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Letters to the Editor

Huge left atrial appendage thrombus in a patient with atrial fibrillation: Successful treatment with tirofiban

, , , &
Pages 333-334 | Received 08 May 2012, Accepted 12 May 2012, Published online: 21 Jun 2012

To the editor

Atrial fibrillation (AF) is the most common chronic arrhythmia and is associated with increased morbidity and mortality. AF is an important cause of cardiac source of embolism and stroke Citation[1], Citation[2]. If AF duration is longer than 48 hours or there is doubt about its duration, at least 3 weeks effective anticoagulation or transesophageal echocardiography (TEE) to rule out thrombus formation is recommended before elective cardioversion because thromboembolic risk increases considerably. If a thrombus is detected in the left atrium or atrial appendage (LAA), guidelines recommend effective anticoagulation with coumadin for at least 3 weeks followed by a repeated TEE. However, guidelines are not illuminative when huge thrombus is detected in LAA Citation[1], Citation[2]. In this article, we report a patient with a history of palpitation and AF for 3 days, for whom TEE revealed a giant, fragmented, mobile thrombus filling LAA and protruding to the left atrium and mitral valve which was successfully treated with the combination of acetylsalicylic acid, unfractionated heparin and tirofiban.

A 68-year-old female with a history of hypertension was admitted to the emergency service with palpitation and dyspnea for the last 3 days. On admission, she had an irregular pulse with a heart rate of 139 bpm and her ECG revealed AF. Her blood pressure was 135/85 mmHg. Rest of the physical examination was normal. Transthoracic echocardiography was normal except diastolic dysfunction. Because we decided to restore sinus rhythm, we performed TEE to exclude any thrombus that revealed a giant, fragmented, mobile thrombus filling LAA and protruding to the left atrium and mitral valve (Panel A, Video). We started acetylsalicylic acid 100 mg daily and unfractionated heparin infusion by adjusting activated clotting time to 250–350 seconds. Control TEE which was performed 5 days after starting heparin showed that there was no change in the thrombus size and characteristics (Panel B). We therefore decreased the dose of unfractionated heparin to keep activated clotting time to 200–250 seconds and added tirofiban infusion 9 cc/h adjusted according to her weight. On the 5th day of the combination of acetylsalicylic acid, unfractionated heparin, and tirofiban, TEE demonstrated that thrombus became smaller but was still mobile, thus we continued the treatment (Panel C). On the 6th day of the combination treatment we observed hematuria, therefore tirofiban dose was reduced to 7 cc/h. Hematuria disappeared on the 8th day. On the 10th day of combination treatment, TEE showed complete lysis of the thrombus (Panel D). The patient was discharged from hospital with warfarin by adjusting international normalized ratio 2:3.

Morbidity and mortality is significantly increased in AF Citation[1], Citation[2]. Most of the physicians attempt to restore sinus rhythm in order to improve symptoms and sometimes survival. If AF duration is longer than 48 hours or there is doubt about its duration, at least 3 weeks effective anticoagulation or TEE to rule out thrombus formation is recommended before elective cardioversion because thromboembolic risk increases considerably. If a thrombus is detected in the left atrium or LAA, guidelines recommend effective anticoagulation with coumadin for at least 3 weeks followed by a repeat TEE. However, guidelines are not illuminative when huge thrombus is detected in LAA Citation[1], Citation[2]. In this article, we report a patient with a history of palpitation and AF for 3 days, for whom TEE revealed a giant, fragmented, mobile thrombus filling the LAA, and protruding to the left atrium and mitral valve, which was successfully treated with the combination of acetylsalicylic acid, unfractionated heparin, and tirofiban, which was not reported previously.

Although thrombus development in LAA in the setting of AF is a well-known issue, development of huge thrombus in non-valvular AF, as in our case, is very rare. Moreover, development of a giant thrombus within 3 days of AF development has not been reported previously although we cannot prove the exact time of the occurrence of the thrombus and AF. Despite the definition of huge thrombus in LAA is somewhat arbitrary, there is no mention and consensus on how to treat this condition in AF guidelines Citation[1], Citation[2]. Heparin infusion itself is often not enough to dissolve the thrombus. Thrombolysis carries high risk of embolization. Surgery seems as a burdensome solution for LAA thrombus. In our view, glycoprotein IIb/IIIa inhibitor infusion might provide an alternative treatment option in this problem. Besides there is an increasing and encouraging evidence regarding non-coronary applications of glycoprotein IIb/IIIa inhibitors such as prosthetic valve thrombus, pulmonary embolism, stroke and right atrial thrombus Citation[3–10]. The potential use of glycoprotein IIb/IIIa inhibitors in these broad spectrum of non-coronary thrombotic conditions need to be tested with randomized studies.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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