Impaired ristocetin–induced Platelet Aggregation in Whole Blood Assessed with a Multiplate© Analyser Suggests a New Mechanism of Antiplatelet Effect of Aspirin and Clopidogrel,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3362-3362 ◽  
Author(s):  
Annick Ankri ◽  
Anne Baranger ◽  
Isabelle Martin-Toutain ◽  
Yves Samson ◽  
Jean-Philippe Collet ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Whole Blood ◽  
Dual Antiplatelet Therapy ◽  
Blood Platelet ◽  
Normal Control Group ◽  
Control Group ◽  
Irreversible Inhibitor ◽  
Blood Samples ◽  
Before And After

Abstract Abstract 3362 The five channel computerized Whole Blood Aggregation instrument (Multiple Platelet Function Analyzer or Multiplate®), assesses platelet aggregation based on a modified whole blood impedance aggregation method. It permits platelet aggregation to be measured after adding commonly used agonists as arachidonic acid (ASPItest), ADP (ADPtest), collagen (COLtest), ristocetin (RISTOtest) and TRAP (TRAPtest), by detecting changes in electrical resistance in whole blood. Instrument handling is easy. Results are available within 9 minutes. Our objective was to evaluate the effect of aspirin (irreversible inhibitor of COX-1) and/or clopidogrel (irreversible inhibitor of the platelet P2Y12 receptor) on whole blood platelet aggregations induced by the 5 agonists using the Multiplate® in patients treated by aspirin and/or clopidogrel. Patients and controls. Two hundred and twenty two consecutive patients were recruited: 83 treated daily by 75 or 100 mg aspirin (group A); 42 treated daily by 75 mg clopidogrel (group C); 70 treated daily by 75 or 100 mg aspirin plus 75mg clopidogrel (group AC) and 27 who were daily on 100 mg aspirin before coronary intervention were tested 12 h after dual loading dose of aspirin between 75 et 500 mg and 75 to 900 mg clopidogrel according to cardiologists' recommendations: group loading aspirin-clopidogrel (LAC). Among group AC, 23 consecutive patients requiring intracranial stent placement of supra-aortic vessel were tested first at preoperative, without antiplatelet therapy, then 1 month after initiation of daily continuous dual antiplatelet therapy by 100 mg aspirin + 75mg clopidogrel. Ninety six volunteers without pathology or drugs influencing platelet functions constitute the normal control group (N). Blood samples. All patient and controls gave informed consent prior to blood sampling. Blood samples were collected by venipuncture or obtained from the arterial sheath directly into vacutainer Becton Dickinson tube containing 0.129M sodium citrate. Results. Patients under medication showing lower aggregation values than the arbitrary cutoff (fifth percentile of the aggregation in the normal control group was selected for each agonist) were classified as abnormal and having biological sensitivity to the agonist tested. Aggregation values above the cutoff with ASPItest or ADPtest for patients on antiplatelet agents were considered as a persistent platelet aggregation and as a biological resistance. According to the literature, resistance to aspirin was found in 8.6% of patients under aspirin alone or in combination and in 25.1% of patients under clopidogrel alone or in combination. Our main result shows an inhibition in platelet aggregation using ristocetin as agonist for 73.9% of patients taking aspirin alone, for 27.8% on clopidogrel and in 94% of patients receiving combination of the 2 drugs. This inhibition appears after aspirin + clopidogrel intake as we could observe it among patients candidates for intracranial stent placement tested before and after one month of treatment by dual antiplatelet therapy. This effect is not related to von Willebrand Factor (vWF) deficiency since the measurement of ristocetin cofactor activity, and vWF antigen carried out among 14 patients exhibiting an inhibition in whole blood platelet aggregation using RISTOtest were normal and unchanged before and after antiplatelet treatment. VWF is essential platelet-to-platelet interactions which is promoted by the binding of VWF with platelet-receptor glycoprotein IbIX (GPIbIX). Our results suggest: 1) aspirin inhibits the interaction of vWF to GP IbIX. This inhibition appears increased by the association of clopidogrel to aspirin. 2) a new mechanism of inhibition of the platelet function GPIbIX-vWF dependant conjointly to inhibition of cyclooxygenase by aspirin and P2Y12 receptor by clopidogrel.Table I:Biological sensibility according to the five tests (%) in the 4 groups testedGroup (n)ASPItestADPtestCOLtestRISTOtestTRAPtestA (83)84.312.038.373.98.4C (42)38.176.219.227.816.7AC (70)90.074.348.288.222.9LAC (27)100.074.163.0100.029.6 Disclosures: No relevant conflicts of interest to declare.

