Background. Trials have shown that novel oral anticoagulants may decrease length of stay versus warfarin. A comparison of length of stay in the treatment of pulmonary embolism (PE) has not been performed outside post hoc analysis of a large clinical trial. Objective. To evaluate if rivaroxaban decreases length of stay compared to warfarin plus enoxaparin in the treatment of PE. Methods. This was a multicenter, retrospective, observational cohort study. Patients were identified based on discharge diagnosis of PE and were excluded if they received anticoagulants prior to admission and had additional indications for anticoagulation or reduced creatinine clearance. The primary endpoint was length of stay. Secondary endpoints included time from initial dose of oral anticoagulant to discharge and length of stay comparison between subgroups. Results. Inclusion criterion was met by 158 patients (82 warfarin, 76 rivaroxaban). The median length of stay was 4.5 days (interquartile range [IQR], 2.7, 5.9) in the warfarin group and 1.8 days (IQR, 1.2, 3.7) in the rivaroxaban group (P < 0.001). Time interval from first dose of oral anticoagulant to discharge was shorter with rivaroxaban (P < 0.001). Conclusions. Patients given rivaroxaban had decreased length of stay versus those given warfarin plus enoxaparin for the treatment of PE.

Angioedema is the abrupt onset of swelling involving the mucosa and submucosa of the skin. It can affect the face, lips, tongue, pharynx, and larynx, causing lifethreatening airflow obstruction. 1,2 Angioedema is mediated by inflammatory cytokines, such as prostaglandin D 2 , leukotrienes, cytokines, bradykinin, and complement components, which cause vasodilation and increase the permeability of capillaries. This allows plasma to leave the intravascular space and cause submucosal swelling. 2 It may be accompanied by urticaria, identifying it as an acute allergic response mediated by histamine. Urticaria differs from angioedema in that it only affects the skin and not the subcutaneous or submucosal tissue and is almost always pruritic. 2 Angioedema without urticaria can be a result of an adverse drug reaction as is the case with angioedema due to angiotensin-converting enzyme (ACE) inhibitors. 1 Approximately 17.5% of patients with cutaneous drug eruptions have angioedema. 3 In addition, it is estimated that angioedema is caused by a drug in 32% of cases. 4 Lastly, ACE-inhibitor use is associated with 25-38% of all angioedema-related emergency department (ED) visits. 5 Simvastatin, as well as atorvastatin, fluvastatin, lovastatin, rosuvastatin, and pravastatin have been associated with postmarketing reports of hypersensitivity reactions, including angioedema. 6-11 A review of the literature reveals 4 case reports of statin-induced angioedema. These reports described a case of atorvastatin-induced angioedema with dermographism and urticaria, atorvastatin-induced angioedema with rash and eosinophilia,

Crouch and Ng co primary author.

Purpose Evidence on the use of antithrombotic pharmacotherapy in patients undergoing revascularization of lower extremities for symptomatic peripheral arterial disease (PAD) is reviewed. Summary Individuals with PAD can experience leg pain, intermittent claudication, critical limb ischemia, and acute limb ischemia. In such patients, revascularization may be indicated to improve the quality of life and to prevent amputations. Antithrombotic therapy is often intensified in the postrevascularization period to prevent restenosis of the index artery and to counteract the prothrombotic state induced by the intervention. Therapeutic modalities include dual antiplatelet therapy (DAPT), anticoagulation, a combination of antiplatelet and anticoagulation therapy, and addition of cilostazol to single antiplatelet therapy. Subgroup analyses of data from randomized clinical trials provided low-quality evidence for the use of DAPT in patients with a below-knee prosthetic bypass graft and anticoagulation for those with a venous bypass graft. Cilostazol, when added to aspirin therapy, has been shown to prevent index vessel reocclusion after an endovascular intervention in patients at low risk for thrombosis in several small randomized trials. Conclusion There is a considerable paucity of high-quality evidence on the optimal antithrombotic regimen for patients undergoing lower extremity revascularization, with no particular therapy shown to consistently improve patient outcomes. The decision to initiate intensified antithrombotic therapy should include a close examination of its risk–benefit profile. The demonstrated benefit of such treatment is restricted to the prevention of index artery reocclusion, while an increased risk of bleeding may lead to significant morbidity and mortality.

The use of thrombolysis in the treatment of intermediate-risk PE is complicated by high rates of bleeding and should be limited to patients who clinically deteriorate rather than given as a standard-of-care treatment in this population. Data for low-dose thrombolysis remain limited.