COMparison ofPlatelet reactivity following prAsugrel and ticagrelor loading dose inST-Segment elevation myocardial infarctIONpatients: The COMPASSION study

Laine, Marc; Gaubert, Mélanie; Frère, Corinne; Peyrol, Michaël; Thuny, Franck; Yvorra, S; Chelini, Virginie; Bultez, Bruno; Luigi, Stephane; Mokrani, Z.; Bessereau, Jacques; Toesca, Richard; Champenois, A.; Dignat-George, Françoise; Paganelli, Franck; Bonello, Laurent

doi:10.3109/09537104.2014.959914

Cited by 17 publications

(20 citation statements)

References 16 publications

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“…In the present study, the number of patients exhibiting HTPR as defined in an international consensus value was low (5.3%) and the number of patients with LTPR was high (55.8%). These rates are consistent with those in the literature, and they confirm the high potency of the drug, which was associated with a lower rate of HTPR compared to prasugrel in a recent study . In addition in our cohort, no baseline characteristic was associated with HTPR on ticagrelor, unlike what was observed with on‐clopidogrel PR, which is influenced by several factors.…”

Section: Discussionsupporting

confidence: 55%

“…These rates are consistent with those in the literature, 17 and they confirm the high potency of the drug, which was associated with a lower rate of HTPR compared to prasugrel in a recent study. 18 In addition in our cohort, no baseline characteristic was associated with HTPR on ticagrelor,…”

Section: Discussionmentioning

confidence: 56%

“…10,12 In addition, we demonstrated that this relationship was also present with prasugrel through a significant link between on-prasugrel PR and thrombotic events. (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24) .03…”

Section: Discussionmentioning

confidence: 99%

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Platelet reactivity inhibition following ticagrelor loading dose in patients undergoing percutaneous coronary intervention for acute coronary syndrome

Laine

Panagides

Frère

et al. 2019

Journal of Thrombosis and Haemostasis

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Background Ticagrelor induces more potent platelet reactivity (PR) inhibition with reduced interindividual variability compared to clopidogrel. Although on‐clopidogrel PR was shown to correlate with ischemia and bleeding events, no study has investigated the relationship between on‐ticagrelor PR and outcome. Objectives We aimed to evaluate the relationship between on‐ticagrelor PR, assessed by the vasodilator‐stimulated phosphoprotein index (VASP), and thrombotic and bleeding events in patients with acute coronary syndrome (ACS) treated by percutaneous coronary intervention (PCI). Methods We performed a prospective, multicenter observational study on patients treated with PCI for ACS. The VASP index was used to assess PR after ticagrelor loading dose (LD). The primary endpoint was the link between major adverse cardiovascular events (MACE) and PR. Results Among the 530 patients with ACS included, 183 (34.5%) were admitted for ST elevation myocardial infarction. We observed high potency and limited interindividual variability after the ticagrelor LD (VASP 19.1% ± 16.6%). At 1 month, 21 (3.8%) MACE and 29 (5.5%) bleedings ≥ 2 according to the Bleedings Academic Research Consortium (BARC) scale were recorded. Neither MACE nor bleeding was associated with PR (P = .34 and P = .78, respectively). However, there was a strong association between PR and the occurrence of definite acute stent thrombosis (P = .03). Platelet reactivity was the only factor associated with acute definite stent thrombosis. Conclusion In patients receiving a ticagrelor LD while undergoing PCI for ACS, PR using the VASP did not predict MACE or bleeding, but it was significantly associated with the occurrence of definite acute stent thrombosis.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 56%

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Platelet reactivity inhibition following ticagrelor loading dose in patients undergoing percutaneous coronary intervention for acute coronary syndrome

Laine

Panagides

Frère

et al. 2019

Journal of Thrombosis and Haemostasis

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“…Prasugrel is a third generation thienopyridine that irreversibly inhibits the platelet P2Y 12 receptors while ticagrelor is a cyclopenthyltriazolo-pyrimidine and a reversible antagonist of this receptor. To date, no study has directly compared ticagrelor and prasugrel regarding clinical outcomes, and small biological studies comparing the effect of both treatments on platelet reactivity have shown contradictory results [8,[18][19][20][21][22][23][24][25][26][27][28][29][30][31]. Thus, it remains uncertain whether or not one agent is superior to another regarding on-treatment platelet reactivity.…”

Section: Introductionmentioning

confidence: 99%

High on-treatment platelet reactivity with ticagrelor versus prasugrel: a systematic review and meta-analysis

