Comparison of Cationic Propyl Gallate and Adenosine Diphosphate for the Meassurement of Aspirin Effectivity with Optical Aggregometry.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3943-3943 ◽  
Author(s):  
Zuzana Motovska ◽  
Zdenka Sujanova ◽  
Sona Wimmerova ◽  
Jan Ardo ◽  
Marcela Skrakova ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Propyl Gallate ◽  
Treated Patient ◽  
High Sensitivity ◽  
Adenosine Diphosphate ◽  
Close Correlation ◽  
Light Transmittance ◽  
Measured Parameter ◽  
Control Group ◽  
Statistical Parameters

Abstract Background. The goal of our interest is to bring attention to standardisation of the aspirin effectiveness examination in patients profiting from (life)long antithrombotic terapy. Optical platelet aggregation tests have been most widely used. Examination with endogenous inductors of platelet aggregation - thrombin, colagen, arachidonic acid, adenosine diphosphate (ADP) has a low specificity and reproducibility. Aim. To compare a newer inductor of platelets aggregation cationic propyl gallate (CPG) with ADP for the examination of aspirin (ASA) efffectivity with optical aggregometry. Methods. We prospectively enrolled 116 consecutive patiens with a stable cardiovascular disease on ASA 100mg/day for ≥ 1 month. The controll group was formed from 62 healthy volunteers, without antithrombotic treatment. Analysis. We investigated platelet aggregation by optical aggregometry (aggregometer LASER 4x, BIOART). CPG and ADP were added as aggregating agents. The measured parameter were: CPG-slope (this parameter expresses steepness of the aggregation curve and also the speed of aggregation (%/minutes)) and ADP-max (the maximum percent change in light transmittance from baseline). Results. Definition. First, we determined the CPG-slope cut-off value for the definition of ASA-non-effective treated patient. We established it on the ground of CPG-slope values in the control group. The values from controll group followed a normal distribution (test Shapiro - Wilk). We calculated the cut-off value using the 95% - confidence interval. The CPG-slope cut-off value was 79 %/min for ASA-effective treated patient. We marked the patients as ASA-non efffective treated when the CPG-slope was ≥ 79%/min. The same way we used to define the cut-off value for ADP-max. We identified the aspirin treatment as uneffective when the value of ADP-max had been > 62%. Comparison. The values of CPG-slope and ADP-max were in a close correlation in the group of patients treated with aspirin. The correlation index (r = 0,671) was highly significant. By CPG-induced optical aggregation were 33,6% ASA-non-effective treated patients. While using both inductors (CPG, ADP) were the proportion of ASA-non-effective treated patients 25%. By both tests (CPG, ADP) were equally divided 71,6% patients. ASA-non-effective treated patients were more commonly obese (46,2%) with hypertension (94,9%) and hypercholesterolemia (73,7%) and were less commonly treated with statins (30,8%) as the aspirin effective treated patients (42,%, 88,2%, 59,2% resp.42,1%). Conclusion. Meassurement of a platelet aggregation by CPG is reproducible with high sensitivity and specificity. The study has also brought attention to the importance of control the cardiovascular risk factors. Figure. Statistical parameters Figure. Statistical parameters

Abstract 3473: The Effect of Cigarette Smoking on the Antiplatelet Effect of Clopidogrel: The Smokers Paradox

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Paul Gurbel ◽  
Joseph Dichiara ◽  
Kevin P Bliden ◽  
Mark J Antonino ◽  
Lawal Lookman
Keyword(s):  
Platelet Aggregation ◽  
Cigarette Smoking ◽  
Metabolic Activation ◽  
Adenosine Diphosphate ◽  
Platelet Inhibition ◽  
Response Variability ◽  
Light Transmittance ◽  
Prior History ◽  
Platelet Response ◽  
Clopidogrel Therapy

