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Artículos de revistas sobre el tema "High on-treatment platelet reactivity"

Autor: Grafiati

Publicado: 10 de marzo de 2023

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1

Ait-Mokhtar, Omar, Laurent Bonello, Saida Benamara y Franck Paganelli. "High on Treatment Platelet Reactivity". Heart, Lung and Circulation 21, n.º 1 (enero de 2012): 12–21. http://dx.doi.org/10.1016/j.hlc.2011.08.069.

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2

Musallam, Anees, Eli I. Lev y Ariel Roguin. "Stent thrombosis in a patient with high on-treatment platelet reactivity despite ticagrelor treatment". European Heart Journal: Acute Cardiovascular Care 4, n.º 1 (22 de mayo de 2014): 85–87. http://dx.doi.org/10.1177/2048872614534563.

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We describe, to the best of our knowledge, the first incidence of stent thrombosis in a patient treated with ticagrelor, who exhibited high on-treatment platelet reactivity (HTPR) according to platelet reactivity testing. He was on clopidrogel and tested for platelet reactivity using the VerifyNow P2Y12 assay. The test showed a PRU of 249 and only 12% platelet inhibition. The patient was then switched to ticagrelor, with a loading dose of 180 mg given. The patient had stent thrombosis three weeks later with an acute myocardial infarction (MI). The patient had good platelet inhibition when started on Ticagrelor treatment (PRU=33), but had HTPR when the stent thrombosis occurred three weeks later (PRU=339).

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3

Cattaneo, Marco. "High on-treatment platelet reactivity – definition and measurement". Thrombosis and Haemostasis 109, n.º 05 (2013): 792–98. http://dx.doi.org/10.1160/th12-10-0758.

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SummaryIn the last decade, several studies revealed inter-patient response variability to antiplatelet agents: patients who display negligible or no responses to these drugs are considered poor responders, or “resistant” to treatment. In order to identify poor responders to an antiplatelet drug, laboratory tests of platelet function that specifically explore the platelet activation pathway that is targeted by the drug should be utilised. In addition, they should be performed both at baseline and during treatment: however, most studies explored platelet function during antiplatelet treatment, in order to identify those patients with “high on-treatment platelet reactivity” (HPR), which exposes them to increased risk of major adverse cardiovascular events (MACE). Many tests of platelet function have been used, most of which are able to identify patients at risk of MACE. Unfortunately, universal cut-off values for HPR have not been clearly established yet. In addition, the concordance among different tests in the identification of patients at risk is very poor and the most effective and safe treatment for patients at risk is still unknown.

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4

Cahoon, William D., Amanda L. Kroll y Denise K. Lowe. "High On-Treatment Platelet Reactivity Associated With Prasugrel". Journal of Pharmacy Technology 31, n.º 1 (8 de agosto de 2014): 38–42. http://dx.doi.org/10.1177/8755122514545776.

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5

Rajendran, Saissan, Devang Parikh, Ibrahim Shugman, John K. French y Craig P. Juergens. "High on Treatment Platelet Reactivity and Stent Thrombosis". Heart, Lung and Circulation 20, n.º 8 (agosto de 2011): 525–31. http://dx.doi.org/10.1016/j.hlc.2011.04.004.

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6

Hayward, Catherine. "Advances in Understanding “High on-Treatment Platelet Reactivity”". Thrombosis and Haemostasis 102, n.º 11 (2009): 799–800. http://dx.doi.org/10.1160/th09-09-0617.

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7

Alexopoulos, Dimitrios, Theodora-Eleni Plakomyti y Ioanna Xanthopoulou. "Variability and treatment of high on-prasugrel platelet reactivity in patients with initial high on-clopidogrel platelet reactivity". International Journal of Cardiology 154, n.º 3 (febrero de 2012): 333–34. http://dx.doi.org/10.1016/j.ijcard.2011.10.031.

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8

Alemanno, Laura, Isabella Massimi, Vanessa Klaus, Maria Guarino, Teresa Maltese, Luigi Frati, Dominick Angiolillo y Fabio Pulcinelli. "Impact of Multidrug Resistance Protein-4 Inhibitors on Modulating Platelet Function and High on-Aspirin Treatment Platelet Reactivity". Thrombosis and Haemostasis 118, n.º 03 (15 de febrero de 2018): 490–501. http://dx.doi.org/10.1055/s-0038-1629920.

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AbstractPlatelet multidrug resistance protein 4 (MRP4) plays a modulating role on platelet activation. Platelet function and thrombus formation are impaired in MRP4 knockout mice models, and, among aspirin-treated patients, high on-aspirin residual platelet reactivity (HARPR) positively correlates with MRP4 levels. To better understand the effects of MRP4 on platelet function, the aim of this investigation was to assess the impact of cilostazol-induced inhibition of MRP4-mediated transport and assess aspirin-induced antiplatelet effects and rates of HARPR in human subjects.Cilostazol-dependent inhibition of MRP4-mediated transport was assessed with the release of the fluorescent adduct bimane-glutathione and aspirin entrapment. Effect of Cilostazol on cAMP inhibition was evaluated by vasodilator-stimulated phosphoprotein (VASP). Platelet function was studied by collagen and TRAP-6-induced platelet aggregation and secretion.Cilostazol reduced the release of bimane-glutathione and enhanced aspirin entrapment demonstrating an inhibitory effect on MRP4 in platelets. VASP phosphorylation was absent until 10 seconds after addition of cilostazol, and becomes evident after 30 seconds. An inhibitory effect on platelet aggregation and secretion was found in activated platelets, with threshold concentration of agonists, 10 seconds after addition of cilostazol, supporting a role of MRP4 on platelet function that is cAMP independent. Cilostazol effects were also shown in aspirin-treated platelets. A reduction of platelet aggregation and secretion were observed in aspirin-treated patients with HARPR.This study supports the role of MRP4 on modulating platelet function which occurs through cAMP-independent mechanisms. Moreover, inhibition of MRP4 induced by cilostazol enhances aspirin-induced antiplatelet effects and reduces HARPR.

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9

Angelo Gaglia, Michael, Rebecca Torguson, Zhenyi Xue, Rajbabu Pakala, Manuel A. Gonzalez, Itsik Ben-Dor, Gabriel Maluenda et al. "PERIPROCEDURAL MYOCARDIAL INFARCTION AND HIGH ON-TREATMENT PLATELET REACTIVITY". Journal of the American College of Cardiology 57, n.º 14 (abril de 2011): E1897. http://dx.doi.org/10.1016/s0735-1097(11)61897-4.

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10

Spiliopoulos, Stavros, George Kassimis, Adam Hatzidakis y Miltiadis Krokidis. "High On-Treatment Platelet Reactivity in Peripheral Endovascular Procedures". CardioVascular and Interventional Radiology 37, n.º 3 (30 de julio de 2013): 559–71. http://dx.doi.org/10.1007/s00270-013-0707-y.