MEASURING WHOLE BLOOD PLATELET AGGREGATION AND ATP-RELEASE WITH A CHRONO-LOG WHOLE BLOOD LUMI-AGGREGOMETER: EFFECT OF STORAGE TIME OF BLOOD SAMPLES

1987 ◽  
Author(s):  
F C Sieders ◽  
A C v Houwelingen ◽  
G Hornstra
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Storage Time ◽  
Bleeding Time ◽  
Atp Release ◽  
Blood Platelet ◽  
Blood Samples ◽  
Before And After ◽  
Positive Correlations ◽  
Blood Platelet Aggregation

The influence of storing blood for either one or two hours after blood sampling, on whole blood platelet aggregation and ATP-release was measured with a Chrono-log whole blood lumi-aggregometer, in 21 healthy male volunteers. Storage of blood samples, gently revolving at 37 °C in an incubator for one hour, caused a significant increase in aggregation and release as compared with results obtained immediately after sampling. After two hours' storage, the values had returned to their initial levels.Significant positive correlations were seen between values obtained before and after storage of blood, and between various aggregation and release parameters. In this study, bleeding time nor hematocrit values were significantly correlated with the aggregation and release parameters. The considerable influence of storage time on whole blood platelet aggregation and ATP-release underlines the importance of performing these determinations immediately after sampling, or possibly after a standardized storage time. Otherwise, comparison of results -obtained either in clinical situations or in trials - will increase variability as a result of which false conclusions may be obtained. This will be illustrated in a small trial using paracetamol.

Response to Dual Antiplatelet Therapy Does Not Impact Bleeding Risks in Patients Undergoing Oral Surgery after Acute Coronary Syndromes

Cardiology ◽  
2015 ◽  
Vol 132 (2) ◽  
pp. 119-123 ◽  
Author(s):  
Damian Dudek ◽  
Wiktor Kuliczkowski ◽  
Jacek Kaczmarski ◽  
Joanna Wiechec ◽  
Edyta Reichman-Warmusz ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Acute Coronary Syndromes ◽  
Dual Antiplatelet Therapy ◽  
Oral Surgery ◽  
Antiplatelet Agent ◽  
Real Life ◽  
Control Group ◽  
Platelet Activity ◽  
Coronary Syndromes

Introduction: Oral surgery (OS) in patients on antecedent dual antiplatelet therapy (DAPT) may be associated with extra bleeding risks. Monitoring platelet activity in such patients may be beneficial for safety when performing OS. Objectives: The aim of this study was to assess whether platelet function during DAPT impacted the risk of bleeding following OS in patients with acute coronary syndromes (ACS). Patients and Methods: Patients who required OS on top of DAPT with aspirin and clopidogrel (n = 55) for invasively treated ACS were included. The control group (n = 33) consisted of patients who underwent OS with no antiplatelet agent. Platelet aggregation before OS was assessed with a Multiplate® analyzer. Bleeding during OS and at days 1, 3, 7 and 10 after surgery was serially evaluated. Results: All 88 patients completed the study. An incomplete response to aspirin or clopidogrel was observed in 43.6% of the patients. In 11% of the cases, an excessive response to clopidogrel was demonstrated. No excessive bleeding upon OS was exhibited in either group during the entire follow-up. Platelet aggregation values and the use of DAPT did not impact the performance of OS. Conclusion: Therapy with clopidogrel and aspirin after ACS does not seem to increase the risk of real-life bleeding following OS, regardless of the platelet activity response to DAPT.

BLOOD PLATELET FUNCTION OF HYPERLIPIDEMIC PATIENTS TREATED WITH BEZAFIBRATE

1987 ◽  
Author(s):  
A Borowska
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Blood Platelet ◽  
Clofibric Acid ◽  
New Drugs ◽  
Control Group ◽  
Lipid Levels ◽  
Before And After ◽  
600Mg Daily ◽  
Layer Chromatography