Background: Wide response variability to clopidogrel therapy has been reported. Clopidogrel is a prodrug that requires metabolic activation by hepatic cytochromes (CYP). Cigarette smoking is an inducer of CYP1A2 and may, therefore, enhance the metabolism of clopidogrel. We sought to examine the effect of cigarette smoking on the platelet response to clopidogrel. Methods: Three hundred thirteen consecutive patients undergoing elective coronary stenting were studied. Platelet aggregation (PA) was assessed by light transmittance aggregometry (LTA) stimulated by 5 and 20μ M adenosine diphosphate. One hundred fourteen patients were on chronic clopidogrel therapy, were not reloaded, and had pre-stenting PA measurements. Pre-and post-stenting PA was measured in 199 patients: 60 were loaded with 300mg and 139 were loaded with 600mg. There were 120 current smokers (smoking within 2 weeks of PCI) and 193 non-smokers (no prior history of smoking). Low PA was defined as the lowest two quartiles of 5μM ADP-induced platelet aggregation (≤ 40%). Results: PA was significantly lower (p ≤ 0.008) in smokers on long term chronic clopidogrel treatment (Table ). Relative platelet inhibition (RPI) was higher in smokers treated with either 300mg or 600mg clopidogrel measured by 5 and 20μM ADP-induced PA. In a multivariate analysis, cigarette smoking was an independent predictor of low PA in patients on chronic clopidogrel therapy and in patients loaded with clopidogrel (r=0.3, p=0.0001). Conclusion: Clopidogrel therapy in smokers is associated with increased platelet inhibition and lower aggregation as compared to non-smokers. The mechanism of the smoking effect deserves further study and may be another cause of response variability to clopidogrel. RPI = 100 x ((baseline aggregation-post-treatment aggregation)/(baseline aggregation))

Changes of platelets’ function in preeclampsia

Open Medicine ◽  
2011 ◽  
Vol 6 (6) ◽  
pp. 696-700
Author(s):  
Goran Babic ◽  
Slobodan Novokmet ◽  
Slobodan Jankovic
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Adenosine Diphosphate ◽  
Control Group ◽  
Adenylate Energy Charge ◽  
Cross Sectional ◽  
Blood Samples ◽  
Metabolic Pool ◽  
Aggregation Of Platelets

AbstractIncreased aggregation of platelets during preeclampsia was shown in several studies, yet several others reported no change. The aim of our study was to investigate platelet aggregation in a group of patients suffering from preeclampsia. In a cross-sectional study blood samples were taken from 89 hospitalized patients in the third trimester of pregnancy: 38 were suffering from mild to moderate preeclampsia and 51 patients were without preeclampsia. From the blood samples platelet aggregation, secretion of adenine nucleotides from platelets, concentration of energy-rich adenine compounds and levels of cyclic adenosine-mono-phosphate and cyclic guanosine mono-phosphate in platelets were measured. In the patients with preeclampsia, the adenosine diphosphate threshold for biphasic aggregation [odds ratio (OR):.75; 95% Confidence Interval (CI): 0.55–1.02; p<0.05], total adenine nucleotides concentration in the metabolic pool of platelets (OR:0.99; CI: 0.62–1.57; p<0.01) and cyclic adenosine-mono-phosphate (OR:0.81; CI: 0.57, 1.14; p<0.05) and cyclic guanosine mono-phosphate (OR:.78; CI: 0.55–1.09; p<0.05) levels in platelets were decreased in comparison with the control group, while adenylate energy charge in the metabolic pool of platelets (OR: >100.00; CI: 0.00->100.00; p<0.05) and secretion of adenosine triphosphate (OR:.13; CI: 0.00–14.26; p<0.05) and adenosine diphosphate (OR:.77; CI: 0.08–36.79; p<0.05) were increased. The results of our study show increased activation and aggregation of platelets in pregnant females with preeclampsia.

scholarly journals Effect of alteplase on platelet function and receptor expression

2019 ◽  
Vol 47 (4) ◽  
pp. 1731-1739 ◽  
Author(s):  
Jun Lu ◽  
Peng Hu ◽  
Guangyu Wei ◽  
Qi Luo ◽  
Jianlin Qiao ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Activation ◽  
Platelet Function ◽  
Adenosine Diphosphate ◽  
Receptor Expression ◽  
Light Transmittance ◽  
Dependent Manner ◽  
Clot Retraction ◽  
Platelet Receptors

