF) comes along with high risk of stroke. This risk continues even after re-establishing sinus rhythm with cardioversion. Aim of this study is to evaluate the contribution of electric cardioversion (EC) to platelet activation and procoagulatory tendency. Methods Extent of platelet activation before and after electric cardioversion was quantified using flow cytometry, impedance aggregation measurements with Multiplate®, and quantification of serum levels of platelet factor 4 (PF4) and ß-thromboglobulin (ß-TG) in patients with AF (N = 10). Results No significant differences were observed in any of the measured parameters comparing the values from before and after cardioversion. Geometric means of P-selectin expression and integrin αIIbβ3 activation were 0.27 (+/- 0.07) and 2.30 (+/- 2.61) before EC and 0.28 (+/- 0.17) and 1.67 (+/- 1.82) after EC. Levels of ß-TG were 110.11 ng/ml (+/- 3.78) before and 110.51 ng/ml (+/- 2.56) after EC, levels of PF4 were 35.64 ng/ml (+/- 12.94) before and 32.40 ng/ml (+/- 4.95) after EC. Platelet aggregation triggered with adenosine diphosphate (ADP), arachidonic acid, collagen, Ristocetin, or thrombin receptor activating peptide (TRAP) revealed results within the normally expected ranges without significant changes before and after EC. Discussion Electric cardioversion has no influence on platelet activation markers which is in agreement with other studies reporting electrical cardioversion to be safe.

Aprotinin: is it prothrombotic?

Perfusion ◽  
2001 ◽  
Vol 16 (5) ◽  
pp. 401-409 ◽  
Author(s):  
M Poullis ◽  
R C Landis ◽  
K M Taylor
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Mechanism Of Action ◽  
Adenosine Diphosphate ◽  
Platelet Membrane ◽  
Calcium Flux ◽  
Thrombin Receptor ◽  
Proteolytic Activation ◽  
Agonist Peptide ◽  
Receptor Family

Controversy continues as to whether aprotinin (Trasylol) is prothrombotic. The recent discovery of the thrombin receptor family, known as the protease-activated receptor family (PAR) has been essential in aiding our understanding of the mechanism of action of aprotinin. Our results show that aprotinin has no effect on platelet aggregation induced by adrenaline, adenosine diphosphate, phorbol-12-myristate-13-acetate, collagen or PAR 1 agonist peptide. However, aprotinin inhibits thrombin-induced platelet activation as assessed by macroaggregation, microaggregation and platelet membrane calcium flux. Aprotinin inhibits proteolytic activation of platelets, but platelets can still be activated by non-proteolytic mechanisms.

Abstract 16292: Selective Platelet Protease-Activated-Receptor (PAR)1 and PAR4 Mediated Thrombin Desensitisation in the Elderly is Correlated With Inflammation and Chronic Thrombin Receptor Stimulation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Sonali R Gnanenthiran ◽  
Gabrielle Pennings ◽  
Caroline Reddel ◽  
Heather Campbell ◽  
Justin Hamilton ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Platelet Activation ◽  
The Elderly ◽  
Elderly Subjects ◽  
Thrombin Receptor ◽  
Receptor Stimulation ◽  
Activation Markers ◽  
Tnf Α ◽  
D Dimer ◽  
Granule Release

