scholarly journals Comparison of Light Transmission Aggregometry With Impedance Aggregometry in Patients on Potent P2Y12 Inhibitors

2020 ◽  
pp. 107424842096870
Author(s):  
Patricia P. Wadowski ◽  
Joseph Pultar ◽  
Constantin Weikert ◽  
Beate Eichelberger ◽  
Irene M. Lang ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Adenosine Diphosphate ◽  
P2y12 Inhibitors ◽  
Coronary Syndrome ◽  
Multiple Electrode Aggregometry ◽  
Impedance Aggregometry ◽  
Light Transmission Aggregometry ◽  
Sensitivity Specificity

Since data on the agreement between light transmission aggregometry (LTA) and multiple electrode aggregometry (MEA) in patients on the more potent P2Y12 inhibitors are missing so far, we investigated if the evaluation of the responsiveness to therapy by LTA can be replaced by MEA in 160 acute coronary syndrome (ACS) patients on dual antiplatelet therapy with aspirin and prasugrel or ticagrelor (n = 80 each). Cut-off values for high on-treatment residual platelet reactivity (HRPR) in response to adenosine diphosphate (ADP) or arachidonic acid (AA) were defined according to previous studies showing an association of HRPR with the occurrence of adverse ischemic outcomes. ADP- inducible platelet aggregation was 33% and 37% (p = 0.07) by LTA and 19 AU and 20 AU (p = 0.38) by MEA in prasugrel- and ticagrelor-treated patients, respectively. AA- inducible platelet aggregation was 2% and 3% by LTA and 15 AU and 16 AU by MEA, (all p ≥ 0.3) in patients on prasugrel and ticagrelor, respectively. By LTA, HRPR ADP and HRPR AA were seen in 5%/5% and in 4%/ 13% of patients receiving prasugrel- and ticagrelor, respectively. By MEA, HRPR ADP and HRPR AA were seen in 3%/ 25% and 0%/24% of prasugrel- and ticagrelor-treated patients, respectively. ADP-inducible platelet reactivity by MEA correlated significantly with LTA ADP in prasugrel-treated patients (r = 0.4, p < 0.001), but not in those receiving ticagrelor (r = 0.09, p = 0.45). AA-inducible platelet aggregation by LTA and MEA did not correlate in prasugrel- and ticagrelor-treated patients. Sensitivity/specificity of HRPR by MEA to detect HRPR by LTA were 25%/99% for MEA ADP and 100%/79% for MEA AA in prasugrel-treated patients, and 0%/100% for MEA ADP and 70%/83% for MEA AA in ticagrelor-treated patients. In conclusion, on-treatment residual ADP-inducible platelet reactivity by LTA and MEA shows a significant correlation in prasugrel- but not ticagrelor-treated patients. However, in both groups LTA and MEA revealed heterogeneous results regarding the classification of patients as responders or non-responders to P2Y12 inhibition.

Platelet aggregation in response to ADP is highly variable in normal donors and patients on anti-platelet medication

2016 ◽  
Vol 54 (7) ◽  
Author(s):  
Eimear Dunne ◽  
Karl Egan ◽  
Siobhán McFadden ◽  
David Foley ◽  
Dermot Kenny
Keyword(s):  
Platelet Aggregation ◽  
Therapeutic Response ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Coronary Intervention ◽  
P2y12 Inhibitors ◽  
Aggregation Response ◽  
Healthy Donors ◽  
Percutaneous Coronary ◽  
Light Transmission Aggregometry

AbstractP2Y12 inhibitors are indicated in patients following percutaneous coronary intervention. Several studies have demonstrated that high on treatment platelet reactivity is correlated with outcomes yet prospective studies of guided therapy have failed to show benefit. There is a paucity of studies on the platelet aggregation response to ADP before P2Y12 therapy is started. The aim of this study was to characterize platelet responses to 20 μM ADP by light transmission aggregometry (LTA) in a homogenous population.Platelet aggregation was assessed in 201 patients on dual antiplatelet therapy, 98 patients on aspirin alone and 47 normal, healthy volunteers free from anti-platelet medication.Consensus guidelines suggest that a platelet aggregation response in response to the agonist ADP of <57% is an adequate therapeutic response to P2Y12 inhibition. Seven healthy donors and 38 patients taking aspirin only had aggregation responses below 57%.The results of our study demonstrate that 15% of normal donors and 38% of patients taking aspirin only would be classified as having a therapeutic response to P2Y12 inhibition using current guidelines.