Objective To investigate the role of alteplase, a widely-used thrombolytic drug, in platelet function. Methods Human platelets were incubated with different concentrations of alteplase followed by analysis of platelet aggregation in response to adenosine diphosphate (ADP), collagen, ristocetin, arachidonic acid or epinephrine using light transmittance aggregometry. Platelet activation and surface levels of platelet receptors GPIbα, GPVI and αIIbβ3 were analysed using flow cytometry. The effect of alteplase on clot retraction was also examined. Results This study demonstrated that alteplase significantly inhibited platelet aggregation in response to ADP, collagen and epinephrine in a dose-dependent manner, but it did not affect ristocetin- or arachidonic acid-induced platelet aggregation. Alteplase did not affect platelet activation as demonstrated by no differences in P-selectin levels and PAC-1 binding being observed in collagen-stimulated platelets after alteplase treatment compared with vehicle. There were no changes in the surface levels of the platelet receptors GPIbα, GPVI and αIIbβ3 in alteplase-treated platelets. Alteplase treatment reduced thrombin-mediated clot retraction. Conclusions Alteplase inhibits platelet aggregation and clot retraction without affecting platelet activation and surface receptor levels.

Smoking and outcomes following guided de-escalation of antiplatelet treatment in acute coronary syndrome patients: a substudy from the randomized TROPICAL-ACS trial

2019 ◽  
Vol 6 (6) ◽  
pp. 372-381 ◽  
Author(s):  
Martin Orban ◽  
Dietmar Trenk ◽  
Tobias Geisler ◽  
Johannes Rieber ◽  
Martin Hadamitzky ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Platelet Aggregation ◽  
Clinical Outcomes ◽  
Smoking Status ◽  
Adenosine Diphosphate ◽  
Antiplatelet Drug ◽  
Control Group ◽  
Antiplatelet Treatment ◽  
Coronary Syndrome ◽  
The Impact

Abstract Aims Prior analyses disclosed variations in antiplatelet drug response and clinical outcomes between smokers and non-smokers, thus the safety and efficacy of any dual antiplatelet therapy (DAPT) de-escalation strategy may differ in relation to smoking status. Hence, we assessed the impact of smoking on clinical outcomes and adenosine diphosphate-induced platelet aggregation following guided de-escalation of DAPT in invasively managed acute coronary syndrome (ACS) patients. Methods and results The multicentre TROPICAL-ACS trial randomized 2610 biomarker-positive ACS patients 1:1 to standard treatment with prasugrel for 12 months (control group) or a platelet function testing guided de-escalation of DAPT. Current smokers (n = 1182) showed comparable event rates between study groups [6.6% vs. 6.6%; hazard ratio (HR) 1.0, 95% confidence interval (CI) 0.64–1.56, P &gt; 0.99]. In non-smokers (n = 1428), a guided DAPT de-escalation was associated with a lower 1-year incidence of the primary endpoint [cardiovascular death, myocardial infarction, stroke, or bleeding ≥ Grade 2 according to Bleeding Academic Research Consortium (BARC) criteria] compared with control group patients (7.9% vs. 11.0%; HR 0.71, 95% CI 0.50–0.99, P = 0.048). This reduction was mainly driven by a lower rate of BARC ≥ Grade 2 bleedings (5.2% vs. 7.7%; HR 0.68, 95% CI 0.45–1.03, P = 0.066). There was no significant interaction of smoking status with treatment effects of guided DAPT de-escalation (Pint = 0.23). Adenosine diphosphate-induced platelet aggregation values were higher in current smokers [median 28 U, interquartile range (IQR: 20–40)] vs. non-smoker [median 24 U (16–25), P &lt; 0.0001] in the control group and in current smokers [median 42 U, IQR (27–68)] vs. non-smoker [median 37 U, IQR (25–55), P &lt; 0.001] in the monitoring group. Conclusion Guided DAPT de-escalation appears to be equally safe and effective in smokers and non-smokers. Regardless of smoking status and especially for those patients deemed unsuitable for 1 year of potent platelet inhibition this DAPT strategy might be used as an alternative antiplatelet treatment regimen.

Is Increased Platelet Aggregation Is a Risk Factor for Cardiovascular Disease in Women With Idiopathic Central Precocious Puberty

2021 ◽  
Author(s):  
Ahmet Bolat ◽  
CENGİZ Zeybek ◽  
ORHAN GÜRSEL ◽  
MEHMET EMRE TAŞÇILAR
Keyword(s):  
Platelet Aggregation ◽  
Precocious Puberty ◽  
Cardiovascular Events ◽  
Platelet Rich Plasma ◽  
Central Precocious Puberty ◽  
Adenosine Diphosphate ◽  
Control Group ◽  
Time Value ◽  
Idiopathic Central Precocious Puberty ◽  
Increased Risk

