HMG CoA reductase inhibitors and the risk of venous thrombosis among postmenopausal women

Leiden University, Leyden, South Holland, Netherlands
Journal of Thrombosis and Haemostasis (Impact Factor: 5.72). 06/2004; 2(5):700-1. DOI: 10.1111/j.1538-7836.2004.00696.x
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Available from: Carine J M Doggen
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    • "Likewise, Doggen et al. found that statin therapy, among postmenopausal women, was associated with reduction in VTE risk (odds ratio [OR] 0.64, 95% CI 0.39-1.07) [15]. The association was observed in patients on simvastatin (OR 0.51, 95% CI 0.29-0.91) "
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    ABSTRACT: Studies have shown that statins have pleiotropic effects on inflammation and coagulation; which may affect the risk of developing venous thromboembolism (VTE). The objective of this study was to evaluate the association between statin therapy during intensive care unit (ICU) stay and the incidence of VTE in critically ill patients. This was a post-hoc analysis of a prospective observational cohort study of patients admitted to the intensive care unit between July 2006 and January 2008 at a tertiary care medical center. The primary endpoint was the incidence of VTE during ICU stay up to 30 days. Secondary endpoint was overall 30-day hospital mortality. Propensity score was used to adjust for clinically and statistically relevant variables. Of the 798 patients included in the original study, 123 patients (15.4%) received statins during their ICU stay. Survival analysis for VTE risk showed that statin therapy was not associated with a reduction of VTE incidence (crude hazard ratio (HR) 0.66, 95% confidence interval (CI) 0.28-1.54, P = 0.33 and adjusted HR 0.63, 95% CI 0.25-1.57, P = 0.33). Furthermore, survival analysis for hospital mortality showed that statin therapy was not associated with a reduction in hospital mortality (crude HR 1.26, 95% CI 0.95-1.68, P = 0.10 and adjusted HR 0.98, 95% CI 0.72-1.36, P = 0.94). Our study showed no statistically significant association between statin therapy and VTE risk in critically ill patients. This question needs to be further studied in randomized control trials.
    Full-text · Article · Nov 2013 · BMC pharmacology & toxicology
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    • "Beyond platelets, statins may inhibit plasmatic pathways of thrombus formation (Undas et al., 2005) and may affect fibrinolytic pathways (Bourcier and Libby, 2000). The first strong evidence of potential association between statin administration and reduced risk of thromboembolism has come from a case control study in postmenopausal women (Doggen et al., 2004) in which statin administration was associated with a slightly lower risk of venous thrombosis. Other case control studies (Lacut et al., 2004; Ramcharan et al., 2009; Sørensen et al., 2009) have also shown reduction in the risk of venous thrombosis ranging from 26 to 58%. "
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    ABSTRACT: Statins, among the most commonly prescribed drugs worldwide, are cholesterol-lowering agents used to manage and prevent cardiovascular and coronary heart diseases. Recently, a multifaceted action in different physiological and pathological conditions has been also proposed for statins, beyond anti-inflammation and neuroprotection. Statins have been shown to act through cholesterol-dependent and -independent mechanisms and are able to affect several tissue functions and modulate specific signal transduction pathways that could account for statin pleiotropic effects. Typically, statins are prescribed in middle-aged or elderly patients in a therapeutic regimen covering a long life span during which metabolic processes, aging, and concomitant novel diseases, including cancer, could occur. In this context, safety, toxicity, interaction with other drugs, and the state of health have to be taken into account in subjects treated with statins. Some evidence has shown a dichotomous effect of statins with either cancer-inhibiting or -promoting effects. To date, clinical trials failed to demonstrate a reduced cancer occurrence in statin users and no sufficient data are available to define the long-term effects of statin use over a period of 10 years. Moreover, results from clinical trials performed to evaluate the therapeutic efficacy of statins in cancer did not suggest statin use as chemotherapeutic or adjuvant agents. Here, we reviewed the pharmacology of the statins, providing a comprehensive update of the current knowledge of their effects on tissues, biological processes, and pathological conditions, and we dissected the disappointing evidence on the possible future use of statin-based drugs in cancer therapy.
    Full-text · Article · Nov 2011 · Pharmacological reviews
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    • "Despite the fact that 70% of patients with VTE are aged over 60[1], there are few studies of risk factors in the elderly. Other studies have analyzed effects of pre-existing statin medication on incident VTE [4-6] or have compared statin use in case control studies of VTE[7-9]. A post hoc analysis of the Heart and Estrogen/progestin Replacement Study (HERS)[4] and analyses of other[5-8], but not all [9], population or case control studies indicated a decreased risk of VTE with statin use. "
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    ABSTRACT: Venous thromboembolic events (VTE), including deep venous thrombosis and pulmonary embolism, are common in older age. It has been suggested that statins might reduce the risk of VTE however positive results from studies of middle aged subjects may not be generalisable to elderly people. We aimed to determine the effect of pravastatin on incident VTE in older people; we also studied the impact of clinical and plasma risk variables. This study was an analysis of incident VTE using data from the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER), a randomized, double-blind, placebo-controlled trial of pravastatin in men and women aged 70-82. Mean follow-up was 3.2 years. Risk for VTE was examined in non-warfarin treated pravastatin (n = 2834) and placebo (n = 2865) patients using a Cox's proportional hazard model, and the impact of other risk factors assessed in a multivariate forward stepwise regression analysis. Baseline clinical characteristics, blood biochemistry and hematology variables, plasma levels of lipids and lipoproteins, and plasma markers of inflammation and adiposity were compared. Plasma markers of thrombosis and hemostasis were assessed in a nested case (n = 48) control (n = 93) study where the cohort was those participants, not on warfarin, for whom data were available. There were 28 definite cases (1.0%) of incident VTE in the pravastatin group recipients and 20 cases (0.70%) in placebo recipients. Pravastatin did not reduce VTE in PROSPER compared to placebo [unadjusted hazard ratio (95% confidence interval) 1.42 (0.80, 2.52) p = 0.23]. Higher body mass index (BMI) [1.09 (1.02, 1.15) p = 0.0075], country [Scotland vs Netherlands 4.26 (1.00, 18.21) p = 0.050 and Ireland vs Netherlands 6.16 (1.46, 26.00) p = 0.013], lower systolic blood pressure [1.35 (1.03, 1.75) p = 0.027] and lower baseline Mini Mental State Examination (MMSE) score [1.19 (1.01, 1.41) p = 0.034] were associated with an increased risk of VTE, however only BMI, country and systolic blood pressure remained significant on multivariate analysis. In a nested case control study of definite VTE, plasma Factor VIII levels were associated with VTE [1.52 (1.01, 2.28), p = 0.044]. However no other measure of thrombosis and haemostasis was associated with increased risk of VTE. Pravastatin does not prevent VTE in elderly people at risk of vascular disease. Blood markers of haemostasis and inflammation are not strongly predictive of VTE in older age however BMI, country and lower systolic blood pressure are independently associated with VTE risk. Not applicable when study undertaken.
    Full-text · Article · Feb 2011 · BMC Geriatrics
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