Titlebook: Handbook for Venous Thromboembolism; Gregory Piazza,Benjamin Hohlfelder,Samuel Z. Goldh Book 2015 Springer International Publishing Switze

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ACME

https://doi.org/10.1007/978-1-4939-2371-7unfractionated heparin, low-molecular-weight heparin, fondaparinux, argatroban, bivalirudin, warfarin, and the non-vitamin K oral anticoagulants (NOACs) rivaroxaban, dabigatran, apixaban, and edoxaban. The NOACs represent a major advance in anticoagulation for VTE with superior safety and equivalent

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https://doi.org/10.1007/978-3-030-27596-9optimal duration and drug regimen requires an individualized assessment of the patient’s long-term risk of recurrence as well as bleeding. Warfarin and non-vitamin K oral anticoagulants (NOACs) have been validated for extended duration anticoagulation to prevent recurrent unprovoked VTE. Aspirin als

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https://doi.org/10.1007/978-1-137-06809-5 persistent macrovascular obstruction, pulmonary vasoconstriction, and a secondary small-vessel arteriopathy. CTEPH used to be considered a rare complication but is now recognized to occur in 2–4 % of patients after PE. While patients may be initially asymptomatic, CTEPH frequently progresses to deb

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https://doi.org/10.1007/978-981-15-2031-0tremity edema, hyperpigmentation, and, in advanced cases, venous ulceration. PTS results in substantial disability, loss of functional status, and health care expenditure. Compression therapy, including graduated compression stockings, comprises the cornerstone of PTS therapy.

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The Short Narratives of E. M. Forstertion of thromboprophylaxis continues to be inconsistent in the U.S., Canada, and worldwide. Quality Improvement initiatives, including decision support-based strategies, have the potential to improve prophylaxis utilization and reduce the incidence of VTE during hospitalization. The approach to VTE

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The Sheer Joy of Celestial Mechanicsdetermine the overall hemodynamic impact. The right ventricle (RV) plays a central role in PE pathophysiology. A sudden increase in RV afterload due to PE can lead to RV dilation and hypokinesis, RV ischemia, and ultimately acute RV failure.