scholarly journals Role of Dipyrone in the High On-Treatment Platelet Reactivity amongst Acetylsalicylic Acid-Treated Patients Undergoing Peripheral Artery Revascularisation

2018 ◽  
Vol 27 (4) ◽  
pp. 356-361 ◽  
Author(s):  
Jan Hartinger ◽  
Robert Novotny ◽  
Jana Bilkova ◽  
Tomas Kvasnicka ◽  
Petr Mitas ◽  
...  
Keyword(s):  
Acetylsalicylic Acid ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Peripheral Artery ◽  
Primary Resistance ◽  
Impedance Aggregometry ◽  
Number Of Patients ◽  
Light Transmission Aggregometry ◽  
Daily Dose ◽  
Induced Aggregation

Objective: To evaluate the effects of dipyrone on sensitivity to aspirin (acetylsalicylic acid [ASA]) in patients who underwent peripheral artery vascular reconstruction. Subjects and Methods: Impedance aggregometry and light transmission aggregometry were used to determine the effects of dipyrone on ASA treatment in 21 patients. Blood samples were drawn in a 7-day period after the surgery. The cut-off value for high on-treatment platelet reactivity (HTPR) was set at < 65% of aggregation inhibition for impedance aggregometry. For light transmission aggregometry the cut-off value for arachidonic acid-induced aggregation was set at > 20% of aggregating platelets, and the cut-off value for epinephrine-induced aggregation was > 44% of aggregating platelets. The cut-off value for each method was derived from a large number of patients treated with a daily dose of 100 mg of ASA. Results: We found HTPR in 14 (67%) of the 21 patients. None had primary resistance to ASA, i.e., after the addition of ASA in vitro all samples showed antiplatelet efficacy. Regression analysis showed a possible correlation between lower efficacy of ASA treatment and higher daily doses of dipyrone (p = 0.005 for impedance aggregometry, p = 0.04 for light transmission aggregometry), higher platelet count (p = 0.005 for impedance aggregometry), and shorter time from surgery (p = 0.03 for impedance aggregometry). Conclusion: HTPR occurs in 67% of ASA-treated patients after lower limb vascular surgery. The occurrence of HTPR correlates with the daily dose of dipyrone. Therefore, dipyrone should not be used as a postoperative analgesic in ASA-treated patients after peripheral artery revascularisation due to its influence on the effectiveness of ASA.

scholarly journals Use of increased concentrations of adenosinediphosphate for high residual platelet reactivity in patients with coronary heart disease

2021 ◽  
Vol 70 (1) ◽  
pp. 129-132
Author(s):  
O.A. Trubacheva ◽  
S.N. Belyaeva ◽  
T.E. Suslova ◽  
I.V. Petrova
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Platelet Rich Plasma ◽  
Adenosine Diphosphate ◽  
Transmission Curve ◽  
Platelet Suspension

Detection of a tendency to increased thrombosis in patients with coronary heart disease (CHD) is of important prognostic value in the selection of drugs aimed at achieving a persistent antithrombotic effect. The aim of the study was to evaluate the use of elevated ADP inducer concentrations to improve the accuracy of ADP-induced platelet aggregation in patients with coronary heart disease. Material and method. Material and method. We studied 48 patients with CHD who were on continuous double antiplatelet therapy for 6 months (aspirin 75mg and clopidogrel 75mg per day). The aggregation activity of the platelet suspension was studied using the Born method G. in the modification of Gabbasov Z. A. Platelet activity was evaluated by the degree of aggregation of platelet-rich plasma along the light transmission curve under the influence of the inducer adenosine diphosphate (ADP) at a concentration of 2 mmol/l and by its own patented method against the background of additional ADP application. Results. In patients, platelet aggregation decreased to 5-35% (p<0.005) compared to the standard values, which are 50-60%. The values of platelet aggregation with the additional introduction of the inducer of aggregation ADP in a ratio of 2:1 to 2 µmol/l for 1, 2, 3, and 4-minute registration of platelet aggregation, resulted in increased aggregation from 55% to 75% (p<0.001), indicating high residual platelet reactivity on the background of double antiplatelet therapy. Correlations of the degree of aggregation for elevated ADP concentrations with multivessel arterial lesion and dyslipidemia were also found, r=0.86 and r=0.92, respectively. Conclusion. The use of elevated concentrations of adenosine diphosphate in platelet aggregation in patients with ischemic heart disease increases the accuracy of assessing ADP-induced platelet aggregation against the background of dual antiplatelet therapy and contributes to the detection of high residual platelet reactivity.

