1,720,992 research outputs found
Management of hypertension in overweight and obese patients: a practical guide for clinicians.
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Combined aspirin-oral anticoagulanttherapy compared with oral anticoagulant therapy alone among patients at risk forcardiovascular disease: a meta-analysis of randomized trials.
Full text linkMeta-analysis: Anticoagulant prophylaxis to prevent symptomatic venous thromboembolism in hospitalized medical patients
No full textBackground: Underutilization of anticoagulant prophylaxis may be due to lack of evidence that prophylaxis prevents clinically important outcomes in hospitalized medical patients at risk for venous thromboembolism.
Purpose: To assess the effects of anticoagulant prophylaxis in reducing clinically important outcomes in hospitalized medical patients.
Data Sources: MEDLINE, EMBASE, and Cochrane databases were searched to September 2006 without language restrictions.
Study selection: Randomized trials comparing anticoagulant prophylaxis with no treatment in hospitalized medical patients.
Data Extraction: Any symptomatic pulmonary embolism (PE), fatal PE, symptomatic deep venous thrombosis, all-cause mortality, and major bleeding. Pooled relative risks and associated 95% Cls were calculated. For treatment effects that were statistically significant, the authors determined the absolute risk reduction and the number needed to treat for benefit (NNTB) to prevent an outcome.
Data Synthesis: 9 studies (n = 19 958) were included. During anticoagulant prophylaxis, patients had significant reductions in any PE (relative risk, 0.43 [Cl, 0.26 to 0.71]; absolute risk reduction, 0.29%; NNTB, 345) and fatal PE (relative risk, 0.38 [Cl, 0.21 to 0.69]; absolute risk reduction, 0.25%; NNTB, 400), a nonsignificant reduction in symptomatic deep venous thrombosis (relative risk, 0.47 [Cl, 0.22 to 1.00]), and a nonsignificant increase in major bleeding (relative risk, 1.32 [Cl, 0.73 to 2.37]). Anticoagulant prophylaxis had no effect on all-cause mortality (relative risk, 0.97 [Cl, 0.79 to 1.19]).
Limitations: 2 of 9 included studies were not double-blind.
Conclusions: Anticoagulant prophylaxis is effective in preventing symptomatic venous thromboembolism during anticoagulant prophylaxis in at-risk hospitalized medical patients. Additional research is needed to determine the risk for venous thromboembolism in these patients after prophylaxis has been stopped
The risk for fatal pulmonary embolism after discontinuing anticoagulant therapy for venous thromboembolism
No full textBACKGROUND: The long-term risk for fatal pulmonary embolism (PE) after treatment of venous thromboembolism (VTE) may be an important factor in the decision to discontinue this treatment. OBJECTIVE: To provide reliable and precise estimates of the annual risk for fatal PE and the case-fatality rate of disease recurrence and to assess these outcomes according to the initial presentation of VTE (deep venous thrombosis [DVT], PE, or both) and its etiology (secondary or idiopathic) in patients who have discontinued anticoagulant therapy. DESIGN: Prospective cohort study. SETTING: Academic medical centers. PATIENTS: Inception cohort of patients with a first episode of symptomatic VTE who discontinued anticoagulant therapy. MEASUREMENTS: Incidence rates of any fatal PE (which included sudden death from possible fatal PE) and definite or probable PE per 100 person-years of follow-up and case-fatality rate of recurrent VTE. RESULTS: Of 2052 patients studied, 1450 had DVT, 310 had PE, and 292 had DVT and PE. The mean duration of previous anticoagulant therapy was 6 months (range, 3 to 39 months), and the mean duration of follow-up after discontinuation of treatment was 54 months (range, 1 to 120 months). The annual risk for any fatal PE and definite or probable fatal PE after discontinuation of anticoagulation was 0.49 events (95% CI, 0.36 to 0.64 events) per 100 person-years and 0.19 events (CI, 0.12 to 0.30 events) per 100 person-years, respectively. The case-fatality rate of recurrent disease was 9.0% (CI, 6.8% to 11.8%) for any fatal PE and 3.8% (CI, 2.4% to 5.9%) for definite or probable fatal PE. LIMITATION: The findings are less pertinent to patients with active cancer, permanent immobility, or high-risk thrombophilia. CONCLUSION: The risk for fatal PE is 0.19 to 0.49 events per 100 person-years for patients who have finished a course of anticoagulant therapy for a first episode of symptomatic VTE. The case-fatality rate for death from recurrent PE is 4% to 9%. This information helps to inform patient prognosis and may assist clinicians in deciding whether to discontinue anticoagulant therapy for VTE
Does celecoxib potentiate the anticoagulant effect of warfarin? A randomized, double-blind, controlled trial.
No full textThe risk of cancer in patients with venous thromboembolism does not exceed that expected in the general population after the first 6 months
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Accuracy of emergency physician-performed ultrasonography in the diagnosis of deep-vein thrombosis. A systematic review and meta-analysis.
No full textOral vitamin K lowers the international normalized ratio more rapidly than subcutaneous vitamin K in the treatment of warfarin-associated coagulopathy: A randomized, controlled trial
No full textBackground: Excessive anticoagulation due to warfarin use is associated with hemorrhage. Subcutaneously administered vitamin K has not been evaluated for the treatment of warfarin-associated coagulopathy, yet it is widely used. Objective: To show that oral vitamin K is more effective than subcutaneous vitamin K in the treatment of warfarin-associated coagulopathy. Design: Randomized, controlled trial. Setting: Two teaching hospitals. Patients: Patients with an international normalized ratio (INR) between 4.5 and 10.0. Intervention: Warfarin therapy was withheld, and 1 mg of vitamin K was given orally or subcutaneously. Measurements: The primary outcome measure was the INR on the day after administration of vitamin K. Secondary outcome measures were hemorrhage and thrombosis during a 1-month follow-up period. Results: 15 of 26 patients receiving oral vitamin K and 6 of 25 patients receiving subcutaneous vitamin K had therapeutic INRs on the day after study drug administration (P = 0.015; odds ratio, 4.32 [95% Cl, 1.13 to 17.44]). Conclusion: Oral vitamin K lowers INR more rapidly than subcutaneous vitamin K in asymptomatic patients who have supratherapeutic INR values while receiving warfarin
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