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11

Mshelbwala, Fakilahyel S., Daniel W. Hugenberg y Rolf P. Kreutz. "Intensified P2Y12 inhibition for high-on treatment platelet reactivity". Journal of Thrombosis and Thrombolysis 50, n.º 3 (9 de marzo de 2020): 619–27. http://dx.doi.org/10.1007/s11239-020-02075-x.

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12

Varol, Ercan y Mehmet Ozaydin. "The relationship between mean platelet volume and high on-treatment platelet reactivity". Anadolu Kardiyoloji Dergisi/The Anatolian Journal of Cardiology 14, n.º 3 (22 de junio de 2014): 308–9. http://dx.doi.org/10.5152/akd.2014.5442.

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13

Wiśniewski, Adam y Karolina Filipska. "The Phenomenon of Clopidogrel High On-Treatment Platelet Reactivity in Ischemic Stroke Subjects: A Comprehensive Review". International Journal of Molecular Sciences 21, n.º 17 (3 de septiembre de 2020): 6408. http://dx.doi.org/10.3390/ijms21176408.

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Clopidogrel is increasingly being used for the secondary prevention of ischemic stroke according to the updated guidelines on acute stroke management. Failure to achieve a drug response is referred to as clopidogrel resistance. Similarly, a higher activation of platelets during clopidogrel therapy—high on-treatment platelet reactivity—is equivalent to a reduced effectiveness of a therapy. Clopidogrel resistance is considered to be a common and multifactorial phenomenon that significantly limits the efficacy of antiplatelet agents. The aim of the current study is to review the latest literature data to identify the prevalance and predictors of clopidogrel high on-treatment platelet reactivity among stroke subjects and to establish the potential impact on clinical outcomes and prognosis. Clinical databases were searched by two independent researchers to select relevant papers on the topic, including all types of articles. Several important predictors contributing to clopidogrel resistance were identified, including genetic polymorphisms, the concomitant use of other drugs, or vascular risk factors, in particular nonsmoking and diabetes. Clopidogrel high on-treatment platelet reactivity has a negative impact on the clinical course of stroke, worsens the early- and long-term prognoses, and increases the risk of recurrent vascular events. Platelet function testing should be considered in selected stroke individuals, especially those predisposed to clopidogrel resistance, for whom an improvement in the efficacy of antiplatelet therapy is essential. This particular group may become the greatest beneficiaries of the modification of existing therapy based on platelet function monitoring.

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14

Frelinger III, Andrew L., Alan D. Michelson, Stephen D. Wiviott, Dietmar Trenk, Franz-Josef Neumann, Debra L. Miller, Joseph A. Jakubowski et al. "Intrinsic platelet reactivity before P2Y12 blockade contributes to residual platelet reactivity despite high-level P2Y12 blockade by prasugrel or high-dose clopidogrel". Thrombosis and Haemostasis 106, n.º 08 (2011): 219–26. http://dx.doi.org/10.1160/th11-03-0185.

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SummaryIt was the objective of this study to determine whether the intrinsic platelet response to adenosine diphosphate (ADP) before thienopyridine exposure contributes to residual platelet reactivity to ADP despite high level P2Y12 blockade by prasugrel (60 mg loading dose [LD]), 10 mg daily maintenance dose [MD]) or high-dose clopidogrel (600 mg LD, 150 mg daily MD). High residual platelet function during clopidogrel therapy is associated with poor clinical outcomes. It remains unknown whether the relationship between platelet reactivity prior to treatment with clopidogrel (300 mg LD, 75 mg daily MD) and residual on-treatment platelet reactivity is maintained after more potent P2Y12 inhibition. PRINCIPLE-TIMI 44 was a randomised, double-blind, twophase crossover study of prasugrel compared with high-dose clopidogrel in 201 patients undergoing cardiac catheterisation for planned percutaneous coronary intervention. ADP-stimulated platelet-monocyte aggregates, platelet surface P-selectin and platelet aggregation were measured pre-treatment, during LD (6 h and 18–24 h) and MD (15 d). Correlations of pre-treatment to on-treatment values were determined by Spearman rank order. Prasugrel resulted in greater platelet inhibition than high-dose clopidogrel for each measure. However, for both drugs, pre-treatment reactivity to ADP predicted 6 h, 18–24 h and 15 day reactivity to ADP (correlations 0.24–0.62 for platelet-monocyte aggregates and P-selectin). In conclusion, a patient's intrinsic platelet response to ADP before exposure to thienopyridines contributes to residual platelet reactivity to ADP despite high level P2Y12 blockade with high-dose clopidogrel or even higher level P2Y12 blockade with prasugrel. Patients who are hyper-responsive to ADP pre-treatment are more likely to be hyper-responsive to ADP on-treatment, which may be relevant to therapeutic strategies.

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15

Kristensen, Steen, Willibald Hochholzer, Franz-Josef Neumann y Dietmar Trenk. "High on-treatment platelet reactivity and P2Y12 antagonists in clinical trials". Thrombosis and Haemostasis 109, n.º 05 (2013): 834–45. http://dx.doi.org/10.1160/th12-08-0588.

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SummaryDual antiplatelet therapy with aspirin and clopidogrel in patients undergoing percutaneous coronary intervention (PCI) and in patients with acute coronary syndromes (ACS) has substantially decreased the rate of cardiovascular events. Within the past decade, the variability in pharmacodynamic response as well as the moderate antiplatelet efficacy of clopidogrel has raised major concerns, since high on-clopidogrel platelet reactivity has consistently been associated with increased risk for ischaemic events in PCI patients. The variability in response could be linked to genetic polymorphisms impacting on activity of cytochrome P450 enzymes as well as clinical and demographic variables, but, taken together, factors identified so far can explain only up to approximately 12% of this variability in adenosine diphosphate-induced platelet aggregation on clopidogrel. Regulatory agencies as well as major cardiac societies suggest the use of other anti-platelet medications or alternative dosing strategies for clopidogrel in patients with reduced effectiveness of clopidogrel. This review will focus on the current status of alternate strategies for more sufficient suppression of high platelet reactivity.

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16

Schrör, Karsten y Kurt Huber. "High on-treatment platelet reactivity - why should we be concerned?" Thrombosis and Haemostasis 109, n.º 05 (2013): 789–91. http://dx.doi.org/10.1160/th13-04-0281.

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17

Lynch, Donald R., Farooq H. Khan, Dhananjay Vaidya y Marlene S. Williams. "Persistent high on-treatment platelet reactivity in acute coronary syndrome". Journal of Thrombosis and Thrombolysis 33, n.º 3 (24 de febrero de 2012): 267–73. http://dx.doi.org/10.1007/s11239-012-0678-x.