Introduction: Platelet activation, by adenosine diphosphate (ADP) via P2Y 12 receptors and thrombin via PAR1 and PAR4, is a key therapeutic target in cardiovascular disease (CVD). The efficacy of antiplatelet agents diminishes in the elderly, but it is unknown whether these pathways change with aging. Hypothesis: Platelet activation pathways change with aging. Methods: Platelet activity was evaluated in young (20-30yrs), middle-aged (40-55yrs) and elderly (≥70yrs) healthy volunteers (n=174). Whole blood aggregometry and flow cytometry (P-selectin: α-granule release; CD63: dense granule release; PAC1 binding: activated GPIIb/IIIa) were performed under basal conditions and post ex vivo stimulation with ADP, thrombin, PAR1 agonist or PAR4 agonist. EC 50 and E max values were derived for each agonist. Receptor cleavage and quantification (P2Y 12 ; PAR1; PAR4; GPIbα) were assessed with flow cytometry. Thrombin generation (D-Dimer) and inflammation (interleukin [IL]-1β; tumour necrosis factor [TNF]-α) were assessed via ELISA. Results: The elderly had higher basal platelet activation markers (P-selectin, CD63, activated GPIIb/IIIa) than the young, with higher basal activity correlating with increasing IL-1β. P2Y 12 receptor density was higher in the elderly and associated with greater ADP-induced platelet aggregation and activation. Elderly subjects had less platelet activation in response to thrombin (higher EC 50 ), demonstrating hyporeactivity to selective stimulation of PAR1 or PAR4, more basal PAR1/PAR4 cleavage, and less inducible PAR1/PAR4 cleavage. This was associated with reduced thrombin binding receptor GPIbα and reduced secondary ADP contribution to thrombin-mediated activation. D-Dimer and TNF-α levels were elevated in the elderly, and inversely correlated with platelet thrombin sensitivity, implying a role of desensitization from chronic thrombin receptor stimulation. Conclusion: Aging is associated with increased basal platelet activation and hyperreactivity to ADP, but selective desensitization to thrombin. The latter appears mediated by chronic thrombin receptor stimulation and inflammation. Age-specific antiplatelet strategies may require selective targeting of these pathways to treat CVD in the elderly.

Effect of Different Dialysis Membranes on Platelet Function. A Tool for Biocompatibility Evaluation

1996 ◽  
Vol 19 (7) ◽  
pp. 404-410 ◽  
Author(s):  
L.B. De Sanctis ◽  
S. Stefoni ◽  
G. Cianciolo ◽  
L. Colì ◽  
A. Buscaroli ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Serum Levels ◽  
Cellulose Triacetate ◽  
Blood Levels ◽  
Functional Evaluation ◽  
Thrombin Time ◽  
Platelet Factor ◽  
Dialysis Membranes ◽  
Membrane Contact ◽  
Fibrinolytic Parameters

Intradialytic coagulative and platelet activation, one of the main consequences of blood-membrane contact, was studied in a group of 5 RDT patients with a comparative evaluation of 3 different dialytic membranes: Cuprophan (CU), Polysulfone (PS) and Cellulose Triacetate (CT). Each patient underwent 5 consecutive dialysis sessions with the above mentioned membranes. Intradialytic platelet activation was studied through a morpho-functional evaluation between the mean platelet volume (MPV) and Serotonin (S), ß-Thromboglobulin (ß-TG) and Platelet Factor 4 (PF4) serum levels. These determinations were made before HD (time 0) and after 30', 120’ and 240'. We also checked the intradialytic status of thrombogenesis and fibrinolysis determining aPTT, thrombin time, fibrinogen, antithrombin III (AT III), α-2 antiplasmin and plasminogen, at the same time intervals. All membranes tested (CU, PS, CT) caused appreciable intradialytic platelet activation, above all after 15’ and at the end of dialysis sessions, more marked for CU than PS or CT. In particular MPV showed a decrease throughout the session (-5% at 30’ and -9% at 240') while S, ßTG and PF4 peripheral blood levels showed a significant increase at the same intervals with CU membrane. Lastly coagulative and fibrinolytic parameters showed no significant differences among any of the membranes tested.

Functional expression of CCR1, CCR3, CCR4, and CXCR4 chemokine receptors on human platelets

Blood ◽  
2000 ◽  
Vol 96 (13) ◽  
pp. 4046-4054
Author(s):  
Kenneth J. Clemetson ◽  
Jeannine M. Clemetson ◽  
Amanda E. I. Proudfoot ◽  
Christine A. Power ◽  
Marco Baggiolini ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Messenger Rna ◽  
Chemokine Receptors ◽  
Polyclonal Antibodies ◽  
Adenosine Diphosphate ◽  
Functional Expression ◽  
Human Platelets ◽  
Platelet Factor ◽  
Platelet Surface ◽  
Stromal Cell Derived Factor