Abstract BackgroundEarly menarche in girls is associated with an increased risk of cardiovascular events later in life, but the role of platelets in this risk has not been investigated during puberty. Here, we evaluated the effects of idiopathic central precocious puberty (ICPP) on platelet aggregation in platelet-rich plasma samples from female patients. MethodsThe study included 40 girls diagnosed with ICPP between February 2012 and June 2016, and a control group consisting of 30 healthy females. Adenosine diphosphate (ADP) and collagen-induced platelet aggregation were studied with photometric aggregometry. ResultsThere was no difference in the platelet count or volume between girls with ICPP and the control group. In addition, the ADP-induced maximum aggregation time, value, and slope did not significantly differ between the study and control groups (p > 0.05). However, the collagen-induced maximum aggregation time, value, and slope were significantly higher in the study group (p < 0.001). ConclusionsIncreased collagen-induced platelet aggregation was detected in girls with ICPP. Thus, early treatment of ICPP may be important because of the increased risk of cardiovascular events later in life. Extensive studies with more patients are needed to determine the mechanisms of platelet dysfunction in girls with ICPP.

The Dysfunction of Platelets in Paroxysmal Nocturnal Hemoglobinuria

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4532-4532
Author(s):  
Rong Fu ◽  
Yinping Meng ◽  
Yihao Wang ◽  
Hui Liu ◽  
Yi Liu ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Conflicts Of Interest ◽  
Adenosine Diphosphate ◽  
Underlying Mechanism ◽  
Control Group ◽  
Type Ii ◽  
Clinical Tests ◽  
Terminal Complement ◽  
Normal Controls ◽  
D Dimer

Abstract Introduction Thrombosis is one of the most dangerous complications in PNH, which can cause high mortality. However, its underlying mechanism remains unclear. To explore the mechanism of thrombosis in PNH, the function of platelets and complements were investigated in our study. Material and Methods Serum level of terminal complement complex (sC5b-9) was detected by ELISA. The quantities of C5b-9,CD61 and CD62p on the membrane of platelets were detected by flow cytometry. Clinical tests were collected, including D-Dimer and platelet aggregation rates induced by adenosine diphosphate (ADP) and arachidonic acid (ARA). Results The serum sC5b-9 level was significantly lower in the PNH/PNH-AA group than that in the control group (p<0.01). The deposition of C5b-9 on CD59- platelets (17.53%±6.27%) was higher than those on CD59+ platelets in PNH/PNH-AA patients(11.33%±5.03%) and normal controls(10.88%±3.58%) (p<0.01). D-dimer was significantly higher in PNH/PNH-AA patients (485ng/dL) than that in normal controls (311ng/dL)(p<0.05),especially in patients with LDH>1000U/L(789ng/dL). CD61 and CD62p expression on CD59+ platelets in PNH patients (76.87%,39.99%) were significantly lower than those in normal controls(98.41%,64.21%)(p<0.05,p<0.01).CD62p expression on CD59- platelets (40.07%) was significantly lower than normal controls(p<0.01). Platelet aggregation stimulated by agonists ADP (37.54±24.25)% and ARA (24.60%) were lower in the PNH/PNH-AA group than that in the control group(59.20±23.30)%, (14.54%) (p < 0.05). Interestingly,CD61 expression on CD59+ platelets in PNH patients was higher in the patients with higher type II PNH clone. Conclusions The function of platelets was inversely inhibited,especially CD59+ platelets even if hypercoagulation continuously exists in PNH/PNH-AA. Disclosures No relevant conflicts of interest to declare.

Pharmacodynamic profiles of dual-pathway inhibition with or without clopidogrel vs dual antiplatelet therapy in patients with atherosclerotic disease

2022 ◽  
Author(s):  
Mattia Galli ◽  
Francesco Franchi ◽  
Fabiana Rollini ◽  
Latonya Been ◽  
Patrick Abou Jaoude ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Thrombin Generation ◽  
Thrombus Formation ◽  
Factor Xa ◽  
Adenosine Diphosphate ◽  
Atherosclerotic Disease ◽  
Light Transmittance ◽  
Dual Pathway ◽  
Pathway Inhibition

