Background: There have been concerns that the antifibrinolytic drug tranexamic acid (TXA) might increase the postoperative risk of cardiovascular events. Our objective was to determine whether perioperative TXA use is associated with cardiovascular events and death within 30 days after primary total hip arthroplasty (THA). Methods: We conducted a nationwide cohort study of cardiovascular outcomes after perioperative exposure to tranexamic acid during THA. We included 45,290 patients who had a THA in the study period of 2006 to 2013; 38,586 received perioperative TXA, and 6,704 did not. Propensity scores were calculated on the basis of age, sex, income, year of surgery, Elixhauser comorbidity index, and a variety of comorbidities and coprescribed medications. The primary outcome was venous thromboembolism. The secondary outcomes were deep venous thrombosis, pulmonary embolism, myocardial infarction, ischemic stroke, and all-cause mortality. Data were analyzed using Cox regression, either in a multivariable model with inclusion of covariates (full cohorts) or in propensity-score-matched cohorts. Results: After propensity score matching, all prognostic covariates balanced well. In the matched cohort, TXA use was not found to significantly increase the risk of venous thromboembolism (hazard ratio [HR] = 1.18; 95% confidence interval [CI] = 0.83 to 1.68), deep vein thrombosis (HR = 1.15; CI = 0.78 to 1.68), pulmonary embolism (HR = 1.50; CI = 0.60 to 3.78), myocardial infarction (HR = 0.83; CI = 0.46 to 1.50), ischemic stroke (HR = 0.89; CI = 0.39 to 2.01), or all-cause mortality (HR = 0.73; CI = 0.41 to 1.28). Similar results were found in the multivariable Cox regression analyses. Conclusions: Our data do not support a detrimental effect of TXA on the risk of cardiovascular events or death following THA. Level of Evidence: Therapeutic Level III. See Instructions for Authors for a complete description of levels of evidence.
Background:Some studies indicate a reduced risk of serious upper gastrointestinal bleeding (UGIB) for users of beta-blockers, but the association remains to be confirmed in larger studies and characterized with respect to differences among beta-blockers. We aimed to assess whether beta-blocker use decreases the risk of UGIB.Methods:We conducted a register-based, population-based case-control study in Denmark. We identified cases with a first validated discharge diagnosis of UGIB during the period 1995–2006. Controls were selected by risk-set sampling in a ratio of 10:1. We estimated crude and adjusted odds ratios (ORs) of the association between current beta-blocker use and the risk of UGIB by using conditional logistic regression and further stratified by selective and non-selective beta-blockers, respectively.Results:We identified 3571 UGIB cases and 35,582 controls. Use of beta-blockers was not found to be associated with a decreased risk of UGIB (adjusted OR 1.10; 95% CI: 1.00–1.21). The association remained neutral after stratification by selective and non-selective beta-blockers, and by single beta-blocker substances. Similarly, we found no association between current beta-blocker use and the risk of UGIB within different subgroups.Conclusions:We found no association between beta-blocker use and UGIB.
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