Effect of Therapeutic INR on Activated Clotting Times, Heparin Dosage, and Bleeding Risk During Ablation of Atrial Fibrillation.

06:00 EDT 4th September 2010 | BioPortfolio

Summary of "Effect of Therapeutic INR on Activated Clotting Times, Heparin Dosage, and Bleeding Risk During Ablation of Atrial Fibrillation."

Effect of INR on Anticoagulation During Ablation of Atrial Fibrillation. Background: Ablation of atrial fibrillation (AF) with international normalized ratio (INR) >/= 2.0 is safe and may reduce thromboembolic complications. Heparin is administered during the procedure, but the effect of elevated INR on heparin requirements and target activation clotting times (ACT) >/= 350 seconds during ablation is unknown. Objectives: To study the effect of INR on intraprocedural anticoagulation during ablation of AF. Methods: We retrospectively studied 427 consecutive patients over an 18-month period when we were transitioning to continuation of warfarin for AF ablation. Baseline INR, procedural ACT measurements, heparin doses and major complications were analyzed according to Group 1 with INR < 2.0 (n = 246) and Group 2 with INR >/= 2.0 (n = 181). Results: In Group 1, the mean INR was lower (1.3 +/- 0.3 s vs 2.4 +/- 0.3; P < 0.001), and the mean heparin dose was greater (106.82 +/- 40.01 vs 77.03 +/- 18.5 U/kg; P < 0.001). A single heparin bolus achieved ACT >/= 350 seconds throughout the procedure in 51 patients (20.7%) in Group 1 compared to 108 patients (59.7%) in Group 2 (P < 0.01). Mean ACT values were higher in Group 2. Symptomatic pericardial effusions were similar (2.4% in Group 1 and 2.2% in Group 2). There were 3 thromboembolic cerebrovascular events in Group 1 and none in Group 2. Femoral hematomas occurred more frequently in Group 1 (8.1%) than in Group 2 (3.3%) (P = 0.007). Conclusions: AF ablation with INR >/= 2.0 provides a consistent anticoagulant milieu during the procedure, with lower heparin requirements that are important to anticipate. (J Cardiovasc Electrophysiol, Vol. pp. 1-7).


Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.

Journal Details

This article was published in the following journal.

Name: Journal of cardiovascular electrophysiology
ISSN: 1540-8167


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Medical and Biotech [MESH] Definitions

The highest dosage administered that does not produce toxic effects. The NOAEL will depend on how closely dosages are spaced (lowest-observed-adverse-effect level and no-observed-effect level) and the number of animals examined. The ultimate objective is usually to determine not the "safe" dosage in laboratory animals but the "safe" dosage for humans. Therefore, the extrapolation most often required of toxicologists is from high-dosage studies in laboratory animals to low doses in humans. (Casarett and Doull's Toxicology: The Basic Science of Poisons, 4th ed)

A proteolytic enzyme obtained from the venom of fer-de-lance (Bothrops atrox). It is used as a plasma clotting agent for fibrinogen and for the detection of fibrinogen degradation products. The presence of heparin does not interfere with the clotting test. Hemocoagulase is a mixture containing batroxobin and factor X activator. EC 3.4.21.-.

Agents acting to arrest the flow of blood. Absorbable hemostatics arrest bleeding either by the formation of an artificial clot or by providing a mechanical matrix that facilitates clotting when applied directly to the bleeding surface. These agents function more at the capillary level and are not effective at stemming arterial or venous bleeding under any significant intravascular pressure.

A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.

A sulfated plasma protein with the MW of approximately 66kDa that resembles ANTITHROMBIN III. The protein is an inhibitor of thrombin in plasma and is activated by dermatan sulfate or heparin. It is a member of the serpin superfamily.


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