Lemesle

Schurtz

Bauters

et al. 2015

Journal of Thrombosis and Haemostasis

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To cite this article: Lemesle G, Schurtz G, Bauters C, Hamon M. High on-treatment platelet reactivity with ticagrelor vs. prasugrel: a systematic review and meta-analysis. J Thromb Haemost 2015; 13: 931-42.Summary. Background: Ticagrelor and prasugrel have shown superiority over clopidogrel. However, it remains unclear if one is superior to another regarding on-treatment platelet reactivity. Objectives: To compare the impact of ticagrelor and prasugrel on high on-treatment platelet reactivity (HTPR). Methods: The PubMed and Cochrane databases were searched for eligible studies in December 2014. Studies were eligible if they compared ticagrelor and prasugrel regarding high on-treatment platelet reactivity (HTPR). Pooled estimates were calculated by using a random-effects model with 95% confidence intervals. Results: We included 14 studies and 1822 patients: 805 and 1017 in the ticagrelor and prasugrel groups, respectively. The rate of HTPR was significantly lower in the ticagrelor group: 1.5% vs. 9.8% (RR = 0.27 [0.14-0.50]). The pre-specified analysis focusing on randomized trials (n = 10) showed consistent results (RR = 0.27 [0.12-0.60]). Conclusion: Our results suggest that ticagrelor allows a higher platelet reactivity inhibition as compared with prasugrel and leads to a further decrease in the rate of HTPR.

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“…In a study by Alexopoulos et al, 27 STEMI patients treated with prasugrel presented 11.5% HTPR 6 h after loading dose administration and 0% 5 days after the treatment initiation, as assessed with the VeryfyNow P2Y12 assay [36]. Similarly, in a study conducted by Laine et al with 44 STEMI patients treated with prasugrel, HTPR measured 6-12 h after a loading dose of prasugrel and defined as VASP index above or equal to 50%, was reported in 4 patients (9,1%) [37]. Prasugrel was also shown to be effective in 44 ACS patients exhibiting HTPR following a clopidogrel loading dose.…”

Section: Discussionmentioning

confidence: 92%

Variability of prasugrel antiplatelet effect in patients with acute coronary syndrome

Kasprzak

Molska²,

Obońska³

et al. 2015

Medical Research Journal

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Background. Many reports have demonstrated excessive variability in response to clopidogrel, the most commonly used P2Y12 receptor antagonist. Clopidogrel resistant patients are at increased risk of cardiovascular (CV) events. Prasugrel is a new P2Y12 inhibitor that provides greater and faster platelet inhibition and reduces CV events more effectively than clopidogrel. The aim of this study was to evaluate the variability and efficacy of prasugrel antiplatelet activity in patients presenting with acute coronary syndrome (ACS). Materials and methods. The study was designed as a prospective, single-center, non-randomized, observational trial. Platelet reactivity (PR) was assessed with the VeryfyNow assay three times during hospitalization in forty-two patients undergoing percutaneous coronary intervention (PCI) for ACS and treated with standard doses of prasugrel. Results. Platelet aggregation with prasugrel displayed relatively high variability. The platelet aggregation was lowest on the 3 rd day of the treatment at 4 p.m. and was significantly different from the measurements obtained on the 3 rd and 4 th day in the morning (6.0 v. 8.5 U; p = 0.0005 and 6.0 v. 36.5 U; p < 0.00001, respectively), with the latter two differing significantly from each other (p = 0.002). All participants were successfully treated with prasugrel achieving PR < 208 PRU in each measurement, whereas 42.9-80.9% (depending on sampling point) of patients presented very low platelet activity. The subgroups of stable and persistent low PR included a higher percentage of active smokers (73.3 v. 40.7%; p = 0.04 and 80.0 v. 43.8%; p = 0.04, respectively). Conclusions. Prasugrel treatment is associated with high variability of PR. Nonetheless, prasugrel is a highly effective antiplatelet drug. Active smoking may predispose to strong and stable on-prasugrel platelet inhibition.

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COMparison ofPlatelet reactivity following prAsugrel and ticagrelor loading dose inST-Segment elevation myocardial infarctIONpatients: The COMPASSION study

Cited by 17 publications

References 16 publications

Platelet reactivity inhibition following ticagrelor loading dose in patients undergoing percutaneous coronary intervention for acute coronary syndrome

Platelet reactivity inhibition following ticagrelor loading dose in patients undergoing percutaneous coronary intervention for acute coronary syndrome

High on-treatment platelet reactivity with ticagrelor versus prasugrel: a systematic review and meta-analysis

Variability of prasugrel antiplatelet effect in patients with acute coronary syndrome

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