Are you Thibaut Petroni?

Claim your profile

Publications (4)11.94 Total impact

  • International journal of cardiology 09/2011; 152(3):410-1. · 6.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aspirin-induced cyclooxygenase (COX)-1 acetylation is irreversible and it is assumed that the platelet thromboxane-A2 aggregation pathway is inhibited for at least 24 hours (h) after aspirin ingestion. However, time course of biological efficacy of daily low-dose aspirin has rarely been assessed in patients with coronary artery disease (CAD). We aimed to assess the 24-h biological efficacy of daily low-dose aspirin in CAD patients. The peak and trough (2 h-24 h) effect of a chronic treatment with once daily dose aspirin were studied in 150 consecutive stable CAD patients. The main outcome measure was light transmission aggregometry (LTA) triggered with 0.5 mg/ml arachidonic acid (AA). In the last 47 consecutive patients, additional tests were conducted at 6, 12, 16, 20 h after last aspirin administration. 4.7% of the patients had significant aggregation (>20% maximal intensity LTA-AA) 2 h after aspirin ingestion and 24.7% at 24 h (p<0.0001). The more precise assessments in the last 47 patients showed that significant platelet aggregation progressively reappeared with time after aspirin intake (2 h--4% of patients, 6 h-- 4%, 12 h--11%, 16 h--16%, 20 h--19% and 24 h--28%). Concordant results were observed using production of thromboxane-B2 and other techniques evaluating AA-induced platelet aggregation/activation. No significant differences were found between lower (75-100 mg/day) and higher (>100 mg/day) dose aspirin. Such aspirin «resistance» at 24 h after ingestion was related to biological inflammatory markers, current smoking and diabetes. In conclusion, once daily aspirin does not provide stable 24-h antiplatelet protection in a significant proportion of CAD patients. Any biological assessment of aspirin efficacy should take time since last aspirin intake into consideration.
    Thrombosis and Haemostasis 02/2011; 105(2):336-44. · 5.76 Impact Factor
  • Archives of Cardiovascular Diseases Supplements 01/2011; 3(1):84-85.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Introduction Aspirin resistance has been widely studied, but few hypothesis are proposed to explain such a mecanism. In our experience, more than a third of patients treated for stable coronary heart disease by aspirin once a day are not protected enough during the hole nycthemer. This could be due to an increased platelet turn-over. The purpose of this study is to compare different platelet turn-over markers. Material and methods In this prospective monocentric study, 50 patients treated for stable coronary heart disease and taking only aspirin as an antiplatelet treatment were included and compared to 55 controls from February to August 2009. Parameters known as to quantify platelet turn-over were measured, including mean platelet volume, reticulated platelets, platelet P selectin and soluble P selectin, and seric thrombopoietin as well. Inflammation markers were measured in both groups and these were usCRP, fibrinogen, VIII factor and von Willebrand factor. Results Mean platelet volume, platelet P selectin, soluble P selectin and seric thrombopoietin were found to be increased in patients more than in controls (p<0,05). Inflammation parameters were noticed to be much higher in patients. No statistical correlation was observed between these different tests, neither with inflammation markers. Conclusion Platelet turn-over is increased at baseline in patients with stable coronary heart disease. Inflammation was found to be much more important among this cohort than in controls. Thus, the absence of statistical correlation between these platelet turn-over markers suggests that some of them better may quantify other parameters, which could be platelet activation. More studies are required to establish whether these parameters could be linked to aspirin resistance.
    Archives of Cardiovascular Diseases Supplements 01/2011; 3(1):20.