Platelets from patients with hyperlipoproteinemia (HLP) are more sensitive to some aggregating agents than platelets from normal persons.On the other hand, it is known that from 15% to 20% of patients with coronary heart disease have primary or secondary HLP.The progress of the knowledge in this field has been expressed in production of the new drugs diminishing HLP.Be-zafibrate is a new derivative of clofibric acid,which has been used in the treatment of HLP.The purpose of our study was and assessment of the effect of bezafi-brate on platelet aggregation and thromboxane (TXB2) generation.The experiments were carried out in 18 patients (7 women and 11 men),aged 32-60 (mean 46 years) with type Ila HLP.The control group of consisted of 10 healthy volunteers.For 6 weeks the patients with HLP were given bezafibrate (Bezalip-Boehringer Mannheim) 600mg daily in divided doses and were taking the same diet as before the treatment.Blood platelet aggregation and 14C arachidonic acid (AA) conversion to thromboxane in washed platelets (using thin-layer-chromatography) were determined before and after bezafibrate administration. The obtained results are presented in the table (mean±S.E.).It is concluded that the main arteriosclerosis-protecting bezafibrate action lies not only in decreasing of lipid levels in serum, but also in normalization of platelet function.

Preservation of collagen-induced whole blood platelet aggregation by tranexamic acid therapy in primary cardiac valve surgery

Perfusion ◽  
2000 ◽  
Vol 15 (6) ◽  
pp. 507-513 ◽  
Author(s):  
Tetsuya Miyashita ◽  
Takahiko Kamibayashi ◽  
Yoshihiko Ohnishi ◽  
Junjiro Kobayashi ◽  
Masakazu Kuro
Keyword(s):  
Cardiac Surgery ◽  
Platelet Aggregation ◽  
Tranexamic Acid ◽  
Platelet Function ◽  
Whole Blood ◽  
Blood Platelet ◽  
Acid Group ◽  
Valve Surgery ◽  
Control Group ◽  
Blood Platelet Aggregation

Haemostatic disorder is one of the most common complications following cardiac surgery with cardiopulmonary bypass (CPB). Tranexamic acid reduces blood loss and allogeneic blood transfusion requirement in cardiac surgery. It had been thought that tranexamic acid inhibited fibrinolysis alone following CPB. In the present study, the haemostatic effects of tranexamic acid (20 mg/kg body weight bolus after induction of anaesthesia followed by continuous infusion at 2 mg/kg/h), including fibrinolysis and platelet function, were investigated in 22 patients (tranexamic acid group n = 12; control group n = 10) undergoing primary cardiac valve surgery. Fibrinolysis following CPB was reduced significantly in the tranexamic acid group. Following protamine administration, the reduction of collagen-induced whole blood platelet aggregation was mitigated significantly in the tranexamic acid group compared with the control group (36% reduction in the tranexamic acid group vs 58% in the control group; p = 0.011), although platelet counts did not differ between the two groups. In conclusion, tranexamic acid not only inhibits fibrinolysis directly, but also may preserve platelet function following CPB.

scholarly journals Whole Blood Platelet Aggregation Test and Prediction of Hemostatic Difficulty After Tooth Extraction in Patients Receiving Antiplatelet Therapy

2017 ◽  
Vol 24 (1) ◽  
pp. 151-156 ◽  
Author(s):  
Yasushi Nagao ◽  
Rikuo Masuda ◽  
Akane Ando ◽  
Mutsumi Nonaka ◽  
Akiko Nishimura ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Whole Blood ◽  
Tooth Extraction ◽  
Point Of Care ◽  
Adenosine Diphosphate ◽  
Blood Platelet ◽  
Test Results ◽  
Test Sensitivity ◽  
Whole Blood Aggregometry

When patients on antiplatelet therapy (APT) require minor invasive surgery, APT is usually continued to limit the risk of thrombosis. However, the possibility of hemostatic difficulties necessitates the monitoring of platelet aggregation to prevent unexpected bleeding. We examined whether whole blood aggregometry as a point-of-care testing (POCT) could be useful as a tool for predicting hemostatic difficulties. Sixty-five patients receiving APT and 15 patients who were not receiving APT were enrolled in the present study; all patients were scheduled to undergo a tooth extraction. Whole blood samples were obtained and were examined using multiple electrode aggregometry. The aggregometry was performed using arachidonic acid (AA), adenosine diphosphate (ADP), and thrombin receptor activating peptide. Hemostatic difficulty was defined as a need for more than 10 minutes of compression to achieve hemostasis. The AA test results were significantly lower in patients treated with aspirin (control: 97.7 [29.0] U, aspirin: 14.5 [7.2] U, P < .001). The ADP test results were also significantly lower in patients treated with a P2Y12 inhibitor (control: 77.7 [21.7] U, P2Y12 inhibitor: 37.3 [20.4] U, P < .01). Six of the examined cases exhibited hemostatic difficulties. The cutoff values for the prediction of hemostatic difficulty were 16.5 U for the AA test (sensitivity, 0.833; specificity, 0.508) and 21 U for the ADP test (sensitivity, 0.847; specificity, 0.500). Our study showed that whole blood aggregometry was useful as a POCT for the prediction of hemostatic difficulties after tooth extraction in patients receiving APT.