Aim: Inhibition of thrombin-mediated signaling processes using a vascular dose of rivaroxaban in adjunct to antiplatelet therapy, known as dual-pathway inhibition (DPI), reduces atherothrombotic events in patients with stable atherosclerotic disease. However, there are limited data on the pharmacodynamic (PD) effects of this strategy. Methods and Results: This investigation was conducted in selected cohorts of patients (n=40) with stable atherosclerotic disease enrolled within a larger prospective PD study who were treated with either aspirin plus clopidogrel (DAPT), aspirin plus rivaroxaban 2.5 mg/bid (DPI) or DAPT plus rivaroxaban 2.5 mg/bid. Multiple PD assays assessing of markers of thrombosis were used. PD endpoints included platelet-mediated global thrombogenicity measured by light transmittance aggregometry (LTA) following stimuli with CATF [collagen‐related peptide +adenosine diphosphate (ADP) +tissue factor (TF)], markers of P2Y12 reactivity, markers of platelet aggregation using LTA following several stimuli (arachidonic acid, ADP, collagen, TF, and TRAP), thrombin generation and thrombus formation. There was no difference in platelet-mediated global thrombogenicity between groups. Rivaroxaban significantly reduced thrombin generation and was associated with a trend towards reduced TF-induced platelet aggregation. Clopidogrel-based treatments reduced markers of P2Y12 signaling and TRAP‐induced platelet aggregation. There were no differences between groups on markers of cyclooxygenase‐1 mediated activity. Conclusions: Compared with DAPT, DPI does not result in any differences in platelet-mediated global thrombogenicity, but reduces thrombin generation. These PD observations support that modulating thrombin generation by means of factor Xa inhibition in adjunct to antiplatelet therapy provides effective antithrombotic effects, supporting the efficacy and safety findings of DPI observed in clinical

Effects of vorapaxar on platelet reactivity and biomarker expression in non-ST-elevation acute coronary syndromes

2014 ◽  
Vol 111 (05) ◽  
pp. 883-891 ◽  
Author(s):  
Susan S. Smyth ◽  
David J. Moliterno ◽  
Tyrus L. Rorick ◽  
Tiziano Moccetti ◽  
Marco Valgimigli ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Reactivity ◽  
Adenosine Diphosphate ◽  
Light Transmittance ◽  
Clinical Event ◽  
Thrombin Receptor ◽  
Coronary Syndrome ◽  
Vasp Phosphorylation ◽  
Potent Inhibition ◽  
St Elevation

SummaryVorapaxar is an antagonist of the protease activated receptor-1 (PAR-1), the principal platelet thrombin receptor. The Thrombin Receptor Antagonist for Clinical Event Reduction (TRACER) trial evaluated vorapaxar compared to placebo in non-ST-elevation (NSTE)-acute coronary syndrome (ACS) patients. It was the study′s objective to assess the pharmacodynamic effects of vorapaxar versus placebo that included aspirin or a thienopyridine or, frequently, a combination of both agents in NSTE-ACS patients. In a substudy involving 249 patients, platelet aggregation was assessed by light transmittance aggregometry (LTA) in 85 subjects (41 placebo, 44 vorapaxar) using the agonists thrombin receptor activating peptide (TRAP, 15 μM), adenosine diphosphate (ADP, 20 μM), and the combination of collagen-related peptide (2.5 μg/ml) + ADP (5 μM) + TRAP (15 μM) (CAT). VerifyNow® IIb/IIIa and vasodilator-stimulated phosphoprotein (VASP) phosphorylation assays were performed, and platelet PAR-1 expression, plasma platelet/endothelial and inflammatory biomarkers were determined before and during treatment. LTA responses to TRAP and CAT and VerifyNow results were markedly inhibited by vorapaxar. Maximal LTA response to TRAP (median, interquartile range) 2 hours post loading dose: placebo 68% (53–75%) and vorapaxar 3% (2–6%), p<0.0001. ADP inhibition was greater in the vorapaxar group at 4 hours and one month (p<0.01). In contrast to the placebo group, PAR-1 receptor number in the vorapaxar group at one month was significantly lower than the baseline (179 vs 225; p=0.004). There were significant changes in selected biomarker levels between the two treatment groups. In conclusion, vorapaxar caused a potent inhibition of PAR-1-mediated platelet aggregation. Further studies are needed to explore vorapaxar effect on P2Y12 inhibition, PAR-1 expression and biomarkers and its contribution to clinical outcomes.

