Light Transmittance Aggregometry Induced by Different Concentrations of Adenosine Diphosphate to Monitor Clopidogrel Therapy: A Methodological Study

2011 ◽  
Vol 33 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Rita Paniccia ◽  
Emilia Antonucci ◽  
Niccolò Maggini ◽  
Marco Miranda ◽  
Eloisa Romano ◽  
...  
Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Paul Gurbel ◽  
Joseph Dichiara ◽  
Kevin P Bliden ◽  
Mark J Antonino ◽  
Lawal Lookman

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))


Author(s):  
Christina C. Rolling ◽  
Julia Tomada ◽  
Andreas M. Frölich ◽  
Brigitte Holst ◽  
Katharina Holstein ◽  
...  

AbstractObjectivesDual platelet inhibition is commonly used for prevention of cardiovascular events in patients undergoing neuroendovascular procedures. Non-responsiveness to platelet inhibitors may be associated with adverse outcomes. The aim of this study was to evaluate the reliability of the platelet function analyzer PFA-100® in comparison to light transmittance aggregometry (LTA) for monitoring clopidogrel and acetylsalicylic acid (ASA) non-responsiveness in a cohort of patients treated for intracranial aneurysm or cranial artery stenosis.MethodsNon-responsiveness to clopidogrel and ASA was assessed by LTA using adenosine diphosphate (ADP) and arachidonic acid and by PFA-100® with the ADP/prostaglandin E1 (PGE1) and collagen/epinephrine cartridges, respectively.ResultsA total of 203 patients (145 females; median age, 57 years) were analyzed. Agreement between the two tests was poor for clopidogrel non-responsiveness (ƙ=0.19) and not better than chance for ASA non-responsiveness (ƙ=0.01). Clopidogrel non-responsiveness by LTA and PFA-100® was associated with higher von Willebrand factor antigen and activity levels. ADP-induced platelet disaggregation was lower in patients with clopidogrel non-responsiveness as assessed by PFA-100®. Clopidogrel non-responsiveness by LTA was associated with a higher prevalence of diabetes and a higher body mass index (BMI). Adverse outcomes (death, thromboembolism, or in-stent thrombosis) occurred in 13% (n=26) of all patients independently of ASA and clopidogrel non-responsiveness as assessed by both devices.ConclusionsOur results show that LTA and PFA-100® are not interchangeable in the assessment of ASA and clopidogrel non-responsiveness in patients undergoing neuroendovascular interventions.


Platelets ◽  
2014 ◽  
Vol 26 (6) ◽  
pp. 608-609 ◽  
Author(s):  
Paul A. Gurbel ◽  
Martin G. Gesheff ◽  
Christopher J. Franzese ◽  
Kevin P. Bliden ◽  
Udaya S. Tantry

2019 ◽  
Vol 47 (4) ◽  
pp. 1731-1739 ◽  
Author(s):  
Jun Lu ◽  
Peng Hu ◽  
Guangyu Wei ◽  
Qi Luo ◽  
Jianlin Qiao ◽  
...  

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.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3943-3943 ◽  
Author(s):  
Zuzana Motovska ◽  
Zdenka Sujanova ◽  
Sona Wimmerova ◽  
Jan Ardo ◽  
Marcela Skrakova ◽  
...  

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


2021 ◽  
Vol 6 (1) ◽  
pp. 31-35
Author(s):  
Charliandri Saputra Wahab ◽  
J. Nugroho Eko Putranto ◽  
Ike Dhiah Rochmawati

Polimorfisme genetik COX-1 (Cyclooxygenase 1) menjadi salah satu faktor penyebab variasi respon terhadap agregasi platelet. Variasi tersebut dapat menimbulkan Coronary Arthery Disease (CAD) pada pasien penyakit jantung koroner (PJK). Penelitian ini dilakukan di RSUD Sidoarjo di Jawa Timur selama 1 bulan yaitu terhitung mulai bulan November hingga Desember 2017 dengan melibatkan 30 pasien. Metode penelitian yang digunakan yaitu Polymerase Chain Reaction (PCR) agar pemeriksaan polimorfisme COX-1 dan metode Light Transmittance  Aggregometry (LTA) untuk pengukuran agregasi platelet. Dari 30 pasien yang terlibat dengan penelitian ini didapatkan jenis polimorfisme COX-1 homozygout (wild type) sebanyak 4 pasien dengan nilai bp pada kisaran rentang 233-243dan Heterozygot sebanyak 26 pasien dengan kisaran rentang 244-294. Analisis yang dilakukan agar mengetahui hubungan antara polimorfisme COX-1 terhadap agregasi platelet pada pasien PJK yaitu analisis inferensial, dimana diperoleh nilai p=0,423. Dari hasil uji analisis yang diperoleh, maka dapat diambil kesimpulan bahwa tidak hubungan antara polimorfisme COX-1 terhadap agrgasi platelet.


Sign in / Sign up

Export Citation Format

Share Document