Effects of rosuvastatin as an adjuvant treatment for deep vein thrombosis

Norberto, Enrique M. San; Gastambide, María Victoria; Taylor, James; García-Sáiz, Irene; Vaquero, Carlos

doi:10.1024/0301-1526/a000507

Cited by 31 publications

(20 citation statements)

References 18 publications

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“…Moreover, the observation of accelerated thrombus resolution and less DVT-induced vein wall scarring suggested that statins protect against the onset of PTS [74]. Lastly, a clinical trial assessed the adjunction of rosuvastatin to the low-molecular-weight heparin (LMWH) bemiparin; after 3 months of follow-up, the CRP level and incidence of PTS were significantly lower in the patients receiving the adjunct statin treatment [76]. However, these preliminary results must be confirmed in large clinical trials.…”

Section: Anti-inflammatory Drugsmentioning

confidence: 99%

Inflammation in deep vein thrombosis: a therapeutic target?

et al. 2019

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Deep vein thrombosis is a common disease associated with a variety of complications including post-thrombotic syndrome as a late complication. It is now clear that in addition to classical deep vein thrombosis triggers such as blood flow disturbance, hypercoagulability, and vessel wall changes, inflammation has a key role in the pathophysiology of deep vein thrombosis, and there is a close relationship between inflammation and coagulation. As attested by changes in several plasma biomarkers, inflammation may have a significant role in the development of post-thrombotic syndrome. Here, we review the link between inflammation and deep vein thrombosis and thus the potential value of anti-inflammatory and/or anticoagulant drugs in the treatment of deep vein thrombosis and the prevention of postthrombotic syndrome.

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Section: Anti-inflammatory Drugsmentioning

confidence: 99%

Inflammation in deep vein thrombosis: a therapeutic target?

et al. 2019

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“…Within apolipoprotein E gene-deleted mice, hyperlipidemia resulted in a significantly elevated level of PAI-1 and an undetectable uPA concentration, so fibrinolysis and thrombus resolution were severely impaired [211]. Rosuvastatin has been shown to reduce these resolution-impairing effects in both mice and trial populations of human patients [212,213].…”

Section: Fibrinolysismentioning

confidence: 99%

Resolution of Deep Venous Thrombosis: Proposed Immune Paradigms

Nicklas

Gordon

Henke

2020

IJMS

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Venous thromboembolism (VTE) is a pathology encompassing deep vein thrombosis (DVT) and pulmonary embolism (PE) associated with high morbidity and mortality. Because patients often present after a thrombus has already formed, the mechanisms that drive DVT resolution are being investigated in search of treatment. Herein, we review the current literature, including the molecular mechanisms of fibrinolysis and collagenolysis, as well as the critical cellular roles of macrophages, neutrophils, and endothelial cells. We propose two general models for the operation of the immune system in the context of venous thrombosis. In early thrombus resolution, neutrophil influx stabilizes the tissue through NETosis. Meanwhile, macrophages and intact neutrophils recognize the extracellular DNA by the TLR9 receptor and induce fibrosis, a complimentary stabilization method. At later stages of resolution, pro-inflammatory macrophages police the thrombus for pathogens, a role supported by both T-cells and mast cells. Once they verify sterility, these macrophages transform into their pro-resolving phenotype. Endothelial cells both coat the stabilized thrombus, a necessary early step, and can undergo an endothelial-mesenchymal transition, which impedes DVT resolution. Several of these interactions hold promise for future therapy. already progressed past the point of anticoagulant efficacy [12,13]. Thus, there is potential clinical utility in investigating and controlling the process by which DVTs resolve in order to provide better care to these later-stage patients, with less bleeding risk. Overview of Venous Thrombus Development in HumansThe time sequence of DVT development and resolution was correctly suggested as early as 1962, based on empirical stains that detected changes in the nanoscopic roughness of clotted material [14]. As Lendrum et. al. remarked, "we consider that the intracytoplasmic granules, which we think are engulfed fibrin, seen in pulmonary phagocytes and in the endothelium of arteries and veins containing thrombus, are better shown by this (methyl-scarlet-blue) method than by any of the others." In fresh clot (whether in deep veins or in diabetic kidneys), platelets and erythrocytes are initially linked in a fine mesh yielding a relatively smooth surface (stage 1). A mat of the medium-textured fibrin replaces the initial thrombus (stage 2), which is gradually replaced by much coarser collagen (stage 3). This staging of clot development quickly became the basis of a pathological guide to grade thrombi [15]. The current three-stage refinement of the DVT grading scheme indicates that the turnover of erythrocyte-rich to fibrin-rich clot in humans is complete approximately seven days after the initial thrombotic event [16], whereas fibrin deposition commences after one day [17]. Various leukocytes, initially neutrophils and later macrophages, are believed to control this progression of DVTs development from a mass of erythrocytes, to fibrin, and finally to collagen [18]. Infiltrating T-lymphocytes and macrophages conta...

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“…The longer the thrombus is adjacent to the vessel wall, the higher the risk of vein wall damage. Fast removal of the thrombus may therefore prevent PTS …”

Section: Thrombus Resolutionmentioning

confidence: 99%

Prevention and treatment of the post‐thrombotic syndrome

Cate‐Hoek

2018

Research and Practice in Thrombosis and Haemostasis

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Essentials Post thrombotic syndrome (PTS) is a complication of deep vein thrombosis (DVT) with limited treatment options.Uniformity of the diagnostic strategy and the use of risk prediction models might improve treatment outcomes.Extending knowledge on the pathophysiology and improving therapeutic options is paramount for progress. PTS management should evolve to a multimodal approach with treatment tailored to individual patients' needs. Post thrombotic syndrome (PTS) is a common chronic complication of deep vein thrombosis of the leg (DVT). Treatment options are limited therefore emphasis is placed on its prevention. Several risk factors have been recognized, but were so far not used for risk stratification or translation into prediction models. Early interventions did not yet result in more successful preventive treatment strategies; for the acute phase of DVT there is equipoise on the value of elastic compression, as well as on catheter directed thrombolysis. There are no drugs specifically targeted at PTS prevention. The use of anticoagulant medication such as direct oral anticoagulants (DOACs) might decrease PTS incidence, but this needs to be corroborated. Both research into more effective treatment options as well as future PTS management may benefit from a uniform diagnostic strategy and the use of prediction rules to better allocate treatment and thereby increase treatment efficacy.

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Effects of rosuvastatin as an adjuvant treatment for deep vein thrombosis

Cited by 31 publications

References 18 publications

Inflammation in deep vein thrombosis: a therapeutic target?

Inflammation in deep vein thrombosis: a therapeutic target?

Resolution of Deep Venous Thrombosis: Proposed Immune Paradigms

Prevention and treatment of the post‐thrombotic syndrome

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