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18

Fileti, Luca, Gianluca Campo y Marco Valgimigli. "Latest Clinical Data on Testing for High On-Treatment Platelet Reactivity". Reviews in Cardiovascular Medicine 12, S1 (20 de enero de 2011): 14–22. http://dx.doi.org/10.3909/ricm12s1s0001.

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19

Massimi, Isabella, Lavinia Lotti, Flavia Temperilli, Massimo Mancone, Gennaro Sardella, Simone Calcagno, Ombretta Turriziani, Luigi Frati y Fabio M. Pulcinelli. "Enhanced platelet MRP4 expression and correlation with platelet function in patients under chronic aspirin treatment". Thrombosis and Haemostasis 116, n.º 12 (noviembre de 2016): 1100–1110. http://dx.doi.org/10.1160/th16-04-0316.

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SummaryPlatelet multidrug resistance protein4 (MRP4)-overexpression has a role in reducing aspirin action. Aspirin in vivo treatment enhances platelet MRP4 expression and MRP4 mediated transport inhibition reduces platelet function and delays thrombus formation. The aim of our work was to verify whether MRP4 expression is enhanced in platelets obtained from patients under chronic aspirin treatment and whether it correlates with residual platelet reactivity. We evaluated changes on mRNA and protein-MRP4 expression and platelet aggregation in four populations: healthy volunteers (HV), aspirin-free control population (CTR), patients who started the treatment less than one month ago (ASA<1 month patients) and aspirinated patients who started the treatment more than two months ago (ASA>2 months patients). In platelets obtained from ASA>2 months patients, it was found a statistically significant MRP4 enhancement of both mRNA and protein expression compared to HV, CTR and ASA<1 month patients. Platelets obtained from ASA>2 months patients that present high levels of platelet MRP4, have higher serum TxB2 levels and collagen-induced platelet aggregation compared to patient with low levels of MRP4 in platelets. In addition collagen induced platelet aggregation is higher in in vitro aspirinated platelets obtained from patients with high levels of MRP4 patients compared to those obtained from patients with low MRP4 levels. We can assert that, in patients under chronic aspirin treatment, platelets that present high MRP4 levels have an increase of residual platelet reactivity, which is due in part to incomplete COX-1 inhibition, and in part to COX-1–independent mechanism.

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20

Wang, Yilong, Yi Lin, Xia Meng, Weiqi Chen, Guohua Chen, Zhimin Wang, Jialing Wu et al. "Effect of ticagrelor with clopidogrel on high on-treatment platelet reactivity in acute stroke or transient ischemic attack (PRINCE) trial: Rationale and design". International Journal of Stroke 12, n.º 3 (23 de febrero de 2017): 321–25. http://dx.doi.org/10.1177/1747493017694390.

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Rationale and aim Little is known about the safety and efficacy of the combination of ticagrelor and aspirin in acute ischemic stroke. This study aimed to evaluate whether the combination of ticagrelor and aspirin was superior to that of clopidogrel and aspirin in reducing the 90-day high on-treatment platelet reactivity for acute minor stroke or transient ischemic attack, especially for carriers of cytochrome P450 2C19 loss-of-function allele. Sample size and design This study was designed as a prospective, multicenter, randomized, open-label, active-controlled, and blind-endpoint, phase II b trial. The required sample size was 952 patients. It was registered with ClinicalTrials.gov (NCT02506140). Study outcomes The primary outcome was the proportion of patients with high on-treatment platelet reactivity at 90 days. High on-treatment platelet reactivity is defined as the P2Y12 reaction unit >208 measured using the VerifyNow P2Y12 assay. Conclusion The Platelet Reactivity in Acute Non-disabling Cerebrovascular Events study explored whether ticagrelor combined with aspirin could reduce further the proportion of patients with high on-treatment platelet reactivity at 90 days after acute minor stroke or transient ischemic attack compared with clopidogrel and aspirin.

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21

Marcucci, Rossella, Anna Maria Gori, Roberto Caporale, Alessandra Fanelli, Rita Paniccia, Maria Zanazzi, Elisabetta Bertoni et al. "High platelet turnover and reactivity in renal transplant recipients patients". Thrombosis and Haemostasis 104, n.º 10 (2010): 804–10. http://dx.doi.org/10.1160/th10-02-0124.

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SummaryRenal transplant recipients (RTRs) patients are at increased risk of cardiovascular morbidity and mortality. We aimed this study to assess reticulated platelets (RP), platelet reactivity and von Willebrand factor (vWF) levels in RTRs patients. In 150 RTRs patients [84 (56%) not on acetylsalicylic acid (ASA) treatment, group A; 66 (44%) on ASA 100 mg treatment, group B] and in 60 healthy control subjects, RP were measured by a Sysmex XE-2100 and were expressed as the percentage of RP of the total optical platelet count (immature platelet fraction; IPF), as the percentage of RP highly fluorescent (H-IPF) and as the absolute number of RP (IPF#). Platelet function was assessed by optical aggregometry (PA) induced by 1 mmol arachidonic acid (AA-PA), 2 and 10 μM ADP (ADP2-PA and ADP10-PA) and 2 μg/ml collagen (Coll-PA). vWF levels were measured by using a miniVidas analyser. Group A and group B showed significant higher values of RP than controls. At a multiple linear regression analysis IPF and IPF# were significantly and positively related to collagen-PA. By analysing group B according to residual platelet reactivity (RPR), we observed a significant higher number of RP among patients with RPR by collagen. Moreover at a multiple logistic regression analysis, IPF# significantly affected the risk of having a RPR by collagen. With regard to vWF, RTRs patients showed higher levels than control subjects. We documented a higher platelet turn-over in both groups of RTRs patients and increased platelet reactivity in RTRs patients not on ASA therapy than controls.

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22

Rosińska, Justyna, Joanna Maciejewska, Robert Narożny, Wojciech Kozubski y Maria Łukasik. "ASSOCIATION OF PLATELET-DERIVED MICROVESICLES WITH HIGH ON-TREATMENT PLATELET REACTIVITY IN CONVALESCENT ISCHEMIC STROKE PATIENTS TREATED WITH ACETYLSALICYLIC ACID". Wiadomości Lekarskie 72, n.º 8 (2019): 1426–36. http://dx.doi.org/10.36740/wlek201908102.