scholarly journals EFFECTS OF ANTIPLATELET TREATMENT ON THROMBOCYTIC AGGREGATING ABILITY IN PATIENTS WITH ISCHEMIC HEART DISEASE AND IN COMBINATION WITH TYPE 2 DIABETES

2019 ◽  
pp. 11-17
Author(s):  
Olena Karpenko
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Cardiovascular Events ◽  
Dual Antiplatelet Therapy ◽  
Control Group ◽  
Antiplatelet Treatment ◽  
Effective Prevention ◽  
Group I

The number of diabetes mellitus (DM) is steadily increasing and such a rapid increase will lead to an increase in cardiovascular events, mainly due to coronary heart disease (CHD), in which coronary atherosclerosis and its progression is one of the causes of mortality. The course of atherosclerosis is closely related to the state of the hemostasis system. The basis for the development of atherosclerosis is arterial thrombosis, with the activation of platelets playing a leading role in the disruption of hemostasis in coronary heart disease, increasing the risk of thrombotic complications. At present, data on the relationship of different hemostasis units in coronary heart disease in combination with diabetes are mixed, complicating the prognosis of adverse effects taking into account the status of platelet hemostasis. Given the relevance of the topic, the purpose of this study was to evaluate the spontaneous and induced platelet aggregation in patients with various forms of acute coronary heart disease (ACHD) and to identify features of platelet aggregation activity in the combination of ACHD and DM.Adequate reduction of platelet functional activity in patients with coronary heart disease receiving antiplatelet treatment is the basis for effective prevention of thrombus formation in the coronary vessels and the development of adverse cardiovascular events. However, according to the data obtained, the highest activation of platelet hemostasis was observed in the group of patients with ACHD in combination with DM, which showed a significant (relative to the control group) increase in the level of spontaneous platelet aggregation by 4.6 times. At the same time, the percentage of patients who had increased the above indicators was significantly lower in the group of patients with ACHD without disorders of carbohydrate metabolism. In patients with ACHD in combination with DM, activation of the spontaneous aggregation rate was also observed, which accelerated the formation of aggregates by 30% compared with the isolated ACHD group (p <0.05). In the study of induced platelet aggregation, it was taken into account that patients in both groups received dual antiplatelet therapy, which had a significant effect on their activity. However, the expected inhibition of aggregation potential was revealed only by the action of arachidonic acid (AA). Thus, the degree of platelet aggregation in response to AA in group I was 1.9 times significantly lower than the control values ​​of 18.8% [12,1; 26,4], in group II - 1,5 times and made 24,38% [21,5; 32.9] (p <0.001 for both cases). According to ADP-induced platelet aggregation, the effect of antiplatelet drugs was less effective. Thus, a moderate decrease in the degree of ADP-aggregation was observed only in the group of isolated ACHD, whose indicators were 1.42 times lower than in the control group (p <0.01). Thus, dual antiplatelet therapy was accompanied by an effective reduction in platelet function only in the group of patients with isolated ACHD.

Effect of Dipyridamole on Spontaneous Platelet Aggregation in Whole Blood Decreases with the Time After Venepuncture: Evidence for the Role of ADP

1987 ◽  
Vol 58 (02) ◽  
pp. 744-748 ◽  
Author(s):  
A R Saniabadi ◽  
G D O Lowe ◽  
J C Barbenel ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Correlation Coefficient ◽  
Whole Blood ◽  
Blood Platelet ◽  
Inhibitory Effect ◽  
Time Interval ◽  
Adp Receptor ◽  
Spontaneous Platelet Aggregation