Whole blood platelet aggregation kinetics under cardiopulmonary bypass: A pilot study

2019 ◽  
Vol 43 (3) ◽  
pp. 208-214
Author(s):  
Tobias Petzold ◽  
Erik Bagaev ◽  
Helen Herzog ◽  
Frank Born ◽  
Dominik Hoechter ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Platelet Aggregation ◽  
Life Support ◽  
Platelet Reactivity ◽  
Extracorporeal Life Support ◽  
Adenosine Diphosphate ◽  
Thrombin Receptor ◽  
Electrode Impedance ◽  
Platelet Counts ◽  
Impedance Aggregometry

Assessing the platelets’ functional status during surgery on cardiopulmonary bypass is challenging. This study used multiple electrode impedance aggregometry (Multiplate®) to create a timeline of platelet aggregation changes as induced by cardiopulmonary bypass in antiplatelet-naive patients undergoing elective surgery for mitral valve regurgitation. We performed six consecutive measurements (T1: pre-operatively, T2: after heparinization, T3: 3 min after establishment of cardiopulmonary bypass, T4: immediately after administration of cardioplegia, T5: 5 min after administration of cardioplegia, and T6: 45 min after administration of cardioplegia). Platelet aggregation was determined after stimulation with 3.2-μg/mL collagen, 6.4-μM adenosine diphosphate, and 32-μM thrombin receptor activating peptide. Five patients were included (age: 64 ± 10 years, one female). We observed a decrease in hematocrit levels by −17.1% ± 3.7% (T1 vs T6) with a drop after establishment of cardiopulmonary bypass (T2 vs T3) and slightly decreasing platelet counts by −6.2% ± 7.7% (T1 vs T6). Immediately after establishment of cardiopulmonary bypass (T2 vs T3), we observed reduced platelet aggregation responses for stimulation with adenosine diphosphate (−19.7% ± 12.8%) and thrombin receptor activating peptide (−19.3% ± 6.3%). Interestingly, we found augmented platelet aggregation for all stimuli 45 min after administration of cardioplegia (T5 vs T6) with the strongest increase for collagen (+83.4% ± 42.8%; adenosine diphosphate: +39.0% ± 37.2%; thrombin receptor activating peptide: +34.5% ± 18.5%). Thus, after an initial drop due to hemodilution upon establishment of cardiopulmonary bypass, platelet reactivity increased over time which was not outweighed by decreasing platelet counts due to mechanical platelet destruction and absorption. These findings have implications for rational transfusion, peri-operative antiplatelet therapy, and for the management of patients on other extracorporeal support, such as extracorporeal life support or extracorporeal membrane oxygenation.

Stability of the high on-treatment platelet reactivity phenotype over time in clopidogrel-treated patients

2011 ◽  
Vol 105 (01) ◽  
pp. 107-112 ◽  
Author(s):  
Juliane Jaitner ◽  
Julia Stegherr ◽  
Tanja Morath ◽  
Siegmund Braun ◽  
Isabell Bernlochner ◽  
...  
Keyword(s):  
Platelet Function ◽  
Large Scale ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Adenosine Diphosphate ◽  
Antiplatelet Treatment ◽  
Chi Square ◽  
Multiple Electrode Aggregometry ◽  
The Stability ◽  
Over Time

