Periprocedural antiplatelet therapy: recommendations for standardized reporting in patients on antiplatelet therapy.

J Thromb Haemost. 2013 May 6;

Authors: Spyropoulos A, Albaladejo P, Godier A, Greinacher A, Hron G, Levy J, Samama C, Douketis J, The Subcommittee on Predictive Variables of the Scientific Standardization Committee of the ISTH

Abstract
The periprocedural management of patients on antiplatelet (AP) therapy such as aspirin (ASA), or P2Y12 receptor antagonists (clopidogrel, ticagrelor, and prasugrel), for the primary or secondary prevention of cardiovascular disease, is an increasingly common clinical problem [1]. Approximately 10 - 15% of normal platelet function is restored for each day of interruption of AP therapy and therefore it would take 7 - 10 days for an entire platelet pool to be restored [2]. Cohort studies involving patients on combined anticoagulant and ASA therapy typically stopped ASA 7-10 days before the procedure or surgery[3-5](,) [6, 7] When resuming AP therapy, the maximum antiplatelet effect of ASA can occur within minutes, and with agents like clopidogrel, when administered with a 150-600 mg loading dose, maximum platelet inhibition can occur within 12 -15 hours after administration [8, 9]. Cohort studies involving patients on anticoagulant therapy and ASA typically resumed ASA within 24 hours for most surgical procedures [6, 7]. This article is protected by copyright. All rights reserved.

PMID: 23647986 [PubMed - as supplied by publisher]

Physicians' compliance with the Padua Prediction Score for preventing venous thromboembolism among hospitalized medical patients.

J Thromb Haemost. 2013 Apr 19;

Authors: Rossetto V, Barbar S, Vedovetto V, Milan M, Prandoni P

Abstract
Hospitalization for acute medical illnesses confers an eight-fold increased risk of venous thromboembolic (VTE) disorders that persists for up to three months and is even higher after discharge than during in-hospital stay [1]. However, in spite of strong evidence in favor of thromboprophylaxis [2-4], several observation studies from various countries found that less than 50% of admitted medical patients at risk receive prophylaxis against VTE [5-8]. This article is protected by copyright. All rights reserved.

PMID: 23601653 [PubMed - as supplied by publisher]

Bleeding risk in warfarinized patients with a therapeutic INR: the effect of low factor IX levels.

J Thromb Haemost. 2013 Apr 13;

Authors: Dargaud Y, Hoffman M, Lefrapper L, Lin FC, Genty A, Chatard B, Marin S, Négrier C, Monroe D

Abstract
OBJECTIVE: Bleeding is the main complication of warfarin therapy, even patients with an INR in the target range can suffer bleeding, suggesting that INR does not perfectly reflect the therapeutic effect of warfarin. We hypothesized the INR might underestimate the level of anticoagulation in a subject with a lower factor IX (FIX) level than average. METHODS & RESULTS: We modeled warfarin anticoagulation in our in vitro thrombin generation (TG) model by adjusting the levels of vitamin K-dependent factors to those of patients with an INR of 2-3. Variation in FIX had a marked effect on TG but had no effect on the PT-INR. A prospective observational, cross-sectional clinical study including 341 consecutive patients admitted to the emergency department with an INR between 2 and 3, showed a statistically lower FIX activity in bleeders (p=0.004) compared to others. No correlation was found between TG capacity and PT-INR results (p=0.36).However, in patients, presenting with warfarin-related hemorrhage, TG was significantly lower (p<0.001) than others. And a correlation on the boundary of significance was observed between TG capacity and FIX levels (p=0.09). CONCLUSION: These data demonstrates that patients who bleed when their PT-INR is in the target range 2-3 might have defective TG related to a lower level of FIX than expected. This article is protected by copyright. All rights reserved.

PMID: 23581252 [PubMed - as supplied by publisher]