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Introduction: Elevated concentrations of platelet-derived microvesicles are found in cerebrovascular diseases. The impact of acetylsalicylic acid on these microvesicles remains inconsistent, despite its well-established effect on platelet aggregation. High residual platelet aggregation is defined as high on-treatment platelet reactivity, while “treatment failure” is the occurrence of vascular events despite antiplatelet treatment. The aim of this study was to determine whether the antiaggregatory effect of acetylsalicylic acid correlates with platelet-derived microvesicles in convalescent ischaemic stroke patients and cardiovascular risk factor controls as well as to evaluate the association between high on-treatment platelet reactivity and recurrent vascular events with the studied platelet-derived microvesicle parameters. Materials and methods: The study groups consisted of 76 convalescent stroke patients and 74 controls. Total platelet-derived microvesicles, annexino-positive microvesicles number, and platelet-derived microvesicles with surface expression of proinflammatory (CD40L, CD62P, CD31) and procoagulant (PS, GPIIb/IIIa) markers were characterized and quantified using flow cytometry. Cyclooxygenase-1-specific platelet responsiveness, with whole blood impedance platelet aggregation under arachidonic acid stimulation and the serum concentration of thromboxane B2, were evaluated. Results: Neither acetylsalicylic acid intake nor modification of its daily dose caused statistically significant differences in the studied microvesicle parameters. Additionally, no statistically significant differences in the studied microvesicle parameters were revealed between high on-treatment platelet reactivity and non-high on-treatment platelet reactivity subjects in either study subgroup. However, elevated concentrations of PAC-1+/CD61+, CD62P+/CD61+ and CD31+/CD61+ microvesicles were found in stroke patients with treatment failure, defined in this study as a recurrent vascular events in a one-year follow-up period. Conclusions: This study revealed no relationship between circulating microvesicle number and platelet aggregation. The procoagulant and proinflammatory phenotype of circulating platelet-derived microvesicles might contribute to acetylsalicylic acid treatment failure.

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Breet, Nicoline, Corine de Jong, Willem Jan Bos, Jochem van Werkum, Heleen Bouman, Johannes Kelder, Thomas Bergmeijer, Felix Zijlstra, Christian Hackeng y Jurriën ten Berg. "The impact of renal function on platelet reactivity and clinical outcome in patients undergoing percutaneous coronary intervention with stenting". Thrombosis and Haemostasis 112, n.º 12 (2014): 1174–81. http://dx.doi.org/10.1160/th14-04-0302.

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SummaryPatients with chronic kidney disease (CKD) have an increased risk of cardiovascular disease. Previous studies have suggested that patients with CKD have less therapeutic benefit of antiplatelet therapy. However, the relation between renal function and platelet reactivity is still under debate. On-treatment platelet reactivity was determined in parallel by ADP- and AA-induced light transmittance aggregometry (LTA) and the VerifyNow® System (P2Y12 and Aspirin) in 988 patients on dual antiplatelet therapy, undergoing elective coronary stenting. Patients were divided into two groups according to the presence or absence of moderate/severe CKD (GFR<60 ml/min/1.73 m2). Furthermore, the incidence of all-cause death, non-fatal acute myocardial infarction, stent thrombosis and stroke at one-year was evaluated. Patients with CKD (n=180) had significantly higher platelet reactivity, regardless of the platelet function test used. Patients with CKD more frequently had high on-clopidogrel platelet reactivity (HCPR) and high on-aspirin platelet reactivity (HAPR) regardless of the platelet function test used. After adjustment for potential confounders, this was no longer significant. The event-rate was the highest in patients with both high on-treatment platelet reactivity (HPR) and CKD compared to those with neither high on-treatment platelet reactivity nor CKD. In conclusion, the magnitude of platelet reactivity as well as the incidence of HPR was higher in patients with CKD. However, since the incidence of HPR was similar after adjustment, a higher rate of co-morbidities in patients with CKD might be the major cause for this observation rather than CKD itself. CKD-patients with HCPR were at the highest risk of long-term cardiovascular events.Clinical Trial Registration: www.clinicaltrials.gov: NCT00352014.

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Nührenberg, Thomas, Michael Amann, Marco Cederqvist, Pascal Kleiner, Christian M. Valina, Dietmar Trenk, Franz-Josef Neumann, Willibald Hochholzer y Christian Stratz. "Impact of reticulated platelets on antiplatelet response to thienopyridines is independent of platelet turnover". Thrombosis and Haemostasis 116, n.º 11 (septiembre de 2016): 941–48. http://dx.doi.org/10.1160/th16-03-0191.

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SummaryReticulated platelets are associated with impaired antiplatelet response to thienopyridines. It is uncertain whether this interaction is caused by a decreased drug exposure due to high platelet turnover reflected by elevated levels of reticulated platelets or by intrinsic properties of reticulated platelets. This study sought to investigate if the impact of reticulated platelets on early antiplatelet response to thienopyridines is mainly caused by platelet turnover as previously suggested. Elective patients undergoing coronary intervention were randomised to loading with clopidogrel 600 mg or prasugrel 60 mg (n=200). Adenosine diphosphate (ADP)-induced platelet reactivity was determined by impedance aggregometry before, at 30, 60, 90, and 120 minutes and at day 1 after loading. Immature platelet count was assessed as marker of reticulated platelets by flow cytometry. Platelet reactivity increased with rising levels of immature platelet count in both groups. This effect was more distinctive in patients on clopidogrel as compared to patients on prasugrel. Overall, immature platelet count correlated well with on-treatment platelet reactivity at all timepoints (p < 0.001). These correlations did not change over time in the entire cohort as well as in patients treated with clopidogrel or prasugrel indicating an effect independent of platelet turnover (comparison of correlations 120 minutes/day 1: p = 0.64). In conclusion, the association of immature platelet count with impaired antiplatelet response to thienopyridines is similar early and late after loading. This finding suggests as main underlying mechanism another effect of reticulated platelets on thienopyridines than platelet turnover.Supplementary Material to this article is available online at www.thrombosis-online.com.

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Verdoia, Monica, Patrizia Pergolini, Roberta Rolla, Matteo Nardin, Lucia Barbieri, Alon Schaffer, Giorgio Bellomo, Paolo Marino, Harry Suryapranata y Giuseppe De Luca. "Platelet Larger Cell Ratio and High-on Treatment Platelet Reactivity During Dual Antiplatelet Therapy". Cardiovascular Drugs and Therapy 29, n.º 5 (octubre de 2015): 443–50. http://dx.doi.org/10.1007/s10557-015-6616-3.

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Sibbing, Dirk, Robert A. Byrne, Isabell Bernlochner y Adnan Kastrati. "High platelet reactivity and clinical outcome – Fact and fiction". Thrombosis and Haemostasis 106, n.º 08 (2011): 191–202. http://dx.doi.org/10.1160/th11-01-0040.

