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Nathalie Hézard

Publications and source records attributed to Nathalie Hézard.

6 recordsLinked to original sources
PubMed2006

Utility of thrombin-generation assay in the screening of factor V G1691A (Leiden) and prothrombin G20210A mutations and protein S deficiency.

BACKGROUND: The thrombin-generation assay has a variety of clinical uses, including diagnosis of thromboembolism-related disease, and particular profiles are associated with thrombophilic risk factors. The aim of this study was to evaluate the use of this assay in screening and identifying patients who require specific thrombophilic testing. METHODS: We used a 2-step approach to perform specific thrombophilic testing and thrombin-generation assays on 169 consecutive patients. The first step was to identify particular profiles of thrombin generation corresponding to each type of thrombophilic risk factor and to determine the pertinent variables related to thrombin generation. We then performed ROC curve analysis for each predefined variable to determine the relevant cutoffs for identification of patients in need of further testing (negative predictive value, 100%). RESULTS: Suggestive profiles were seen in factor V Leiden (n = 49) and prothrombin (n = 12) mutations and in protein S deficiency (n = 12). ROC curves showed that factor V Leiden may be excluded when the difference between lag times obtained in the absence and presence of activated protein C (APC) is >1.5 min and that prothrombin G20210A may also be excluded when the peak thrombin concentration is 63%. CONCLUSION: The thrombin-generation assay represents a promising tool for screening thrombophilic risk factors, particularly in patients who are carriers of factor V Leiden or prothrombin G20210A mutations and patients with protein S deficiency.

Adult↗
PubMed2003

Unexpected persistence of platelet hyporeactivity beyond the neonatal period: a flow cytometric study in neonates, infants and older children.

Previous studies, using flow cytometry, have reported a lower platelet reactivity in neonates compared to adults. Only few studies were carried out in older children, and results were controversial in terms of age to reach adult platelet function. We studied a total of 125 healthy neonates, infants and older children, and 15 adults. alphaIIbbeta3 expression on resting and activated platelets was lower in all children, with an impaired capability of alphaIIbbeta3 activation (PAC1 and bound fibrinogen). This defect was observed until the age of fifteen with a gradual recovery with age. In neonates, we observed a defect of GPIalpha internalization, and demonstrated that this defect persisted in older children as well. In contrast with alphaIIbbeta3 integrin activation, we did not observe a gradual age-dependent recovery. These unexpected results point out the need for reference values in childhood.

Adolescent↗
PubMed2002

PFA-100 and flow cytometry: can they challenge aggregometry to assess antiplatelet agents, other than GPIIbIIIa blockers, in coronary angioplasty?

INTRODUCTION: Platelet response to inhibitors varies widely, leading to a higher risk of abrupt closure events in insufficiently treated-coronary heart disease patients. The aim of this study was to compare, in patients under various antiplatelet regimens, three platelet function assays: aggregometry, PFA-100 and flow cytometry. These assays stand for available tests, as "ready-to-use" device (PFA-100) and sophisticated assay (cytometry). We chose the setting of percutaneous coronary intervention as a standardized procedure to determine which test was appropriate to detect the effect of (1) an aspirin bolus in patients under long-term aspirin treatment, and (2) ticlopidin in case of stent implantation. METHODS: Fifty patients under oral aspirin treatment were randomized to receive a bolus of 500 mg aspirin before angioplasty (n=25). Ticlopidin was given at a 500 mg loading dose in the case of stent implantation (n=38). Platelet function was assessed before, at 2 and 24 h after angioplasty. RESULTS: Considering aspirin antiplatelet effect, the following was observed: (1) a lack of further inhibition after the bolus whatever assay was used and (2) a disagreement between aggregometry and PFA-100 to classify patients as being poor or good aspirin responders (kappa were 0.11 and 0.28 between ADP 4 or 6 microM aggregation, respectively, and PFA-100). Another finding was the good performance of flow cytometry, which evaluated GPIIbIIIa activation, and aggregometry, to detect ticlopidin the day after the loading dose. In contrast, PFA-100 was insensitive to ticlopidin. CONCLUSION: Current assays are not interchangeable to monitor antiplatelet treatment in daily practice.

Angioplasty, Balloon, Coronary↗