Can we prevent venous thrombosis with statins: an epidemiologic review into mechanism and clinical utility

Lijfering, Willem M.; Biedermann, Joseph S.; Kruip, Marieke J.H.A.; Leebeek, Frank W.G.; Rosendaal, Frits R.; Cannegieter, Suzanne C.

doi:10.1080/17474086.2016.1245137

Cited by 16 publications

(15 citation statements)

References 77 publications

(88 reference statements)

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“…It has been postulated that modulation of fibrin clot structure and function represents an additional beneficial effect of this widely used medications that have been shown to reduce the risk of VTE [87]. …”

Section: Antithrombotic Agents and Fibrin Clot Propertiesmentioning

confidence: 99%

Prothrombotic Fibrin Clot Phenotype in Patients with Deep Vein Thrombosis and Pulmonary Embolism: A New Risk Factor for Recurrence

Undas

2017

BioMed Research International

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Prothrombotic fibrin clot phenotype, involving faster formation of dense meshwork composed of thinner and highly branched fibers that are relatively resistant to plasmin-induced lysis, has been reported in patients with not only myocardial infarction or stroke, but also venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT), and/or pulmonary embolism (PE). Prothrombotic fibrin clot phenotype, in particular prolonged clot lysis time, is considered a novel risk factor for VTE as well as venous thrombosis at unusual location, for example, cerebral sinus venous thrombosis, retinal vein obstruction, and Budd-Chiari syndrome. Growing evidence from observational studies indicates that abnormal fibrin clot properties can predict recurrent DVT and PE and they are involved in serious complications of VTE, for example, thromboembolic pulmonary hypertension and postthrombotic syndrome. The purpose of this article is to review our current understanding of the role of fibrin clot structure and function in venous thrombosis with emphasis on clinical issues ranging from prognosis to therapy.

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Section: Antithrombotic Agents and Fibrin Clot Propertiesmentioning

confidence: 99%

Prothrombotic Fibrin Clot Phenotype in Patients with Deep Vein Thrombosis and Pulmonary Embolism: A New Risk Factor for Recurrence

Undas

2017

BioMed Research International

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“…It is also correlated with higher levels of factor VIII. Despite this, hsCRP does not appear to be a driving factor of thrombus formation (43). It is also not clear the ordering of VTE and inflammation despite an association between the two.…”

Section: Statins and Inflammationmentioning

confidence: 87%

“…Inhibition of NOX2 activation causes downstream effects via platelet thromboxane A2 (TxA2) and 8-iso-PGF2alpha formation (47). In vitro studies support this idea with mechanisms that include TxA2 (43), however, the Statins Reduce Thrombophilia trial (START) investigated the effect of rosuvastatin on TxA2-mediated platelet activation and found that it is unlikely that this is the etiology (43). Another mechanism may involve peroxisome proliferator activated receptors that are involved in inflammatory responses (47).…”

Section: Statins and Inflammationmentioning

confidence: 99%

“…It has been shown that idiopathic VTE can be characterized by lower plasma fibrin clot permeability, thicker fibers and prolonged clot lysis time making this a potential target for treatment (52). Studies that demonstrate rapid alterations in fibrin clot structure/function with statin use have not had consistent outcomes (43). vWF and D-dimer may be affected by statin therapy but the studies are poor (43).…”

Section: Statins and Inflammationmentioning

confidence: 99%

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Statins as a preventative therapy for venous thromboembolism

Wallace

Albadawi

Hoang

et al. 2017

Cardiovasc. Diagn. Ther.

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The anti-inflammatory effects of statins have likely not been used to their fullest extent, particularly in reducing venous thromboembolic events. Current therapy for thrombotic events hinges on anticoagulation via heparin, warfarin or new oral anticoagulants. Interventional procedures with thrombectomy may also play a critical role. Unfortunately, thrombotic events can occur and recur despite meticulous anticoagulation therapy. Venous thromboembolism (VTE) includes both deep vein thrombosis (DVT) and pulmonary embolism (PE), two complicated and prevalent diseases that can cause chronic disease states such as post-thrombotic syndrome (PTS). In 2009 the JUPITER trial demonstrated that rosuvastatin may be effective when dealing with vascular inflammation by providing an anti-inflammatory effect. Multiple subsequent studies have looked at this association with some promising findings. The mechanism of action for statins is not entirely understood but there has been a variety of proposals and subsequent testing of inflammatory biomarkers. Additional prospective trials are needed to confirm the possible benefit of VTE reduction through an anti-inflammatory effect, but if this can be shown then statins may become a safe adjunctive therapy for VTE prevention.

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“…Most of them are observational studies and were performed in selected populations of patients with CVD. 81 The only RCT supporting the effect of statins on decreasing VTE risk was published in 2009. In the JUPITER trial, 13 17,802 apparently healthy individuals, with normal cholesterol levels, were randomized to receive rosuvastatin at 20 mg per day or placebo and were followed for a median period of 1.9 years.…”

Section: Statins To Prevent First Venous Thromboembolismmentioning

confidence: 99%

Statin Therapy to Revert Hypercoagulability and Prevent Venous Thromboembolism: A Narrative Review

Orsi

Cannegieter

Lijfering

2019

Semin Thromb Hemost

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Venous thromboembolism (VTE) causes a major disease burden worldwide, so that effective preventive measures are warranted. Although oral anticoagulation is effective in preventing VTE episodes, bleeding complications are a major concern that may lead to treatment avoidance. Statin therapy, which is widely used for prevention of arterial cardiovascular disease, is a promising alternative treatment for VTE prophylaxis, as the drug may affect hemostasis without increasing the risk of bleeding. In the past years, clinical studies have suggested that statins can interfere with blood coagulation and, in turn, reduce the risk of VTE. These effects, however, are still regarded with skepticism, as the underlying mechanisms by which statins may affect hemostasis in humans are not clear and data showing that statin therapy reduces VTE risk mostly came from observational studies, while only one randomized trial was conducted to evaluate this issue. In this review, the authors summarize the currently available evidence regarding the effect of statin therapy on coagulation and on VTE prevention. Recent randomized data showed that statin therapy, in particular rosuvastatin, leads to decreased levels of coagulation factors in patients with prior VTE. This evidence provides a reasonable basis for interventional studies necessary to establish the efficacy of statins on reducing the risk of incident and recurrent VTE.

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Can we prevent venous thrombosis with statins: an epidemiologic review into mechanism and clinical utility

Cited by 16 publications

References 77 publications

Prothrombotic Fibrin Clot Phenotype in Patients with Deep Vein Thrombosis and Pulmonary Embolism: A New Risk Factor for Recurrence

Prothrombotic Fibrin Clot Phenotype in Patients with Deep Vein Thrombosis and Pulmonary Embolism: A New Risk Factor for Recurrence

Statins as a preventative therapy for venous thromboembolism

Statin Therapy to Revert Hypercoagulability and Prevent Venous Thromboembolism: A Narrative Review

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