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SummaryIn patients suffering from acute coronary syndromes or undergoing percutaneous coronary intervention, oral antiplatelet treatment is routinely administered with the primary aim of inhibiting platelet-mediated thrombus formation and subsequent abrupt vessel occlusion. Simultaneous inhibition of blood platelet cyclooxygenase-1 by aspirin and of the P2Y12 receptor by clopidogrel or prasugrel is currently recommended in this setting. Inter-individual response variability to aspirin and especially to clopidogrel is the subject of much debate as evidence has grown over the years linking an attenuated response to treatment with the occurrence of ischaemic events. Consequently, the clinical entity of high (on-treatment) platelet reactivity (HPR) was born and subsequently characterised in numerous studies over the last decade. Until recently, alternative treatment options were limited in patients exhibiting HPR. At present the antiplatelet therapy landscape is changing with the advent of prasugrel and ticagrelor as alternative and more potent treatment options. Different tests for monitoring platelet function are available and are being increasingly employed in research projects and clinical routine. These tests may prove useful for achieving optimal platelet inhibition for the individual patient, and several centres now incorporate such testing in day-to-day practice. Widespread adoption of this practice and incorporation into clinical guidelines awaits the results of ongoing trials in which treatment is changed based on platelet function monitoring. This review aims to summarise available facts and fiction in relation to platelet function testing and reactivity with a particular focus on P2Y12 receptor inhibition in patients undergoing coronary stent placement.

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Wiśniewski, Adam, Joanna Sikora, Agata Sławińska, Karolina Filipska, Aleksandra Karczmarska-Wódzka, Zbigniew Serafin y Grzegorz Kozera. "High On-Treatment Platelet Reactivity Affects the Extent of Ischemic Lesions in Stroke Patients Due to Large-Vessel Disease". Journal of Clinical Medicine 9, n.º 1 (17 de enero de 2020): 251. http://dx.doi.org/10.3390/jcm9010251.

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Background: Excessive platelet activation and aggregation plays an important role in the pathogenesis of ischemic stroke. Correlation between platelet reactivity and ischemic lesions in the brain shows contradictory results and there are not enough data about the potential role of stroke etiology and its relationships with chronic lesions. The aim of this study is to assess the relationship between platelet reactivity and the extent of ischemic lesions with the particular role of etiopathogenesis. Methods: The study involved 69 patients with ischemic stroke, including 20 patients with large-vessel disease and 49 patients with small-vessel disease. Evaluation of platelet reactivity was performed within 24 h after the onset of stroke using two aggregometric methods (impedance and optical), while ischemic volume measurement in the brain was performed using magnetic resonance imaging (in diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) sequences) at day 2–5 after the onset of stroke. Results: In the large-vessel disease subgroup, a correlation was found between platelet reactivity and acute ischemic focus volume (correlation coefficient (R) = 0.6858 and p = 0.0068 for DWI; R = 0.6064 and p = 0.0215 for FLAIR). Aspirin-resistant subjects were significantly more likely to have a large ischemic focus (Odds Ratio (OR) = 45.00, 95% Confidence Interval (CI) = 1.49–135.36, p = 0.0285 for DWI; OR = 28.00, 95% CI = 1.35–58.59, p = 0.0312 for FLAIR) than aspirin-sensitive subjects with large-vessel disease. Conclusion: In patients with ischemic stroke due to large-vessel disease, high on-treatment platelet reactivity affects the extent of acute and chronic ischemic lesions.

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Cattaneo, Marco. "Diagnosis and Management of High Platelet Reactivity on Treatment with Clopidogrel". Seminars in Thrombosis and Hemostasis 38, n.º 07 (3 de octubre de 2012): 645–51. http://dx.doi.org/10.1055/s-0032-1326785.

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Meves, Saskia H., Kay D. Schröder, Heinz G. Endres, Christos Krogias, Jan C. Krüger y Horst Neubauer. "Clopidogrel High-on-Treatment Platelet Reactivity in Acute Ischemic Stroke Patients". Thrombosis Research 133, n.º 3 (marzo de 2014): 396–401. http://dx.doi.org/10.1016/j.thromres.2013.12.002.

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30

Johnston, L. R., J. Michel, A. Ramanathan, A. La Flamme, A. Sasse, P. D. Larsen y S. A. Harding. "High on Treatment Platelet Reactivity in a New Zealand ACS Population". Heart, Lung and Circulation 20, n.º 6 (junio de 2011): 389–90. http://dx.doi.org/10.1016/j.hlc.2011.03.043.

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Polzin, Amin, Mathias Schleicher, Holger Seidel, Rüdiger E. Scharf, Marc W. Merx, Malte Kelm y Tobias Zeus. "High on-treatment platelet reactivity in transcatheter aortic valve implantation patients". European Journal of Pharmacology 751 (marzo de 2015): 24–27. http://dx.doi.org/10.1016/j.ejphar.2015.01.028.

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Jover, Eva, José M. Rodríguez, Agustina Bernal, Ana B. Arroyo, Juan A. Iniesta, Isabel Sánchez Guiú, Constantino Martínez, Vicente Vicente, María L. Lozano y José Rivera. "High on-treatment platelet reactivity in patients with ischemic cerebrovascular disease". Blood Coagulation & Fibrinolysis 25, n.º 6 (septiembre de 2014): 604–11. http://dx.doi.org/10.1097/mbc.0000000000000118.

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Gaglia, Michael A., Rebecca Torguson, Rajbabu Pakala, Manuel A. Gonzalez, Itsik Ben-Dor, Gabriel Maluenda, Michael Mahmoudi et al. "High on-treatment platelet reactivity is associated with periprocedural myocardial infarction". Cardiovascular Revascularization Medicine 12, n.º 3 (mayo de 2011): 193. http://dx.doi.org/10.1016/j.carrev.2011.02.012.

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34

Gaglia, Michael A., Rebecca Torguson, Rajbabu Pakala, Manuel A. Gonzalez, Itsik Ben-Dor, Gabriel Maluenda, Michael Mahmoudi et al. "High on-treatment platelet reactivity is associated with periprocedural myocardial infarction". Cardiovascular Revascularization Medicine 12, n.º 3 (mayo de 2011): e15. http://dx.doi.org/10.1016/j.carrev.2011.04.282.

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35

Gaglia, Michael A., Rebecca Torguson, Rajbabu Pakala, Manuel A. Gonzalez, Itsik Ben-Dor, Gabriel Maluenda, Michael Mahmoudi et al. "Chronic renal insufficiency is associated with high on-treatment platelet reactivity". Cardiovascular Revascularization Medicine 12, n.º 3 (mayo de 2011): e29-e30. http://dx.doi.org/10.1016/j.carrev.2011.04.321.

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36

Mohring, Annemarie, Kerstin Piayda, Lisa Dannenberg, Saif Zako, Theresa Schneider, Kirsten Bartkowski, Bodo Levkau et al. "Thromboxane Formation Assay to Identify High On-Treatment Platelet Reactivity to Aspirin". Pharmacology 100, n.º 3-4 (2017): 127–30. http://dx.doi.org/10.1159/000477303.

