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  Vol. 65 No. 9, September 2008 TABLE OF CONTENTS
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Anticoagulation After Cardioembolic Stroke

To Bridge or Not to Bridge?

Hen Hallevi, MD; Karen C. Albright, DO, MPH; Sheryl Martin-Schild, MD, PhD; Andrew D. Barreto, MD; Sean I. Savitz, MD; Miguel A. Escobar, MD; Nicole R. Gonzales, MD; Elizabeth A. Noser, MD; Kachi Illoh, MD; James C. Grotta, MD

Arch Neurol. 2008;65(9):1169-1173. Published online July 14, 2008 (doi:10.1001/archneur.65.9.noc70105).

Background  Most patients with cardioembolic stroke require long-term anticoagulation. Still, uncertainty exists regarding the best mode of starting long-term anticoagulation.

Design, Setting, and Patients  We conducted a retrospective review of all patients with cardioembolic stroke admitted to our center from April 1, 2004, to June 30, 2006, and not treated with tissue plasminogen activator. Patients were grouped by treatment: no treatment, aspirin only, aspirin followed by warfarin sodium, intravenous heparin sodium in the acute phase followed by warfarin (heparin bridging), and full-dose enoxaparin sodium combined with warfarin (enoxaparin bridging). Outcome measures and adverse events were collected prospectively. Laboratory values were captured from the records.

Main Outcome Measures  Symptomatic hemorrhagic transformation, stroke progression, and discharge modified Rankin Scale score.

Results  Two hundred four patients were analyzed. Recurrent stroke occurred in 2 patients (1%). Progressive stroke was the most frequent serious adverse event, seen in 11 patients (5%). Hemorrhagic transformation occurred in a bimodal distribution—an early benign hemorrhagic transformation and a late symptomatic hemorrhagic transformation. All of the symptomatic hemorrhagic transformation cases were in the enoxaparin bridging group (10%) (P = .003). Systemic bleeding occurred in 2 patients (1%) and was associated with heparin bridging (P = .04).

Conclusions  Anticoagulation of patients with cardioembolic stroke can be safely started with warfarin shortly after stroke. Heparin bridging and enoxaparin bridging increase the risk for serious bleeding.


Author Affiliations: Department of Neurology, University of Texas at Houston Medical School (Drs Hallevi, Martin-Schild, Barreto, Savitz, Gonzales, Noser, Illoh, and Grotta) and Department of Hematology (Dr Escobar), University of Texas Health Science Center at Houston; and Department of Neuroscience, University of California, San Diego (Dr Albright).



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