Evidence that pre-existent variability in platelet response to ADP accounts for 'clopidogrel resistance': a rebuttal.

Journal of Thrombosis and Haemostasis (Impact Factor: 5.55). 06/2007; 5(5):1087-8; author reply 1089-90. DOI: 10.1111/j.1538-7836.2007.02509.x
Source: PubMed
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    ABSTRACT: Percutaneous coronary interventions associated with a need for long-term dual anti-platelet therapy are steadily increasing. Accordingly, reports of severe perioperative complications in this high-risk group of patients are also increasing. Complications can be categorized into two groups: coronary ischemia or myocardial infarction due to acute stent thrombosis or increased blood loss. Risk of stent thrombosis is higher compared to the risk of bleeding. The article discusses the perioperative management based on an informative case report and recent evidence: Elective surgery has to be postponed until the end of dual anti-platelet therapy. Management of patients planned for semi-elective surgery should be individualized with interdisciplinary consensus. If clopidogrel is withdrawn, aspirin should be administered throughout the perioperative period. Careful surgical technique is required. If surgery is planned within 12 months, implantation of bare metal stents is recommended.
    Wiener Medizinische Wochenschrift 10/2009; 159(19-20):501-6. DOI:10.1007/s10354-009-0715-3
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    ABSTRACT: This study sought to evaluate the relationship between platelet reactivity and atherosclerotic burden in patients undergoing percutaneous coronary intervention (PCI) with pre-intervention volumetric intravascular ultrasound (IVUS) imaging. Atherosclerosis progresses by the pathologic sequence of subclinical plaque rupture, thrombosis, and healing. In this setting, increased platelet reactivity may lead to more extensive arterial thrombosis at the time of plaque rupture, leading to a more rapid progression of the disease. Alternatively, abnormal vessel wall biology with advanced atherosclerosis is known to enhance platelet reactivity. Therefore, it is possible that by either mechanism, increased platelet reactivity may be associated with greater atherosclerotic burden. This study included patients who underwent PCI with pre-intervention IVUS imaging and platelet reactivity functional assay (P2Y(12) reaction units) performed >16 h after PCI, after the stabilization of clopidogrel therapy (administered before PCI). Platelet reactivity >230 P2Y(12) reaction units defined high on-treatment platelet reactivity (HPR). Among 335 patients (mean age 65.0 years, 71% men), there were 109 patients with HPR (32.5%) and 226 without HPR (67.5%), with HPR being associated with diabetes and chronic renal insufficiency. By IVUS analysis, patients with HPR had significantly greater target lesion calcium lengths, calcium arcs, and calcium indexes. Furthermore, patients with HPR tended to have longer lesions and greater volumetric dimensions, indicating higher plaque volume, larger total vessel volume, and also greater luminal volume, despite similar plaque burden. By multivariate analysis controlling for baseline clinical variables, HPR was the single consistent predictor of all IVUS parameters examined, including plaque volume, calcium length, and calcium arc. Increased platelet reactivity on clopidogrel treatment, defined as >230 P2Y(12) reaction units, is associated with greater coronary artery atherosclerotic disease burden and plaque calcification.
    JACC. Cardiovascular imaging 05/2012; 5(5):540-9. DOI:10.1016/j.jcmg.2011.12.019 · 6.99 Impact Factor
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    ABSTRACT: BACKGROUND: In the present study, the influence of bacterial infection, lipopolysacharides (LPS) and hydroxyethyl starch (HES) on platelet function in a parallel plate flow chamber were measured. Experiments were performed with non-activated and protease-activating-receptor (PAR) 4 agonist activated platelets. Comparative measurements were in vivo capillary bleeding time, platelet function analyzer and impedance aggregometry. RESULTS: PAR 4 agonist did not increase platelet adhesion of platelets from dogs with bacterial inflammation in the flow chamber in contrast to platelets of healthy dogs. Except from impedance aggregometry with lower sensitivity and specificity, PFA did not detect platelet dysfunctions in dogs with infection. In vitro addition of LPS or HES significantly reduced platelet covered area after PAR-activation. CONCLUSIONS: The flow chamber detects platelet dysfunctions in dogs with inflammatory diseases. In vitro addition of LPS highlights the inhibiting effect of bacterial wall components on platelet function. Platelet dysfunction induced by infection could possibly also be diagnosed after treatment of sepsis with colloids has commenced. The flow chamber could be a useful tool to detect sepsis associated platelet dysfunction given that larger prospective trials confirm these findings from a proof of concept study.
    BMC Veterinary Research 06/2013; 9(1):112. DOI:10.1186/1746-6148-9-112 · 1.74 Impact Factor

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