Platelets are known to contain platelet factor 4 and β-thromboglobulin, α-chemokines containing the CXC motif, but recent studies extended the range to the β-family characterized by the CC motif, including RANTES and Gro-α. There is also evidence for expression of chemokine receptors CCR4 and CXCR4 in platelets. This study shows that platelets have functional CCR1, CCR3, CCR4, and CXCR4 chemokine receptors. Polymerase chain reaction detected chemokine receptor messenger RNA in platelet RNA. CCR1, CCR3, and especially CCR4 gave strong signals; CXCR1 and CXCR4 were weakly positive. Flow cytometry with specific antibodies showed the presence of a clear signal for CXCR4 and weak signals for CCR1 and CCR3, whereas CXCR1, CXCR2, CXCR3, and CCR5 were all negative. Immunoprecipitation and Western blotting with polyclonal antibodies to cytoplasmic peptides clearly showed the presence of CCR1 and CCR4 in platelets in amounts comparable to monocytes and CCR4 transfected cells, respectively. Chemokines specific for these receptors, including monocyte chemotactic protein 1, macrophage inflammatory peptide 1α, eotaxin, RANTES, TARC, macrophage-derived chemokine, and stromal cell–derived factor 1, activate platelets to give Ca++ signals, aggregation, and release of granule contents. Platelet aggregation was dependent on release of adenosine diphosphate (ADP) and its interaction with platelet ADP receptors. Part, but not all, of the Ca++ signal was due to ADP release feeding back to its receptors. Platelet activation also involved heparan or chondroitin sulfate associated with the platelet surface and was inhibited by cleavage of these glycosaminoglycans or by heparin or low molecular weight heparin. These platelet receptors may be involved in inflammatory or allergic responses or in platelet activation in human immunodeficiency virus infection.

Correlation of Specific Platelet Activation Markers with Carotid Arterial Wall Thickness

1995 ◽  
Vol 74 (03) ◽  
pp. 943-948 ◽  
Author(s):  
Habib M Ghaddar ◽  
Jorge Cortes ◽  
Veikko Salomaa ◽  
Jeremy D Kark ◽  
C Edward Davis ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Platelet Activation ◽  
Wall Thickness ◽  
Arterial Wall ◽  
White Men ◽  
Basic Question ◽  
Activation Markers ◽  
Platelet Factor ◽  
Arterial Wall Thickness ◽  
Carotid Arterial

SummaryMany studies have shown inereased platelet activation in patients with coronary artery, cerebrovascular and peripheral vascular diseases. However, the temporal relationship between platelet activation and arterial atherosclerosis is unclear. To answer this basic question, we measured the plasma concentrations of two specific platelet activation markers, β-thromboglobulin (βTG) and platelet factor 4 (PF4) in 459 cases with increased carotid arterial wall thickness and 459 age-, sex- and race-matched controls selected from a cohort of 15,800 men and women, aged 45-64 who participated in the Atherosclerosis Risk in Communities Study. These participants had no acute vascular symptoms or known cardiovascular disease. The mean values of βTG and PF4 were significantly higher in cases than in controls. However, when analyzed by quartiles using conditional logistic regression, only βTG exhibited a significant association with carotid wall thickness, while PF4 did not. The odds ratio (OR) determined by multivariate logistic regression analysis was significantly higher for the uppermost quartile of βTG (OR=1.7, 95% Cl 1.1-2.5) compared to the lower 3 quartiles. This OR was 2.3 in white men (95% Cl 1.2-4.2), 1.4 in white women (95% Cl 0.6-3.0) and 1.0 in blacks (95% Cl 0.4-2.5).This study indicates that plasma βTG may be useful as a marker for early atherosclerosis in middle aged adults, particularly in white men. It also suggests that platelet activation has an independent role in the pathogenesis of atherosclerosis, although the possibility that this may be a response to carotid atherosclerosis cannot be excluded.

scholarly journals Platelet Counts and Platelet Activation Markers in Obese Subjects