SummaryInterindividual response variability to clopidogrel treatment is a well established phenomenon. In recent studies and ongoing large-scale trials where patients with high on-treatment platelet reactivity (HPR) to clopidogrel are being randomised to an intensified antiplatelet treatment, confirmation of the HPR phenotype is based on one single platelet function assessment. The stability of the HPR phenotype over time has never been investigated but should be considered crucial for justification of intensified antiplatelet treatment regimens beyond clinical trials. The goal of this study was to test for the stability of the HPR phenotype over time in clopidogrel-treated patients. Patients (n=31) under chronic clopidogrel treatment (75 mg/day) were investigated by serial adenosine diphosphate (ADP)-induced platelet aggregation assessment with multiple electrode aggregometry (MEA) on a Multiplate analyser and light transmission aggregometry (LTA) at three different time points (once per week) during monitored antiplatelet treatment. On the basis of a cut-off level approach (468 AU*min for MEA, 53% for LTA) patients were classified into patients with (n=27) or without (n=4) HPR. For MEA, the phenotype was stable in 93.5% (n=29) of patients whereas 6.5% (n=2) crossed the cut-off level. For LTA, the phenotype was stable in 68% (n=21) of patients whereas 32% (n=10) patients crossed the cut-off level (chi-square P=0.01 for comparison of pheno-type stability between both assays). In conclusion, the HPR phenotype is stable over time in the majority of clopidogrel-treated patients. Comparative assessment of phenotype stability across available platelet function assays warrants further investigation.

Evaluation of Residual Platelet Reactivity in Patients Treated with Aspirin and or Clopidogrel: Comparison of Results Obtained On Multiplate®, PFA-100TM and Classical Light Transmission Aggregometry.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3129-3129
Author(s):  
Annick Ankri ◽  
Isabelle Martin-Toutain ◽  
Anne Baranger ◽  
Marie-Claude Couty ◽  
Jean Philippe Collet ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Biological Activities ◽  
Impedance Aggregometry ◽  
Increased Risk ◽  
Light Transmission Aggregometry ◽  
Group A ◽  
Platelet Functions ◽  
Good Agreement

Abstract Abstract 3129 Poster Board III-66 Residual platelet reactivity (RPR), despite antiplatelet therapy (AT), is currently associated with an increased risk of recurrent ischemic events and is linked to a biological resistance to AT. We determined whether whole blood impedance aggregometry using the Multiplate® (Dynabyte and IL France) detects the effects of AT as reliably as does classical light transmission aggregometry (LTA) (PAP-8, Biodis). We compared also results with those obtained on PFA-100TM (Siemens). Patients and Methods Ninety-three controls, healthy volunteers or patients without intake of AT or other drugs or pathology impairing platelet functions and 182 consecutive patients on AT were studied. Among patients, 61 received Aspirin 100mg (group A), 36 Clopidogrel 75mg (group C) and 85 the association of the two drugs. Among these 85 patients, 58 received continuously Aspirin 75mg and Clopidogrel 75mg (group AC) and 27 received a loading dose for both drugs before coronarography (group LAC). Venous blood samples were obtained on Becton Dickinson vacutainer containing citrate 0.129M. Multiplate® measures change in electrical resistance as arbitrary aggregation units (AU) over time. Aggregation is quantified as AU and area under the curve (AUC) of AU.min. On LTA, aggregation was quantified according to manufacturer's recommendations as AUC. “Resistance” to Aspirin or Aspirin RPR was determined on Multiplate® (M) using arachidonic acid at 0.5 mM (ASPITEST), in LTA with arachidonic acid at 1 mM (AA-LTA) and on PFA-100TM using the cartridge with membrane coated with epinephrine (PFA-EPI). In the same way, “resistance” to Clopidogrel was determined on M using ADP at 6.4 μM (ADPTEST), in LTA with the presence of ADP at 10 μM (ADP-LTA) and occlusion time on PFA-100TM using cartridge with membrane coated with ADP (PFA-ADP). Results All patients were tested on M, 169 on PFA-100TM and 37 with LTA. Significant correlations (p<.0001) were observed between ASPITEST and AA-LTA (r = .771), ASPITEST and PFA-EPI (r = -.42), AA-LTA and PFA-EPI (r = -.47), ADPTEST and ADP-LTA (r = .6) ADPTEST and PFA-ADP (r = -.39) and ADP-LTA and PFA-ADP (r = -.56). To define RPR on M and LTA, cut-off values (5th percentile) were determined from controls for each inducer. Treated patients presenting reactivity higher than the threshold value were considered as ‘resistant’. For PFA-100TM, results of patients under cut-off point defined by the manufacturer were considered as ‘resistant’. The frequency of “resistant” patients according to the different platelet functions tests was: a) for Aspirin: 10% on M, 4.5% with LTA and 32.8% with PFA-EPI. b) for Clopidogrel 23.1% on M 16.1% with LTA and 54.5% with PFA-ADP. A good agreement was found between ASPITEST and AA-LTA and between ADPTEST and ADP-LTA (respectively 92% and 88.7%). On the other hand, results on comparison between ASPITEST and PFA-EPI and LTA and PFA-EPI were respectively 70% and 72.6%. Results for ADPTEST and PFA-ADP were 69% and 72.3% for ADP-LTA and PFA-ADP. A significant gradation of mean AUC was observed using ASPITEST on M between all groups of subjects: controls (mean = 494±176); group A (mean = 214±186); group C (mean = 310±198); group AC (mean = 118±109); group LAC (mean = 74±45). Similar results are obtained with LTA and on PFA-100TM (except for the group C, Clopidogrel alone). Thus, a potentiating effect of Aspirin by the association with Clopidogrel may be postulated in this study. Using ADPTEST to assess the treatment response by clopidogrel, mean AUC were significantly lower for all group of patients with Clopidogrel than for controls. No gradient has been observed. Mean AUC of patients with Aspirin alone was similar to controls. In conclusion, our results confirm that Multiplate® is more effective than PFA-100TM in monitoring patients on AT. The good agreement between Multiplate® and LTA could lead to use the Multiplate® in first intention to detect RPR in these patients. Furthermore the easiness of Multiplate® use may contribute to development of new studies on biological activities of AT. Disclosures No relevant conflicts of interest to declare.