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Platelet inhibition by aspirin is indispensable in the secondary prevention of cardiovascular events. Nevertheless, impaired aspirin antiplatelet effects (high on-treatment platelet reactivity [HTPR]) are frequent. This is associated with an enhanced risk of cardiovascular events. The current gold standard to evaluate platelet hyper-reactivity despite aspirin intake is the light-transmittance aggregometry (LTA). However, pharmacologically, the most specific test is the measurement of arachidonic acid (AA)-induced thromboxane (TX) B2 formation. Currently, the optimal cut-off to define HTPR to aspirin by inhibition of TX formation is not known. Therefore, in this pilot study, we aimed to calculate a TX formation cut-off value to detect HTPR defined by the current gold standard LTA. We measured platelet function in 2,507 samples. AA-induced TX formation by ELISA and AA-induced LTA were used to measure aspirin antiplatelet effects. TX formation correlated nonlinearly with the maximum of aggregation in the AA-induced LTA (Spearman's rho R = 0.7396; 95% CI 0.7208-0.7573, p < 0.0001). Receiver operating characteristic analysis and Youden's J statistics revealed 209.8 ng/mL as the optimal cut-off value to detect HTPR to aspirin with the TX ELISA (area under the curve: 0.92, p < 0.0001, sensitivity of 82.7%, specificity of 90.3%). In summary, TX formation ELISA is reliable in detecting HTPR to aspirin. The calculated cut-off level needs to be tested in trials with clinical end points.

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37

Gibbins, Jonathan, Rekha Rana, Dalia Khan, Susie Shapiro, Henri Grech y Karthik Ramasamy. "Multiple Myeloma Treatment Is Associated with Enhanced Platelet Reactivity". Blood 132, Supplement 1 (29 de noviembre de 2018): 3300. http://dx.doi.org/10.1182/blood-2018-99-116006.

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Abstract Multiple myeloma (MM) is associated with elevated levels of thrombotic disease. Poor mobility due to bone disease and older age are contributory factors but a satisfactory molecular or cellular explanation for this has not been established. Furthermore, the treatment of newly-diagnosed or relapsed MM patients with immunomodulatory drugs increases thrombosis risk. In this study, we therefore sought to determine whether platelet function and/or haemostasis is altered during the clinical progression from the benign monoclonal gammopathy of underdetermined significance (MGUS) to the smouldering myeloma (SM, untreated) state, and to establish the impact of lenalidomide therapy in MM patients on platelet reactivity. Patients (MGUS (N=10), SM (N=10) MM (N=4), healthy volunteer/control (N=10)) were recruited at the myeloma clinics at the Royal Berkshire and Oxford University Hospital Trusts. Single blood samples were obtained from controls, MGUS and smoldering myeloma participants. For patients undergoing therapy (lenalidomide, dexamethasone and anti-coagulant or anti-platelet therapy), samples were taken at predose Cy1, Cy1 D14, Cy1 D28 (a week free from lenalidomide administration), and Cy4 D14. All blood samples were taken less than 12 hours from Lenalidomide dosing, and analysis performed within 4 hours. High throughput platelet function analysis was performed on platelet-rich plasma and washed platelets to measure platelet aggregation, secretion and fibrinogen binding in response collagen, collagen-related peptide (a collagen receptor GPVI-selective ligand), ADP, thrombin receptor activatory peptide (TRAP), the thromboxane mimetic U46619 and epinephrine, and full concentration-response profiles obtained for each. The levels of key platelet receptors including GPVI, CD61, CD41b, CD36 and CD31, were also measured by flow cytometry and remained unaltered between groups. In comparison with control samples, platelet functional responses (maximal response, maximal gain and EC50) from MGUS and smoldering myeloma patients were unaltered (EC50: ADP 1µM, collagen-related peptide (CRP-XL) 0.1µg/ml, U46619 1µM, TRAP 1.6µM, epinephrine 1.3µM). Similarly circulating levels of platelet-bound fibrinogen and P-selectin exposure were unaltered (control: 709±194 AU, MGUS: 581±129 AU, SM: 655±148 AU 9 (Mean±SD)). In MM patients during therapy, the levels of these platelet responses (aggregation, fibrinogen binding and P-selectin exposure - a marker for a-granule secretion) were increased 2-4 fold. In most patients this was notable at week 2 and had declined approximately 50% by week 4 of cycle 1 but remained above predose levels, and remained elevated to a similar level in drug cycle 4. The study of further patients (including Bortezomib treated patients as controls) will be required in order to validate these findings which suggest that (1) baseline platelet function is not substantially compromised in MM and SM, (2) lenalidomide and other immunomodulatory drugs may be able to modulate platelets in patients causing increased platelet reactivity, and (3) effects noted are lenalidomide-dependent and not related to inflammatory state secondary to disease response. The effects of exposure of platelets to lenalidomide in vitro in the presence or absence of dexamethasone and a proteasome inhibitor are being tested to explore potential direct effects of the drugs on circulating platelets. Results from these experiments will also be presented. Disclosures Gibbins: Celgene Corporation: Research Funding. Rana:Celgene Corporation: Research Funding. Khan:Celgene Corporation: Research Funding. Shapiro:Freeline Therapeutics Ltd: Consultancy. Grech:Novartis: Other: sponsorship for scientific meetings. Ramasamy:Janssen: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Amgen: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Takeda: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Celgene: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding.

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38

Pedersen, Oliver Buchhave, Leonardo Pasalic, Erik Lerkevang Grove, Steen Dalby Kristensen, Anne-Mette Hvas y Peter H. Nissen. "Advanced Flow Cytometry Using the SYTO-13 Dye for the Assessment of Platelet Reactivity and Maturity in Whole Blood". Methods and Protocols 6, n.º 1 (13 de enero de 2023): 8. http://dx.doi.org/10.3390/mps6010008.

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Newly produced immature platelets are larger, contain higher amounts of residual RNA, and are more reactive than mature platelets. Flow cytometry using the SYTO-13 dye is a method for the subdivision of immature platelets from mature platelets based on the labelling of intracellular platelet RNA, enabling the simultaneous investigation of the reactivity of each platelet population. This method provides detailed information on several aspects of platelet physiology using a combination of platelet surface markers and agonists. Currently, no standardized protocol exists across laboratories. Here, we describe a flow cytometry protocol in detail to investigate platelet reactivity and its relation to platelet maturity. We analyzed 20 healthy individuals with the protocol and compared the platelet subpopulation with the highest SYTO-13 labelling (in the first quintile, “SYTO-high”) corresponding to the most immature platelets (highest RNA content) with the platelet subpopulation with the lowest SYTO-13 labelling (in the fifth quintile, “SYTO-low”) corresponding to the mature platelets with the lowest RNA content. SYTO-high platelets had overall significantly increased platelet reactivity compared with that of SYTO-low platelets. The presented method may be a valuable research tool for the analysis of platelet reactivity and its relation to platelet maturity.

