Data were extracted and collected from PubMed, Google Scholar, Scopus, and Cochrane library from the overall term clinical and animal studies published in English between 1990 and April 2022.

Effect of Raloxifene on Stroke and Venous Thromboembolism
Lori Mosca and his colleagues conducted research on this subject, based on which the absolute increased risk for VTE associated with raloxifene was 0.12 per 100 woman-years. The incidence of pulmonary embolism, deep vein thrombosis, or retinal vein thrombosis individually did not differ significantly between treatment groups [11].

In accordance with findings from other trials, raloxifene did increase the risk for VTE in RUTH. The risk of VTE is increased 2- to 3-fold with estrogen plus progestin or tamoxifen [12-14]; in the STAR trial, the risk of VTE was lower in women assigned raloxifene versus tamoxifen [15].

The totality of evidence suggests that menopausal hormone therapy and SERMs are associated with increased risk of VTE, including pulmonary embolism and deep vein thrombosis, and that the absolute risk increase varies depending on the type of agent and the underlying risk of VTE [11].

Tamoxifen is also effective in venous thromboembolism as the raloxifene
Tamoxifen reduces breast cancer incidence among healthy women, but is associated with an increased risk of venous thrombosis. studied the 6-month effects of tamoxifen on venous thrombosis risk factors in women without cancer. One hundred and eleven women at one center who were participants in a multicenter breast cancer prevention trial were randomized, in double-blind fashion, to receive 20 mg/d of tamoxifen or placebo. The activated protein C (APC) ratio and concentrations of antithrombin, protein C antigen, and total protein S were measured at baseline and 6 months of treatment. None of the factors changed over 6 months in placebo-treated women. Among tamoxifen-treated women, antithrombin and protein S, but not protein C or APC ratio were reduced. Sequential antithrombin concentrations with tamoxifen were 114% and 104% (P = 0·001 compared with placebo). Sequential protein S concentrations with tamoxifen were 18·42 and 17·30 µg/ml (P = 0·02 compared with placebo). Reductions in antithrombin and protein S were greater in postmenopausal women, but did not differ by other risk factors for venous thrombosis, such as body mass index. Reductions of antithrombin and protein S, but not protein C or APC resistance, might relate to the increased risk of venous thrombosis associated with tamoxifen treatment [16].

Despite such benefits rendered by the agent, there has been heightened concern that tamoxifen use increases the risk of thrombotic complications [17]. One meta-analysis showed that those treated with tamoxifen had an 82% increased risk of ischemic stroke [18]. In randomized trials, the association between the risk of thromboembolic events and the use of tamoxifen was also significant [19.20] The first two years after the initiation of tamoxifen therapy, which was also the case for our patient, was considered to be the most vulnerable time to developing venous thromboembolic complications [21] After diagnosis of CVT, the case patient took anastrozole in place of tamoxifen. The anastrozole is a new aromatase inhibitor and known to have fewer thromboembolic complications [22].

Even though the mechanisms by which tamoxifen increases the risk of thrombosis have yet to be elucidated, alterations in the concentrations of natural anticoagulants have been implicated [23].

A case illustrates concurrent CVT and DVT suspected to have arisen from the use of tamoxifen [24].