Functional impact of high clopidogrel maintenance dosing in patients undergoing elective percutaneous coronary interventions

2008 ◽  
Vol 99 (01) ◽  
pp. 161-168 ◽  
Author(s):  
Esther Bernardo ◽  
Jorge Palazuelos ◽  
Bhaloo Desai ◽  
Ian Weisberg ◽  
Fernando Alfonso ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Maintenance Dose ◽  
Platelet Reactivity ◽  
Adenosine Diphosphate ◽  
Coronary Intervention ◽  
Platelet Inhibition ◽  
Relative Increase ◽  
Light Transmittance ◽  
Functional Impact ◽  
Percutaneous Coronary

SummaryThe currently recommended maintenance dose of clopidogrel is often associated with inadequate platelet inhibition, suggesting the need for a higher dose. The aim of this pilot study was to assess the functional impact of a high (150 mg/day) maintenance dose of clopidogrel in patients undergoing elective percutaneous coronary intervention (PCI).This is a prospective, randomized, platelet function study which was performed in elective PCI patients assigned to treatment with either a 75 mg (n=20) or 150 mg (n=20) daily maintenance dose of clopidogrel for 30 days;afterwards, all patients resumed standard dosing. Platelet aggregation was performed using light transmittance aggregometry following 20 μM and 5 μM adenosine diphosphate (ADP) stimuli 30 days after randomization and 30 days after resuming standard dosing. Patients treated with 150 mg/day clopidogrel had lower 20 μMADP-induced platelet aggregation compared to patients on 75 mg/day (52.1±9% vs. 64.0±8%; p<0.001; primary endpoint).The dose-dependent effect was confirmed by the absolute and relative increase in platelet aggregation after resuming standard dosing (p<0.001). No changes were observed in patients randomized to standard dosing. Parallel findings were observed following 5 μM ADP stimuli for all assessments. A broad variability in clopidogrel-induced antiplatelet effects was observed irrespective of dosing. In conclusion, a 150 mg/day maintenance dose regimen of clopidogrel is associated with reduced platelet reactivity and enhanced platelet inhibition compared to that achieved with the currently recommended 75 mg/day in patients undergoing elective PCI.

Aspirin failure in patients presenting with acute cerebrovascular ischaemia

2011 ◽  
Vol 106 (08) ◽  
pp. 240-247 ◽  
Author(s):  
Saeed H. M. Halawani ◽  
David J. P. Williams ◽  
John Webster ◽  
Michael Greaves ◽  
Isobel Ford
Keyword(s):  
Platelet Aggregation ◽  
Ischaemic Stroke ◽  
High Sensitivity ◽  
Adenosine Diphosphate ◽  
Platelet Inhibition ◽  
Antiplatelet Drug ◽  
Platelet Response ◽  
Reactive Protein ◽  
Fibrinogen Binding ◽  
Von Willebrand

SummaryAspirin is the most commonly used antiplatelet drug for prevention of ischaemic stroke. In order to determine the prevalence and nature of aspirin failure, we studied 51 adults admitted with suspected ischaemic stroke and already prescribed daily aspirin. Within 48 hours (h) of onset, blood and urine samples were collected to assess platelet aggregation, activation and aspirin response by a range of methods. All tests were then repeated on a second sample taken 24 h after witnessed administration of 75 mg or 150 mg aspirin. At entry to the study, incomplete response to aspirin, measured by arachidonic acid (AA)-stimulated platelet aggregation, was found in 43% of patients. Following in-hospital aspirin administration, there was a significant decrease in AA-aggregation (p=0.001) suggesting poor adherence to therapy prior to admission. However, residual aggregation (10–15%) persisted in 11 subjects – suggesting alternative causes. In incomplete responders on admission, platelet aggregation with adenosine diphosphate (ADP) was significantly higher compared with responders (p<0.05) but there were no significant differences in collagen aggregation, platelet fibrinogen binding or P-selectin expression, plasma von Willebrand factor, fibrinogen, high-sensitivity C-reactive protein, or the urinary metabolite, 11-dehydro-TxB2. Incomplete platelet inhibition is common around the time of acute cerebrovascular ischaemic events in patients prescribed aspirin. Up to 50% of these observations appear due to incomplete adherence to aspirin therapy. Intervention studies are required to determine the clinical relevance of measured platelet response to aspirin in terms of outcome, and the effectiveness of improved pharmacotherapy for stroke prevention.

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