Platelet and Microvesicles Derived in Venous Thromboembolism: Call to Be Aware

Short Communication

Venous Thromboembolism (VTE) affects a number of individuals it is frequently diagnosed in patients hospitalized for chronic diseases (i.e.cardiac, cerebral, inflammatory disease, trauma, surgical procedures) or having thrombophilia (i.e.factor V Leiden, mutation of pro thrombin G210A, deficiency of protein c and S, anti thrombin 3rd deficiency, mutation of MTHFR enzyme, hyperomocisteinemia) [1-7]. Hypercoagulative condition plays a crucial role for VTE consequently, factors of coagulative cascade are highly considered both as patogenethic tools, and in threatening the VTE. Diversely, there is a few interest on the role played by Platelets (P) in VTE. P is widely accepted as a pivotal mechanism involved in arterial thrombosis in fact anti platelet drugs are assigned both to prevent and to cure arterial thrombosis (Figure 1). However, there are such evidences from studies on pathophisyologic role of P and on possible efficacy of anti platelet drugs in preventing the VTE or in reducing its frequency [8-12]. Acetil salicilic acid was considered for VTE prophylaxis, achieving to the risk reduction of VTE in primary and in secondary prevention. Genetic and functional activation of P, spatial or volumetric modifications were found in specific setting of VTE patients (i.e. cancer, anti phospholipid syndrome, hematologic malignancy etc.) [13-15]. However, role of P in VTE is still debated or no cleared. About P in VTE, I believe as noteworthy to highlight on microvesicles P derived as a specific pathway of clot activation in VTE. Briefly, Microparticles (MPs) are phospholipid vesicles potentially derived from the bloodstream cells (leukocyte, platelet) and from endothelial cells. Tissue Factor (TF) and Phospholipids (Phsp) are two active players leading to procoagulant capability of MPs. In this light it is noteworthy to note that surface of P derived MPs is able to bind coagulative VIII, IX, V, and X activated factors of coagulative cascade [14].

    

    

    Figure 1: Mechanisms involved in provoking thrombosis. Figure focuses
both on Virchow’s triade components, on platelet and on platelet derived
miscovesicles.