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39

Armstrong, Paul C., Thomas Hoefer, Rebecca B. Knowles, Arthur T. Tucker, Melissa A. Hayman, Plinio M. Ferreira, Melissa V. Chan y Timothy D. Warner. "Newly Formed Reticulated Platelets Undermine Pharmacokinetically Short-Lived Antiplatelet Therapies". Arteriosclerosis, Thrombosis, and Vascular Biology 37, n.º 5 (mayo de 2017): 949–56. http://dx.doi.org/10.1161/atvbaha.116.308763.

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Objective— Aspirin together with thienopyridine P2Y 12 inhibitors, commonly clopidogrel, is a cornerstone of antiplatelet therapy. However, many patients receiving this therapy display high on-treatment platelet reactivity, which is a major therapeutic hurdle to the prevention of recurrent thrombotic events. The emergence of uninhibited platelets after thrombopoiesis has been proposed as a contributing factor to high on-treatment platelet reactivity. Here, we investigate the influences of platelet turnover on platelet aggregation in the face of different dual-antiplatelet therapy strategies. Approach and Results— Traditional light transmission aggregometry, cytometry, advanced flow cytometric imaging, and confocal microscopy were used to follow the interactions of populations of platelets from healthy volunteers and patients with stable cardiovascular disease. Newly formed, reticulated platelets overproportionately contributed to, and clustered at, the core of forming aggregates. This phenomenon was particularly observed in samples from patients treated with aspirin plus a thienopyridine, but was absent in samples taken from patients treated with aspirin plus ticagrelor. Conclusions— Reticulated platelets are more reactive than older platelets and act as seeds for the formation of platelet aggregates even in the presence of antiplatelet therapy. This is coherent with the emergence of an uninhibited subpopulation of reticulated platelets during treatment with aspirin plus thienopyridine, explained by the short pharmacokinetic half-lives of these drugs. This phenomenon is absent during treatment with ticagrelor, because of its longer half-life and ability to act as a circulating inhibitor. These data highlight the important influences of pharmacokinetics on antiplatelet drug efficacies, especially in diseases associated with increased platelet turnover.

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Bernlochner, Isabell, Steven Steinhubl, Siegmund Braun, Tanja Morath, Juliane Jaitner, Julia Stegherr, Julinda Mehilli et al. "Association between inflammatory biomarkers and platelet aggregation in patients under chronic clopidogrel treatment". Thrombosis and Haemostasis 104, n.º 12 (2010): 1193–200. http://dx.doi.org/10.1160/th10-05-0266.

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SummaryInflammatory processes in the vessel wall are associated with progression of atherosclerosis and myocardial infarction. Both high levels of C-reactive protein (CRP) and high on-clopidogrel treatment platelet reactivity (HPR) have been linked to an increased risk of ischaemic events after percutaneous coronary intervention (PCI). The aim of this study was to explore the association between biomarker levels of inflammation and platelet reactivity. Stable patients (n=1,223) eligible for this study were under chronic antiplatelet treatment with aspirin and clopidogrel due to prior coronary stent placement. ADP-induced platelet aggregation (in AU*min) was measured on a Multiplate analyser. The primary outcome measure of this retrospective study was the ADP-induced platelet aggregation in patients with versus those without elevated CRP levels. Of the patients 15.5% (n=189) showed elevated CRP levels (≥5 mg/l). Platelet aggregation (median [interquartile range]) was significantly higher in patients with elevated CRP levels compared to patients with normal (<5 mg/l) CRP levels (305 [202–504] AU*min vs. 218 [144–384] AU*min; p<0.001). A multivariable linear regression model that adjusted for known predictors of HPR confirmed a significant independent association between elevated CRP levels and high ADP-induced platelet aggregation values (p=0.0002). Elevated WBC count and fibrinogen levels were also associated with higher platelet aggregation values (p<0.001 for both). In conclusion, elevated levels of CRP, WBC count and fibrinogen were significantly associated with high platelet reactivity in patients under chronic clopidogrel treatment. Whether a direct relation between platelets and inflammation exists, as well as the clinical impact of our results, warrants further investigations.

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41

Marcucci, Rossella, Roberto Caporale, Rita Paniccia, Eloisa Romano, Gian Franco Gensini, Rosanna Abbate, Anna Maria Gori y Francesca Cesari. "Relationship between high platelet turnover and platelet function in high-risk patients with coronary artery disease on dual antiplatelet therapy". Thrombosis and Haemostasis 99, n.º 11 (2008): 930–35. http://dx.doi.org/10.1160/th08-01-0002.

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SummaryA high platelet turnover rate produce a population of immature reticulated platelets (RP) that could confer, despite of antiplatelet drugs, a residual platelet reactivity (RPR) in coronary artery disease (CAD) patients. To assess the influence of RP on platelet reactivity in CAD patients on dual antiplatelet therapy we measured RP in 372 patients by using the Sysmex XE-2100 haematology analyzer and platelet function by optical platelet aggregometry (PA) on platelet-rich-plasma induced by 1 mmol arachidonic acid (AA-PA) and 10 μM ADP (ADP-PA). RPR was defined as either AA-PA >20% or ADP-PA >70%. RP were expressed as a percentage of RP of the total optical platelet count (immature platelet fraction; IPF) and as the percentage of RP highly fluorescent (higly fluorescent immature platelet fraction; H-IPF). Moderate but significant positive correlations between PA, IPF, H-IPF, and mean platelet volume (MPV) were found. According to tertiles of IPF, H-IPF and MPV, a significant trend for an increase of platelet aggregation by AA and ADP was evidenced. Furthermore, a significant difference for IPF, H-IPF and MPV between patients with and without RPR was observed. A linear regression analysis showed that IPF, H-IPF and MPV significantly affected PA measured by AA and ADP. At multivariate linear regression analysis these associations were confirmed. Moreover, a logistic regression analysis demonstrated that IPF, H-IPF and MPV significantly influenced the risk of RPR, and in the multivariate model these results remained significant. This study indicates that a high rate of platelet turnover is a new mechanism associated with platelet reactivity in high risk CAD patients on dual antiplatelet therapy.

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42

Berger, Martin, Alexander Dressel, Marcus E. Kleber, Winfried März, Peter Hellstern, Nikolaus Marx y Katharina Schütt. "Platelet Reactivity and Cardiovascular Mortality Risk in the LURIC Study". Journal of Clinical Medicine 12, n.º 5 (28 de febrero de 2023): 1913. http://dx.doi.org/10.3390/jcm12051913.