2008 ◽  
Vol 2008 ◽  
pp. 1-6 ◽  
Author(s):  
Dorit Samocha-Bonet ◽  
Dan Justo ◽  
Ori Rogowski ◽  
Nili Saar ◽  
Subchi Abu-Abeid ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Platelet Activation ◽  
Annexin V ◽  
High Sensitivity ◽  
Serum Levels ◽  
Normal Weight ◽  
Morbidly Obese ◽  
Activation Markers ◽  
Platelet Counts ◽  
Hs Crp

Objective. In this work we studied the correlation between platelet count, platelet activation, and systemic inflammation in overweight, obese, and morbidly obese individuals.Methods and subjects. A total of 6319 individuals participated in the study. Complete blood counts, high sensitivity C-reactive protein (hs-CRP) serum levels, and body mass index (BMI) were measured during routine checkups. Platelet activation markers were studied among 30 obese (BMI = 41 8 kg/m2) and 35 nonobese (BMI = 24 3 kg/m2) individuals. Platelet activation status was evaluated by flow cytometry using specific antibodies against the activated platelet membrane glycoprotein IIb/IIIa, p-selectin (CD-62 p), and binding of Annexin-V to platelet anionic phospholipids.Results. Overweight, obese, and morbidly obese females had significantly elevated platelet counts () compared with normal-weight females. No significant elevation of platelet counts was observed in the male subgroups. A significant age adjusted correlation between BMI and platelet counts () was found among females. This correlation was attenuated () after adjustment for hs-CRP concentrations. The flow cytometry analysis of platelets showed no significant differences in activation marker expression between nonobese and obese individuals.Discussion. Obesity may be associated with elevated platelet counts in females with chronic inflammation. Obesity is not associated with increased platelet activation.

Aspirin-Responsive, Migraine-Like Transient Cerebral and Ocular Ischemic Attacks and Erythromelalgia in JAK2V617F-Positive Essential Thrombocythemia and Polycythemia Vera

2014 ◽  
Vol 133 (1) ◽  
pp. 56-63 ◽  
Author(s):  
Jan Jacques Michiels ◽  
Zwi Berneman ◽  
Alain Gadisseur ◽  
King H. Lam ◽  
Hendrik De Raeve ◽  
...  
Keyword(s):  
Polycythemia Vera ◽  
Platelet Activation ◽  
Essential Thrombocythemia ◽  
Ex Vivo ◽  
Time Lapse ◽  
Blurred Vision ◽  
Activation Markers ◽  
Platelet Factor ◽  
Cox 1

Migraine-like cerebral transient ischemic attacks (MIAs) and ocular ischemic manifestations were the main presenting features in 10 JAK2V617F-positive patients studied, with essential thrombocythemia (ET) in 6 and polycythemia vera (PV) in 4. Symptoms varied and included cerebral ischemic attacks, mental concentration disturbances followed by throbbing headaches, nausea, vomiting, syncope or even seizures. MIAs were frequently preceded or followed by ocular ischemic events of blurred vision, scotomas, transient flashing of the eyes, and sudden transient partial blindness preceded or followed erythromelalgia in the toes or fingers. The time lapse between the first symptoms of aspirin-responsive MIAs and the diagnosis of ET in 5 patients ranged from 4 to 12 years. At the time of erythromelalgia and MIAs, shortened platelet survival, an increase in the levels of the platelet activation markers β-thromboglobulin and platelet factor 4 and also in urinary thromboxane B2 were clearly indicative of the spontaneous in vivo platelet activation of constitutively JAK2V617F-activated thrombocythemic platelets. Aspirin relieves the peripheral, cerebral and ocular ischemic disturbances by irreversible inhibition of platelet cyclo-oxygenase (COX-1) activity and aggregation ex vivo. Vitamin K antagonist, dipyridamole, ticlopidine, sulfinpyrazone and sodium salicylate have no effect on platelet COX-1 activity and are ineffective in the treatment of thrombocythemia-specific manifestations of erythromelalgia and atypical MIAs. If not treated with aspirin, ET and PV patients are at a high risk of major arterial thrombosis including stroke, myocardial infarction and digital gangrene.