Cross validation of the Multiple Electrode Aggregometry

2009 ◽  
Vol 102 (08) ◽  
pp. 397-403 ◽  
Author(s):  
Jolanta Siller-Matula ◽  
Ghazaleh Gouya ◽  
Michael Wolzt ◽  
Bernd Jilma
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Cross Validation ◽  
Platelet Reactivity ◽  
Adenosine Diphosphate ◽  
Multiple Electrode Aggregometry ◽  
Vasp Phosphorylation ◽  
Function Analyzer ◽  
Platelet Function Analyzer ◽  
Multiple Electrode

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.

Inter-patient variability and impact of proton pump inhibitors on platelet reactivity after prasugrel

2012 ◽  
Vol 107 (02) ◽  
pp. 338-345 ◽  
Author(s):  
Wiktor Kuliczkowski ◽  
Dan Atar ◽  
Victor Serebruany ◽  
Dániel Aradi
Keyword(s):  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Maintenance Phase ◽  
Loading Dose ◽  
Platelet Activity ◽  
Coronary Syndrome ◽  
Impedance Aggregometry ◽  
The Impact

SummaryAlthough there is considerable variability of platelet reactivity among patients treated with clopidogrel, little is known about inter-individual differences and possible role of proton pump inhibitors (PPIs) after prasugrel. We defined the extent of inter-patient variability, and evaluated the impact of PPI interaction in prasugrel-treated patients with acute coronary syndrome (ACS). Between January 2010 and May 2011, 104 prospective, high-risk patients with ACS were recruited into this multicentre, prospective, observational study. Twelve to 24 hours after receiving 60 mg loading dose of prasugrel, light transmission aggregometry (LTA) and whole blood impedance aggregometry (Multiplate) were used to assess platelet activity. Platelet function measurements were repeated during maintenance phase on reduced (5 mg) or on conventional (10 mg) doses of prasugrel. High platelet reactivity (HPR) was defined according to the consensus document of the Working Group on High On-Treatment Platelet Reactivity (LTA:>46%; Multiplate:>47U). Compared to maintenance doses, 60 mg loading dose of prasugrel provided significantly greater platelet reactivity inhibition (p<0.05). There were no significant differences between the conventional and reduced maintenance doses. Notably, a remarkable inter-patient variability was present in platelet reactivity after all doses of prasugrel, and the prevalence of HPR was significantly higher during the maintenance doses (p<0.05). Although median platelet reactivity values were consistently higher when prasugrel was used in combination with PPIs, these differences were not significant (p≥0.17). Despite potent platelet inhibition, inter-patient variability is present after all tested doses of prasugrel. The 60 mg loading dose is superior to conventional and reduced maintenance doses in terms of platelet reactivity inhibition and regarding the prevention of HPR.

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