Abstract-Arterial thrombosis results from endovascular injury and, to a lesser extent, alterations in hemostatic equilibrium. Although multiple hereditary and acquired hemostatic risk factors have been described in the pathophysiology of venous thrombosis, the degree and type of abnormalities that contribute to arterial thrombosis are less well understood. Endothelial cell injury with the elaboration of proinflammatory mediators stimulates the process of arterial thrombosis. Although this is most often the result of endovascular injury attributable to atherosclerotic disease, other disease states can elicit a similar response as well. Similarly, once thrombosis has been initiated, variations in the activity of coagulation proteins and endogenous anticoagulants, as well as the kinetics of platelet aggregation, may alter the effectiveness of thrombus formation. Epidemiological studies have identified several acquired or inherited states that may result in endothelial damage or altered hemostatic equilibrium, thereby predisposing patients to arterial thrombosis. These include hyperhomocysteinemia, elevated C-reactive protein, antiphospholipid antibodies, elevated fibrinogen, Factor VII, plasminogen activator inhibitor-1 (PAI-1), hereditary thrombophilias, and platelet hyper-reactivity. This review explores our present understanding of these risk factors in the development of arterial thrombotic events. At present, the literature supports a role for hyperhomocysteinemia, elevated C-reactive protein, and elevated fibrinogen as risk factors for arterial thrombosis. Similarly, the literature suggests that lupus anticoagulants and, to a lesser extent, elevated titers of cardiolipin IgG antibodies predispose to arterial vascular events. In certain subsets of patients, including those with concomitant cardiac risk factors, Ͻ55 years of age, and women, hereditary thrombophilias such as carriership of the factor V Leiden and the prothrombin G20210A mutations may confer a higher risk of arterial thrombosis. However, the data on Factor VII, PAI-1, and platelet receptor polymorphisms are contradictory or lacking.

In this large cohort of non-critically ill hospitalized patients, we identified several independent risk factors for nosocomial gastrointestinal bleeding. With further validation at other medical centers, the risk model derived from these factors may help clinicians to direct acid-suppressive medication to those most likely to benefit.

As part of the Choosing Wisely Campaign, the Society of Hospital Medicine identified reducing inappropriate use of acid-suppressive medication for stress ulcer prophylaxis as one of 5 key opportunities to improve the value of care for hospitalized patients. We designed a computerized clinical decision support intervention to reduce use of acid-suppressive medication for stress ulcer prophylaxis in hospitalized patients outside of the intensive care unit at an academic medical center. Using quasi-experimental interrupted time series analysis, we found that the decision support intervention resulted in a significant reduction in use of acid-suppressive medication with stress ulcer prophylaxis selected as the only indication, a non-significant reduction in overall use, and no change in use on discharge. We found low rates of use of acid-suppressive medication for the purpose of stress ulcer prophylaxis even before the intervention, and continuing preadmission medication was the most commonly selected indication throughout the study. Our results suggest that attention should be focused on both the inpatient and outpatient settings when designing future initiatives to improve the appropriateness of acid-suppressive medication use.

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AAIM is the largest academically focused specialty organization representing departments of internal medicine at medical schools and teaching hospitals in the United States and Canada. As a consortium of five organizations, AAIM represents department chairs and chiefs; clerkship, residency, and fellowship program directors; division chiefs; and academic and business administrators as well as other faculty and staff in departments of internal medicine and their divisions.

The management of antithrombotic medications in patients requiring invasive procedures is a common problem in hospital medicine, for which there is limited evidence to guide clinical decision making. Existing guidelines do not address many hospital‐based procedures and have not kept pace with the introduction of newer antiplatelet and anticoagulant medications. This article provides a conceptual framework for the periprocedural management of antithrombotic therapy, with a focus on the procedures that hospitalists are most likely to perform and the pharmacology of the common and newer antithrombotic medications. Journal of Hospital Medicine 2014;9:337–346. © 2014 Society of Hospital Medicine

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