59 results match your criteria: "Hopital Universitaire Nord[Affiliation]"

Ticagrelor versus prasugrel in diabetic patients with an acute coronary syndrome. A pharmacodynamic randomised study.

Thromb Haemost

February 2014

Laurent Bonello, MD, PhD, Department of cardiology, Hôpital universitaire nord, Chemin des bourrely, 13015 Marseille, France, Tel.: +33 491 968 858, Fax: +33 491 968 979, E-mail:

Optimal P2Y12 receptor blockade is critical to prevent ischaemic recurrence in patients undergoing percutaneous coronary intervention (PCI). We aimed to compare the level of platelet reactivity (PR) inhibition achieved by prasugrel and ticagrelor loading dose (LD) in diabetic acute coronary syndrome (ACS) patients undergoing PCI. We performed a single-center prospective open-label randomised trial.

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Dual antiplatelet therapy with aspirin and a P2Y12 receptor blocker is a key strategy to reduce platelet reactivity and to prevent thrombotic events in patients treated with percutaneous coronary intervention. In an earlier consensus document, we proposed cutoff values for high on-treatment platelet reactivity to adenosine diphosphate (ADP) associated with post-percutaneous coronary intervention ischemic events for various platelet function tests (PFTs). Updated American and European practice guidelines have issued a Class IIb recommendation for PFT to facilitate the choice of P2Y12 receptor inhibitor in selected high-risk patients treated with percutaneous coronary intervention, although routine testing is not recommended (Class III).

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Dual antiplatelet therapy is critical to inhibit platelet reactivity in order to prevent ischemic recurrences in stented patients. However, studies have observed a variable blockade of the P2Y12 adenosine diphosphate receptor between patients following clopidogrel intake. This interindividual variability in the biological response is not uncommon with clopidogrel (about 50%) and even prasugrel (20%).

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A randomized trial of platelet reactivity monitoring-adjusted clopidogrel therapy versus prasugrel therapy to reduce high on-treatment platelet reactivity.

Int J Cardiol

October 2013

Département de cardiologie, Hôpital universitaire nord, Aix-Marseille Univ., Marseille, France; INSERM UMRS 608, UFR de pharmacie, Marseille, France. Electronic address:

Background: Peri-procedural platelet reactivity (PR) inhibition is critical in patients undergoing percutaneous coronary intervention (PCI). High on-treatment PR (HTPR) was associated with recurrent ischemic events in acute coronary syndrome (ACS) patients undergoing PCI. We aimed to compare a strategy of clopidogrel loading dose-adjustment (CDA) according to PR monitoring with standard prasugrel therapy to reduce the rate of patients exhibiting HTPR.

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Background: The level of platelet reactivity (PR) inhibition obtained after P2Y12-ADP receptor antagonist loading dose (LD) is associated with the ischemic and bleeding risk following percutaneous coronary intervention (PCI) in acute coronary syndromes (ACS).

Objective: We aimed to evaluate the level of PR inhibition achieved by a 180 mg LD of ticagrelor and the rate of high on-treatment platelet reactivity (HTPR) in ACS patients undergoing PCI.

Methods: We performed a multicentre prospective observational study enrolling ACS patients undergoing PCI.

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Background: Post-treatment platelet reactivity (PR) is associated with ischemic and bleeding events in patients receiving P2Y12 receptor antagonists.

Objectives: We aimed to study the relationship between post-treatment PR after a 60-mg loading dose (LD) of prasugrel and 1-year thrombotic and bleeding events.

Method: Patients were prospectively included in this multicenter study if they had a successful percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) and received prasugrel.

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Mobilization of CD34+ KDR+ endothelial progenitor cells predicts target lesion revascularization.

J Thromb Haemost

September 2012

Département de cardiologie, Hôpital universitaire nord, Faculté de médecine, Aix Marseille Université, Marseille, France.

Background: Endothelial lesion and regeneration are critical events in the process leading to in-stent restenosis (ISR) after bare metal stent (BMS) percutaneous coronary intervention (PCI).

Objectives: To prospectively investigate the relationship between biomarkers reflecting endothelial turnover and the occurrence of ISR.

Methods: We performed a multicenter prospective observational study that included 156 patients undergoing elective PCI with BMS.

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In patients with acute coronary syndromes undergoing percutaneous coronary intervention, the combination of aspirin and clopidogrel, a P2Y12 adenosine diphosphate (ADP) receptor antagonist, is the gold standard of antiplatelet therapy. Two more potent P2Y12 ADP receptor antagonists are now available. Pharmacodynamic studies have revealed a large interindividual variability in the biological response to clopidogrel that is primarily related to variable active metabolite generation, depending on clinical factors, drug-drug interactions, and genetic polymorphisms.

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Optimal platelet reactivity (PR) inhibition is critical to prevent thrombotic events in primary percutaneous coronary intervention (PCI). We aimed to determine the relationship between high on-treatment platelet reactivity (HTPR) and ST-elevation myocardial infarction (STEMI) following a 600 mg loading dose (LD) of clopidogrel. We performed a prospective monocentre study enrolling patients on clopidogrel undergoing PCI.

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Introduction: Inter-individual variability in clopidogrel responsiveness is dependent on genetic polymorphisms. We aimed to investigate the impact of 3 genetic polymorphisms involved in clopidogrel metabolism on a strategy of dose-adjustment according to platelet reactivity (PR) monitoring.

Material And Methods: [corrected] This prospective multicenter study enrolled 498 ACS patients undergoing PCI.

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Unveiling the mysteries of clopidogrel metabolism and efficacy.

