Plasma levels of platelet-derived microvesicles are associated with risk of future venous thromboembolism

• Published in: Journal of Thrombosis and Haemostasis
• Main Authors: Snir, Omri, Wilsgård, line, Latysheva, Nadezhda, Ullsten-Wahlund, Casper, Brækkan, Sigrid Kufaas, Hindberg, Kristian Dalsbø, Hansen, John Bjarne
• Format: Article in Journal/Newspaper
• Language: English
• Published: Elsevier 2022
• Subjects: Tromsø
• Online Access: https://hdl.handle.net/10037/28780; https://doi.org/10.1111/jth.15638

Background - Microvesicles (MVs) are small double‐membrane encapsulated particles shed from cells. Case‐control studies have reported elevated plasma levels of platelet‐derived MVs (PDMVs) in patients with venous thromboembolism (VTE). However, it is not known whether high PDMV levels is a risk factor or a consequence of the acute VTE event. Objectives - To investigate the association between PDMVs in plasma and risk of future incident VTE. Methods - We performed a population‐based nested case‐control study with 314 VTE cases and 705 age‐ and sex‐matched controls (from The Tromsø Study) to investigate the association between the proportion of PDMVs (PDMVs%) in plasma and risk of future incident VTE. MVs isolated from plasma sampled at baseline (i.e., before VTE) were stained for platelet markers and analyzed by flow cytometry. PDMVs% were defined as the number of PDMVs divided by the total number of MVs. Odds ratios (ORs) with 95% confidence intervals (CI) for VTE risk were estimated across quartiles of PDMVs%. Results - Subjects with PDMVs% in the highest quartile had an OR for VTE of 1.78 (95% CI: 1.21–2.64) and 1.99 (95% CI: 1.24–3.26) for provoked VTE, compared to those in the lowest quartile. The association was moderately affected by multivariable adjustment for age, sex, body mass index, C‐reactive protein, platelet count, and cancer. The OR for VTE was higher when the time between blood sampling and event was shorter. Conclusions - Our results show that high proportions of PDMVs are associated with future risk of incident VTE and imply a role of platelet activation in the pathogenesis of VTE.