Factors influencing the level of circulating procoagulant microparticles in acute pulmonary embolism

Cardiology Department, Saint-Antoine University and Medical School, Assistance Publique-Hôpitaux de Paris, université Pierre-et-Marie-Curie, 75571 Paris cedex 12, France.
Archives of cardiovascular diseases (Impact Factor: 1.84). 06/2010; 103(6-7):394-403. DOI: 10.1016/j.acvd.2010.06.005
Source: PubMed


Flow cytometry has shown levels of platelet-derived microparticles (PMPs) and endothelial-derived microparticles (EMPs) to be elevated in deep-vein thrombosis. Cardiovascular risk factors can also contribute to hypercoagulability due to circulating procoagulant microparticles (CPMPs).
To investigate in a case-control study the respective contribution of pulmonary embolism and cardiovascular risk factors to the level of hypercoagulability due to CPMPs.
CPMP, PMP and EMP levels were measured in 45 consecutive patients (age 67.9 +/- 11.6 years; 66.7% men) admitted to an intensive care unit for acute pulmonary embolism (APE), 45 healthy control subjects with no history of venous thromboembolism or vascular risk factors (Controls(noCVRFs)), and 45 patients with cardiovascular risk factors (Controls(CVRFs)). APE was diagnosed by spiral computed tomography or scintigraphy. CPMP levels were assessed using a prothrombinase assay on platelet-depleted plasma (results expressed as nmol/L equivalent).
CPMP levels were higher in APE patients than in Controls(noCVRFs) (medians 4.7 vs 3.2 nmol/L, interquartile ranges [IQRs] 2.9-11.1 vs 2.3-4.6 nmol/L; p=0.02). Similar results were reported for PMPs (medians 2.2 vs 1.9 nmol/L, IQRs 1.7-5.8 vs 1.4-2.4 nmol/L; p=0.02), whereas EMP levels were not significantly different. However, CPMP procoagulant activity was not significantly different in APE patients and Controls(CVRFs).
CPMPs and PMPs were significantly elevated in APE patients vs Controls(noCVRFs), but this correlation was not significant when APE patients were compared with Controls(CVRFs). Our observations highlight the importance of adjusting for the presence of cardiovascular risk factors in conditions in which microparticle levels are raised.

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Available from: Franck Boccara, Oct 07, 2015
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    • "Pulmonary hypertension can be caused by chronic thromboembolic disease (CTEPH)[61]. Pulmonary embolism, as in many diseases in which apoptosis occurs[62], results in shedding of microparticles (MP)[63]. MP are shed from apoptotic sites, circulate via plasma, and act on distant sites to effect inflammation, hemostasis, and thrombosis[64]. "
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    PROTEOMICS - CLINICAL APPLICATIONS 02/2015; 9(1-2). DOI:10.1002/prca.201400157 · 2.96 Impact Factor
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    • "There was a dramatic increase in platelet activation (35.2 vs 5.0 fluorescence intensity units for P-selectin; P<0.0001) in the setting of VTE, which was found in the recent study by Chirinos et al37. Likewise, elevated PMPs were detected in patients with VTE in two other studies34,35, and a strong correlation was found between total MPs and PMPs (ρ=0.99, P<0.0001) and between PMPs and TF-bearing MPs (ρ=0.94, "
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