SummarySpontaneous platelet aggregation (SPA) was studied in human whole blood at 3, 5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter, SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of citrated blood at 37° C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10 μM at each time interval; (b) 0.5-100 μM at 3 and 30 minutes and (c) 15 μM in combination with 100 μM adenosine, 8 μM 2-chloroadenosine (2ClAd, an ADP receptor blocker) and 50 μM aspirin. There was a rapid decrease in the inhibitory effect of Dipy with the time after venepuncture; the correlation coefficient was -0.533. At all the concentrations studied, Dipy was more effective at 3 minutes than at 30 minutes after venepuncture. A combination of Dipy with adenosine, 2ClAd or aspirin was a more effective inhibitor of SPA than either drug alone. However, when 15 μM Dipy and 10 μM Ad were added together, the inhibitory effect of Dipy was not increased significantly, suggesting that Dipy inhibits platelet aggregation independent of Ad. The increase in SPA with the time after venepuncture was abolished when blood was taken directly into the anticoagulant containing 5 μM 2ClAd. It is suggested that ADP released from the red blood cells is responsible for the increased platelet aggregability with the time after venepuncture and makes a serious contribution to the artifacts of in vitro platelet function studies.

Platelet Aggregation in Whole Blood: The Role of Thromboxane A2 and Adenosine Diphosphate

1985 ◽  
Vol 54 (03) ◽  
pp. 612-616 ◽  
Author(s):  
A J Carter ◽  
S Heptinstall
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Adenosine Diphosphate ◽  
Blood Platelet ◽  
Thromboxane B2 ◽  
Lipoxygenase Inhibitor ◽  
Thromboxane Synthase Inhibitor ◽  
Synthase Inhibitor

SummaryThe platelet aggregation that occurred in whole blood in response to several aggregating agents (collagen, arachidonic acid, adenosine diphosphate, adrenaline and thrombin) was measured using an Ultra-Flo 100 Whole Blood Platelet Counter. The amounts of thromboxane B2 produced were measured by radioimmunoassay. The effects of various inhibitors of thromboxane synthesis and the effects of apyrase, an enzyme that destroys adenosine diphosphate, were determined.Platelet aggregation was always accompanied by the production of thromboxane B2, and the amounts produced depended on the nature and concentration of the aggregating agent used. The various inhibitors of thromboxane synthesis - aspirin and flurbiprofen (cyclo-oxygenase inhibitors), BW755C (a cyclo-oxygenase and lipoxygenase inhibitor) and dazoxiben (a selective thromboxane synthase inhibitor) - did not markedly inhibit aggregation. Results obtained using apyrase showed that adenosine diphosphate contributed to the aggregation process, and that its role must be acknowledged when devising means of inhibiting platelet aggregation in vivo.

Blood platelet-derived microparticles release and bubble formation after an open-sea air dive

2012 ◽  
Vol 37 (5) ◽  
pp. 888-892 ◽  
Author(s):  
Jean-Michel Pontier ◽  
Emmanuel Gempp ◽  
Mihaela Ignatescu
Keyword(s):  
Platelet Aggregation ◽  
Decompression Sickness ◽  
Blood Platelets ◽  
Water Immersion ◽  
Bubble Formation ◽  
Blood Platelet ◽  
Field Conditions ◽  
Control Group ◽  
Open Sea ◽  
Experimental Group

Bubble-induced platelet aggregation offers an index for evaluating decompression severity in humans and in a rat model of decompression sickness. Endothelial cells, blood platelets, or leukocytes shed microparticles (MP) upon activation and during cell apoptosis. The aim was to study blood platelet MP (PMP) release and bubble formation after a scuba-air dive in field conditions. Healthy, experienced divers were assigned to 1 experimental group (n = 10) with an open-sea air dive to 30 msw for 30 min and 1 control group (n = 5) during head-out water immersion for the same period. Bubble grades were monitored with a pulsed doppler according to Kissman Integrated Severity Score (KISS). Blood samples for platelet count (PC) and PMP (annexin V and CD41) were taken 1 h before and after exposure in both groups. The result showed a decrease in post-dive PC compared with pre-dive values in experimental group with no significant change in the control group. We observed a significant increase in PMP values after the dive while no change was revealed in the control group. There was a significant positive correlation between the PMP values after the dive and the KISS bubble score. The present study highlighted a relationship between the post-dive decrease in PC, platelet MP release, and bubble formation. Release of platelet MPs could reflect bubble-induced platelet aggregation and could play a key role in alteration of the coagulation. Further studies must investigate endothelial and leukocyte MP release in the same field conditions.

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