Clin Pharmacol Ther

December 2011

Department of Cardiology, Hôpital Universitaire Nord, Faculté de Médecine de Marseille, Marseille, France.

Clopidogrel is an important antiplatelet agent, but a considerable variability in the biological effect of the drug has been observed. Additionally, patients with insufficient platelet reactivity inhibition following a loading dose (LD) of clopidogrel have a poor outcome. The mechanisms of variability are dependent on genetic polymorphisms of enzymes involved in clopidogrel metabolism.

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Atherosclerotic renal artery stenosis is frequent and is associated with a high incidence of morbidity and mortality, with a strong correlation with coronary artery disease, (Kalra et al., 2005; Cheung et al., 2002; Guo et al.

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Rate of nuisance bleedings and impact on compliance to prasugrel in acute coronary syndromes.

Am J Cardiol

December 2011

Département de Cardiologie, Hôpital Universitaire Nord, Faculté De Médecine, Université de la Méditerranée, Marseille, France.

Antiplatelet agents are critical to prevent thrombotic events in patients with acute coronary syndromes, particularly those who undergo percutaneous coronary intervention. Prasugrel is a potent P2Y(12)-adenosine diphosphate receptor antagonist that is superior to clopidogrel in such patients. Previous studies have observed that nuisance and internal bleedings were relatively frequent in patients under clopidogrel therapy and were associated with noncompliance.

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Objectives: The aim of this study was to investigate the relationship between platelet reactivity (PR) after a loading dose (LD) of prasugrel and thrombotic events.

Background: Post-treatment PR has been shown to be strongly associated with the occurrence of major adverse cardiac events (MACE) after percutaneous coronary intervention (PCI) in the clopidogrel era. Prasugrel is a new P2Y(12)-adenosine diphosphate receptor with a higher potency on PR.

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Most ST-elevation myocardial infarctions are related to atherothrombosis and benefit from emergent percutaneous coronary intervention. On the other hand, type-A aortic dissection is a less frequent but deadly disease requiring emergent surgery. In the present case, we aimed to report the case of a patient who presented with aortic dissection responsible for STEMI and cardiogenic shock related to a compressive hematoma of the left main trunk.

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Objectives: We aimed to investigate whether clopidogrel-induced inhibition of platelet reactivity could reduce the level of circulating endothelial cells (CEC), reflecting the endothelial injury induced by percutaneous coronary intervention (PCI).

Background: Clopidogrel loading dose before percutaneous coronary angioplasty (PCI) reduces platelet activation through a selective and irreversible blockade of the adenosine diphosphate (ADP) receptor P2Y(12). The impact of clopidogrel on endothelial cells has been scarcely studied.

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Consensus and future directions on the definition of high on-treatment platelet reactivity to adenosine diphosphate.

J Am Coll Cardiol

September 2010

Department of Cardiology, Institut National de la Santè et de la Recherche Médicale Unité Mixte de Recherche 608, Hôpital Universitaire Nord, Faculté de Médecine, Marseille, France.

The addition of clopidogrel to aspirin treatment reduces ischemic events in a wide range of patients with cardiovascular disease. However, recurrent ischemic event occurrence during dual antiplatelet therapy, including stent thrombosis, remains a major concern. Platelet function measurements during clopidogrel treatment demonstrated a variable and overall modest level of P2Y(12) inhibition.

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Objectives: We aimed to investigate the biological impact of a tailored clopidogrel loading dose (LD) according to platelet reactivity monitoring in carriers of the cytochrome (CYP) 2C19*2 loss-of-function polymorphism undergoing percutaneous coronary intervention for an acute coronary syndromes.

Background: CYP2C19*2 polymorphism is associated with reduced clopidogrel metabolism and a worse prognosis after percutaneous coronary intervention.

Method: A prospective multicenter study enrolling 411 patients with non-ST-segment elevation acute coronary syndrome undergoing percutaneous coronary intervention was performed.

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Clopidogrel responsiveness (CR) following a loading dose (LD) predicts thrombotic events after percutaneous coronary interventions (PCI). Some of the mechanisms involved in large inter-individual variability in CR may be varied. We therefore postulated that there may be an intra-individual variability in CR.

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Fractional flow reserve is a simple and efficient tool to assess the severity of an intermediate lesion in order to determine the optimal therapy. However there are some limitations to its use. We observed that in patients with an occluded artery, FFR measurements in the vessel supplying collaterals can be underestimated leading to inappropriate therapy.

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Clopidogrel has decreased the rate of thrombotic events in patients undergoing percutaneous coronary intervention. However, two major limitations of the drug have been involved in the persistence of a relatively high rate of adverse events. The recent literature suggested that improved platelet reactivity inhibition using a higher or tailored dose of clopidogrel, or a more potent agent, could reduce the rate of events.

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Introduction: High on-treatment platelet reactivity (HTPR) after clopidogrel loading dose (LD) is associated with a high risk of thrombotic events after percutaneous coronary intervention(PCI). We have demonstrated that HTPR could be overcome in the majority of cases using LD adjustment resulting in an improved clinical outcome. However this strategy failed in nearly 10% of patients with HTPR.

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Stent thrombosis remains a significant pitfall of percutaneous coronary intervention (PCI). A recent trial observed that an adjusted loading dose (LD) of clopidogrel according to platelet monitoring decreases the rate of major adverse cardiovascular events after PCI. We investigated if such a strategy of a tailored clopidogrel LD according to platelet reactivity monitoring could decrease the rate of stent thrombosis.

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A paradigm shift in anti-platelet therapy?

Platelets

December 2008

Département de cardiologie, Hôpital universitaire nord de Marseille, Faculté de medecine de Marseille, Marseille, France.

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