Platelet Function in Patients with Chronic Coronary Heart Disease on Long-Term Anticoagulant Therapy: Effect of Anticoagulant Stopping

Vallés, Juana; Aznar, Justo; Santos, Teresa; Villa, Piedad; Fernández, Angeles

doi:10.1159/000216877

Cited by 3 publications

(2 citation statements)

References 26 publications

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“…51,52 Furthermore, a surgical procedure may induce a hypercoagulable state through mechanisms that include vessel-wall injury and fibrinolysis inhibition. [53][54][55] In 3 prospective studies that have investigated periprocedural bridging anticoagulation with LMWH, 25,26,56 thromboembolic events occurred in 1 (0.8%) of 128 of patients, an event rate that is consistent with our findings.…”

Section: Commentsupporting

confidence: 86%

Low-Molecular-Weight Heparin as Bridging Anticoagulation During Interruption of Warfarin

Douketis¹,

Johnson²,

Turpie³

2004

Arch Intern Med

309

213

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Section: Commentsupporting

confidence: 86%

Low-Molecular-Weight Heparin as Bridging Anticoagulation During Interruption of Warfarin

Douketis¹,

Johnson²,

Turpie³

2004

Arch Intern Med

309

213

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“…Hence, a 10% per year risk of thromboembolism translates to a daily risk of ~0.03%, or a 1-in-3650 probability of an event. If stopping oral anticoagulation induces a transient "rebound" hypercoagulable state [55][56][57][58][59][60] or starting anticoagulation induces a transient "paradoxical" hypercoagulable state, 51 the daily risk of thromboembolism may be underestimated. However, there is no convincing clinical evidence to support either of these phenomena.…”

Section: Qualifying Remarksmentioning

confidence: 99%

Management of Anticoagulation in Patients Who Require Invasive Procedures

2003

Seminars in Vascular Medicine

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When orally anticoagulated patients need to have surgery, the goals of management are to minimize the risks of thromboembolism and of bleeding from the invasive procedure. Some invasive procedures can be performed while patients are fully or partially anticoagulated because bleeding is rare and/or easily controlled. When it is necessary to reverse oral anticoagulant therapy it should be interrupted for as short a time as possible, usually 4 or 5 days. Intravenous unfractionated heparin or therapeutic-dose subcutaneous low-molecular-weight heparin (LMWH) can be given as "bridging therapy" to reduce the risk of thromboembolism while oral anticoagulation is interrupted. However, the risks and benefits of bridging therapy are uncertain. Bridging therapy, particularly with LMWH, may not be very effective at preventing embolism in patients with atrial fibrillation or mechanical heart valves, and it may be associated with bleeding. My preference is to minimize the time that patients are off oral anticoagulant therapy, generally restarting warfarin the day of surgery; reserve bridging therapy for those at highest risk of thromboembolism; and to use "prophylactic" rather than "therapeutic" doses of heparin after major surgery. As major surgery markedly increases the risk of venous thromboembolism, postoperative bridging therapy should be considered for patients without an inferior vena caval filter that have had proximal deep vein thrombosis or pulmonary embolism during the previous month.

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Warfarin Withdrawal

Palareti

Legnani

1996

Clinical Pharmacokinetics

130

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Warfarin, like all the 4-hydroxycoumarin compounds, has an asymmetric carbon atom. The clinically available warfarin preparations consist of a racemic mixture of equal amounts of 2 distinct S and R isomers, the former being 4-times more potent as anticoagulant and more susceptible to drug interaction. Warfarin is highly water soluble and rapidly absorbed from the stomach and the upper gastrointestinal tract; its plasma concentrations peak 60 to 90 minutes after oral administration. Warfarin binds to the enzyme vitamin K 2,3-epoxide reductase in liver microsomes, stopping the cycle of vitamin K and reducing gamma-carboxylation of the precursors of vitamin D-dependent pro- and anticoagulant factors. A variable fraction of the binding with the target enzyme, albeit small, can be reversed by competitive displacers, such as dithiol-reducing agent activity. Differences in dithiol-reducing activity have been suggested as a contributing factor to the wide interindividual differences in sensitivity to oral anticoagulants. The anticoagulant effect is caused by a small fraction of the drug, since most (97 to 99%) is protein bound (mainly to albumin) and ineffective. Drugs that can displace the albumin binding will increase the action of warfarin, even though this effect is counteracted by a more rapid elimination of the drug. The elimination half-life of warfarin varies greatly among individuals, ranging from 35 to 45 hours; the S isomer has, however, an average half-life shorter than the R isomer. The plasma levels of vitamin K-dependent proteins are determined by a dynamic equilibrium between their synthesis and half-life times. The delay before warfarin takes effect reflects the half-life of the clotting proteins; the levels of factor VII and protein C (with shorter half-lives) are reduced earlier, reaching steady inhibited levels in about 1 day, whereas factor II takes more than 10 days. Oral anticoagulant therapy (OAT) with warfarin or other coumarin derivatives is increasingly administered to patients for primary or secondary prevention of various arterial or venous thromboembolic diseases. If in some clinical conditions OAT is given indefinitely, in others--such as venous thromboembolism or after tissue heart valve replacement--anticoagulants are usually given only for the high risk period of thrombotic complication. A recent large prospective study performed by the Italian Federation of Anticoagulation Clinics showed that about 30% of the patients who began OAT for various clinical indications stopped treatment at different times, confirming that withdrawal from OAT is an occurrence that affects a large number of patients. The expression 'rebound phenomenon' was adopted to indicate a hypercoagulant condition occurring after warfarin withdrawal. A possible more frequent recurrence of thromboembolism after cessation of anticoagulation became a matter of controversy and many clinical studies, mostly observational and noncontrolled, reported on the issue with inconsistent results. Most authoritative commentators agreed ...

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Platelet Function in Patients with Chronic Coronary Heart Disease on Long-Term Anticoagulant Therapy: Effect of Anticoagulant Stopping

Cited by 3 publications

References 26 publications

Low-Molecular-Weight Heparin as Bridging Anticoagulation During Interruption of Warfarin

Low-Molecular-Weight Heparin as Bridging Anticoagulation During Interruption of Warfarin

Management of Anticoagulation in Patients Who Require Invasive Procedures

Warfarin Withdrawal

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