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Background: The clinical and prognostic implications of platelet reactivity (PR) testing in a P2Y12-inhibitor naïve population are poorly understood. Objectives: This explorative study aims to assess the role of PR and explore factors that may modify elevated mortality risk in patients with altered PR. Methods: Platelet ADP-induced CD62P and CD63 expression were measured by flow-cytometry in 1520 patients who were referred for coronary angiography in the Ludwigshafen Risk and Cardiovascular Health Study (LURIC). Results: High- and Low-platelet reactivity to ADP were strong predictors of cardiovascular and all-cause mortality and risk equivalent to the presence of coronary artery disease. (High platelet reactivity 1.4 [95% CI 1.1–1.9]; Low platelet reactivity: 1.4 [95% CI 1.0–2.0]). Relative weight analysis indicated glucose control (HbA1c), renal function ([eGFR]), inflammation (high-sensitive C-reactive protein [hsCRP]) and antiplatelet therapy by Aspirin as consistent mortality risk modifiers in patients with Low- and High-platelet reactivity. Pre-specified stratification of patients by risk modifiers HbA1c (<7.0%), eGFR (>60 mL/min/1.73 m2) and CRP (<3 mg/L) was associated with a lower mortality risk, however irrespective of platelet reactivity. Aspirin treatment was associated with reduced mortality in patients with high platelet reactivity only (p for interaction: 0.02 for CV-death [<0.01 for all-cause mortality]. Conclusions: Cardiovascular mortality risk in patients with High- and Low platelet reactivity is equivalent to the presence of coronary artery disease. Targeted glucose control, improved kidney function and lower inflammation are associated with reduced mortality risk, however independent of platelet reactivity. In contrast, only in patients with High-platelet reactivity was Aspirin treatment associated with lower mortality.

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Biolik, Grzegorz, Dariusz Gajniak, Maciej Kubicz, Damian Ziaja, Krzysztof Ziaja y Wacław Kuczmik. "The Influence of Inflammation on Fibrinogen Turnover and Redistribution of the Hemostatic Balance to a Prothrombotic State in High On-Treatment Platelet Reactivity-Dual Poor Responder (HTPR-DPR) Patients". Mediators of Inflammation 2019 (17 de julio de 2019): 1–6. http://dx.doi.org/10.1155/2019/3767128.

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Knowledge about the influence of inflammation on platelet function and relocation of hemostatic balance to hypercoagulable state is still unclear. We compared two groups of patients who suffer from acute vs. chronic inflammatory process and additionally present high on-treatment platelet reactivity-dual platelet resistance. We did not found any differences in platelet aggregation between both investigated groups, but patients who suffer from chronic inflammation presented stronger relocation of the hemostatic balance to the hypercoagulability. A high concentration of prothrombin fragment F1+2 together with higher activity of von Willebrand factor in critical limb ischemia shows more exaggerated fibrinogen turnover although the blood concentration of this factor was in normal range. We concluded that high on-treatment platelet reactivity-dual platelet resistance and intensified inflammation are linked with elevated platelet and fibrinogen turnover to counteract proper hemostatic balance in favor of a prothrombotic state.

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44

Nooney, Vivek B., Yuliy Chirkov y John Horowitz. "PT209 “High On-treatment” Platelet Reactivity, But Not Pre-treatment Hyperaggregability, Predicts Clopidogrel Response". Global Heart 9, n.º 1 (marzo de 2014): e208. http://dx.doi.org/10.1016/j.gheart.2014.03.1977.

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45

Akinosoglou, Karolina, Angelos Perperis, Spyridoula Theodoraki, Dimitrios Alexopoulos y Charalambos Gogos. "Sepsis favors high-on-clopidogrel platelet reactivity". Platelets 29, n.º 1 (21 de junio de 2017): 76–78. http://dx.doi.org/10.1080/09537104.2017.1319919.

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46

Hills, Robert K. "High on‐treatment platelet reactivity—an OPTIMAl solution, or a better solution?" British Journal of Haematology 196, n.º 2 (3 de noviembre de 2021): 272–73. http://dx.doi.org/10.1111/bjh.17944.

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47

Stolarek, Wioleta, Michał Kasprzak, Joanna Sikora, Emilia Siemińska y Grzegorz Grześk. "High on-treatment platelet reactivity to aspirin in patients after myocardial infarction". Biomedicine & Pharmacotherapy 147 (marzo de 2022): 112618. http://dx.doi.org/10.1016/j.biopha.2022.112618.

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48

Szymezak, Jean, Caroline Moreau, Marie-Anne Loriot, Eric Durand, Hubert Van Viet, Michel Desnos y Pascale Gaussem. "High on-clopidogrel platelet reactivity: Genotyping Can help to optimize antiplatelet treatment". Thrombosis Research 128, n.º 1 (julio de 2011): 92–95. http://dx.doi.org/10.1016/j.thromres.2011.01.012.

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49

Harding, S., L. Johnston, J. Michel, A. Ramanathan, A. La Flamme, A. Sasse y P. Larsen. "High on Treatment Platelet Reactivity is Common and Differs Among Ethnic Groups". Heart, Lung and Circulation 20 (enero de 2011): S34—S35. http://dx.doi.org/10.1016/j.hlc.2011.05.088.

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50

Psaila, Bethan, James B. Bussel, Matthew D. Linden, Bracken Babula, Youfu Li, Marc R. Barnard, Chinara Tate, Kanika Mathur, Andrew L. Frelinger y Alan D. Michelson. "In vivo effects of eltrombopag on platelet function in immune thrombocytopenia: no evidence of platelet activation". Blood 119, n.º 17 (26 de abril de 2012): 4066–72. http://dx.doi.org/10.1182/blood-2011-11-393900.

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Abstract The effects of eltrombopag, a thrombopoietin-receptor agonist, on platelet function in immune thrombocytopenia (ITP) are not fully characterized. This study used whole blood flow cytometry to examine platelet function in 20 patients receiving eltrombopag treatment at days 0, 7, and 28. Platelet surface expression of activated GPIIb/IIIa, P-selectin, and GPIb was measured with and without low and high adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP) concentrations. Before eltrombopag treatment with no ex vivo agonist, platelet activation was higher in ITP patients than controls. Platelet GPIb and activated GPIIb/IIIa expression without added agonist was unchanged following eltrombopag treatment, whereas a slight increase in P-selectin was observed. Expression of P-selectin and activated GPIIb/IIIa in response to high-dose ADP was lower during eltrombopag treatment than at baseline. Eltrombopag led to a slight increase in platelet reactivity to TRAP only in responders to eltrombopag but not to levels above those in controls; whole blood experiments demonstrated that this increase was probably because of higher platelet counts rather than higher platelet reactivity. In conclusion, although thrombocytopenic ITP patients have higher baseline platelet activation than controls, eltrombopag did not cause platelet activation or hyper-reactivity, irrespective of whether the platelet count increased.

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