Increased platelet aggregation and in vivo platelet activation after granulocyte colony-stimulating factor administration

2011 ◽  
Vol 105 (04) ◽  
pp. 655-662 ◽  
Author(s):  
Alexander Spiel ◽  
Johann Bartko ◽  
Michael Schwameis ◽  
Christa Firbas ◽  
Jolanta Siller-Matula ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Controlled Trial ◽  
Adenosine Diphosphate ◽  
Thrombin Receptor ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Neutrophil Recovery ◽  
Stimulating Factor

SummaryGranulocyte colony-stimulating factor (G-CSF) stimulates the bone marrow to produce granulocytes and stem cells and is widely used to accelerate neutrophil recovery after chemotherapy. Interestingly, specific G-CSF receptors have been demonstrated not only on myeloid cells, but also on platelets. Data on the effects of G-CSF on platelet function are limited and partly conflicting. The objective of this study was to determine the effect of G-CSF on platelet aggregation and in vivo platelet activation. Seventy-eight, healthy volunteers were enrolled into this randomised, placebo-controlled trial. Subjects received 5 μg/kg methionyl human granulocyte colony-stimulating factor (r-metHuG-CSF, filgrastim) or placebo subcutaneously for four days. We determined platelet aggregation with a whole blood impedance aggregometer with various, clinically relevant platelet agonists (adenosine diphosphate [ADP], collagen, arachidonic acid [AA], ristocetin and thrombin receptor activating peptide 6 [TRAP]). Filgrastim injection significantly enhanced ADP (+40%), collagen (+60%) and AA (+75%) -induced platelet aggregation (all p<0.01 as compared to placebo and p<0.001 as compared to baseline). In addition, G-CSF enhanced ristocetin-induced platelet aggregation (+18%) whereas TRAP-induced platelet aggregation decreased slightly (-14%) in response to filgrastim. While baseline aggregation with all agonists was only slightly but insignificantly higher in women than in men, this sex difference was enhanced by G-CSF treatment, and became most pronounced for ADP after five days (p<0.001). Enhanced platelet aggregation translated into a 75% increase in platelet activation as measured by circulating soluble P-selectin. G-CSF enhances platelet aggregation and activation in humans. This may put patients suffering from cardiovascular disease and cancer at risk for thrombotic events.

scholarly journals Low-Level Laser Irradiation Exerts Antiaggregative Effect on Human Platelets Independently on the Nitric Oxide Metabolism and Release of Platelet Activation Markers

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Piotr Rola ◽  
Adrian Doroszko ◽  
Ewa Szahidewicz-Krupska ◽  
Paweł Rola ◽  
Piotr Dobrowolski ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Platelet Aggregation ◽  
Laser Irradiation ◽  
Platelet Activation ◽  
Activation Markers ◽  
Platelet Factor ◽  
Low Level ◽  
Low Level Laser ◽  
Level Laser ◽  
No Bioavailability

Aim. The goal of the study is to develop a model allowing to investigate precisely the effect of low-level laser therapy (LLLT) on platelet aggregation and to verify the hypothesis regarding the role of the nitric oxide (NO) bioavailability and platelet activation markers in modulating platelet aggregation. Methods. A total of 41 healthy volunteers at the age of 21–45 years were investigated. At first, platelet aggregation in response to three agonists (TRAP, ADP, and collagen) was evaluated following previous exposure to different doses of laser radiation (λ = 662 nm) to assess the dose-response effect. Subsequently, plasma levels of platelet activation markers (PF4—platelet factor-4 and sP-selectin) as well as the substrate for nitric oxide synthase, L-arginine, and its competitive inhibitors (ADMA—asymmetric dimethylarginine and SDMA—symmetric dimethylarginine) were measured. Results. All doses of laser irradiation significantly reduced the aggregation. However, the most pronounced effect was observed for 19.7 J/cm2. No significant differences in the levels of platelet activation markers nor in the nitric-oxide-metabolic-pathway compounds between analyzed groups were noted. Conclusions. We have demonstrated in the established in vitro experimental model that the LLLT in a reproducible manner decreases the whole blood platelet aggregation regardless of the NO bioavailability or changes in the platelet activation markers.

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