HMG-CoA reductase inhibitors, other lipid-lowering medication, antiplatelet therapy, and the risk of venous thrombosis

Ramcharan, Alexius; Stralen, Karlijn J. van; Snoep, Jaapjan D.; Mantel‐Teeuwisse, Aukje K.; Rosendaal, Frits R.; Doggen, Carine J.M.

doi:10.1111/j.1538-7836.2008.03235.x

Cited by 103 publications

(93 citation statements)

References 33 publications

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“…The comparison suggested a decreased risk of venous thrombosis for simvastatin compared to pravastatin users (OR 0.14; 95 % CI 0.02 -0.88). This observation is in contrast to the results of Ramcharan et al [21], showing a benefi cial preventative eff ect of DTV with pravastatin, which was higher in comparison to simvastatin (OR 95 %CI 0.48 vs. 0.51). Rahimi et al [4] conducted a meta-analysis of 22 RCTs with > 100,000 patients, comparing statin users with controls.…”

Section: Discussioncontrasting

confidence: 56%

Effects of rosuvastatin as an adjuvant treatment for deep vein thrombosis

Norberto

Gastambide

Taylor

et al. 2016

Vasa

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Summary:Background: Statins have been reported to help prevent the development and the recurrence of deep vein thrombosis (DVT). We conducted a prospective randomized clinical trial to compare the effects of rosuvastatin plus a low-molecular-weight heparin (LMWH), bemiparin, with conventional LMWH therapy in the treatment of DVT. Patients and methods: In total, 234 patients were randomized into two groups, 116 in the LMWH group and 118 in the statin plus LMWH group. All patients underwent lower limb duplex ultrasound and analytic markers at diagnosis and three months of follow-up. The fi nal analysis included 230 patients. Results: No signifi cant differences were observed in D-dimer levels after three months of follow-up between patients treated with LMWH+rosuvastatin compared to the LMWH group (802.51 + 1062.20 vs. 996.25 + 1843.37, p = 0.897). The group of patients treated with statins displayed lower levels of CRP (4.17 + 4.27 vs. 22.39 + 97.48, p = 0.018) after three months of follow-up. The Villalta scale demonstrated signifi cant differences between groups (3.45 + 6.03 vs. 7.79 + 5.58, p = 0.035). There was a signifi cant decrease in PTS incidence (Villalta score> 5) in the rosuvastatin group (38.3 % vs. 48.5%, p = 0.019). There were no differences in EuroQol score between groups. Conclusions: Adjuvant rosuvastatin treatment in patients diagnosed of DVT improve CRP levels and diminish PTS incidence.

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Section: Discussioncontrasting

confidence: 56%

Effects of rosuvastatin as an adjuvant treatment for deep vein thrombosis

Norberto

Gastambide

Taylor

et al. 2016

Vasa

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“…Statins also have antiinflammatory and antithrombotic activities (39,40). Several studies have found that statin therapy is associated with a significant reduction in the incidence of venous thromboembolism (VTE) (41)(42)(43). Interestingly, statins also inhibit TF expression in monocytes and macrophages, both in vitro and in vivo (27,29,31,39,(44)(45)(46)(47).…”

Section: Introductionmentioning

confidence: 99%

Monocyte tissue factor–dependent activation of coagulation in hypercholesterolemic mice and monkeys is inhibited by simvastatin

Owens¹,

Passam²,

Antoniak³

et al. 2012

J. Clin. Invest.

163

138

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Hypercholesterolemia is a major risk factor for atherosclerosis. It also is associated with platelet hyperactivity, which increases morbidity and mortality from cardiovascular disease. However, the mechanisms by which hypercholesterolemia produces a procoagulant state remain undefined. Atherosclerosis is associated with accumulation of oxidized lipoproteins within atherosclerotic lesions. Small quantities of oxidized lipoproteins are also present in the circulation of patients with coronary artery disease. We therefore hypothesized that hypercholesterolemia leads to elevated levels of oxidized LDL (oxLDL) in plasma and that this induces expression of the procoagulant protein tissue factor (TF) in monocytes. In support of this hypothesis, we report here that oxLDL induced TF expression in human monocytic cells and monocytes. In addition, patients with familial hypercholesterolemia had elevated levels of plasma microparticle (MP) TF activity. Furthermore, a high-fat diet induced a time-dependent increase in plasma MP TF activity and activation of coagulation in both LDL receptor-deficient mice and African green monkeys. Genetic deficiency of TF in bone marrow cells reduced coagulation in hypercholesterolemic mice, consistent with a major role for monocyte-derived TF in the activation of coagulation. Similarly, a deficiency of either TLR4 or TLR6 reduced levels of MP TF activity. Simvastatin treatment of hypercholesterolemic mice and monkeys reduced oxLDL, monocyte TF expression, MP TF activity, activation of coagulation, and inflammation, without affecting total cholesterol levels. Our results suggest that the prothrombotic state associated with hypercholesterolemia is caused by oxLDL-mediated induction of TF expression in monocytes via engagement of a TLR4/TLR6 complex.

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“…Similarly, in a retrospective cohort study from Canada, statin use was associated with a 22% decreased risk of DVT compared with thyroid replacement therapy (adjusted HR, 0.78; 95% CI, 0.69-0.87; p-value not mentioned) among 125 862 patients 65 years old 16 . The statin-induced reduction in the risk of venous thrombosis was also documented in other trials [17][18][19] .…”

Section: I a L D I S T R I B U T I O N U N A U T H O R I Z E D U S mentioning

confidence: 74%