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CASE REPORT
Year : 2014  |  Volume : 24  |  Issue : 2  |  Page : 64-65

Thrombophilia-related complications in the treatment of a left atrial appendage thrombus: A case report


Cardiology Unit and Echo-Lab of Emergency Department, Madonna del Soccorso Hospital, San Benedetto del Tronto, Italy

Date of Web Publication1-Jul-2014

Correspondence Address:
Vito Maurizio Parato
Department of Cardiology Unit of Emergency, Madonna del Soccorso Hospital, 3-7 via Manara, 63074 San Benedetto del Tronto, Marche
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2211-4122.135621

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  Abstract 

Trans-esophageal echocardiography (TEE) revealed a left atrial appendage (LAA) thrombus in an 84-year-old woman with nonvalvular atrial fibrillation not known before our evaluation. In her medical history, there were hypertension, dyslipidemia and a previous pulmonary embolism. She was taking warfarin at time of our evaluation and presented signs and symptoms of heart failure. Together with heart failure treatment, intravenous anticoagulation with unfractionated heparin was initiated. Treatment was complicated by additional right lower limb embolic event and the LAA thrombus remained unchanged. Testing revealed heterozygosity for both the factor V Leiden and the methylenetetrahydrofolate reductase C677T mutations inducing resistance to activated protein C. The patient refused transcatheter closure of the left atrial appendage.

Keywords: Left atrial appendage, thrombophilia, thrombus, trans-esophageal echocardiography


How to cite this article:
Parato VM, Scarano M, Labanti B. Thrombophilia-related complications in the treatment of a left atrial appendage thrombus: A case report. J Cardiovasc Echography 2014;24:64-5

How to cite this URL:
Parato VM, Scarano M, Labanti B. Thrombophilia-related complications in the treatment of a left atrial appendage thrombus: A case report. J Cardiovasc Echography [serial online] 2014 [cited 2019 Dec 9];24:64-5. Available from: http://www.jcecho.org/text.asp?2014/24/2/64/135621


  Introduction Top


Atrial fibrillation (AF) is epidemiologically the most common cardiac arrhythmia, and it is responsible for 15-20% of all ischemic strokes and 26% of all embolic events. Thrombophilias represent an evolving story that continues to stir controversy for care providers and patients. The predominant thrombophilic mutations include the factor V Leiden mutation, prothrombin gene mutation G20210A, methylenetetrahydrafolate reductase C667T, and deficiencies of the natural anticoagulants proteins C and S, and antithrombin. [1],[2],[3]


  Case report Top


An 84-year-old woman was referred to our institution because of palpitations and dyspnea started 1 week before. In her medical history there were hypertension, dyslipidemia and a previous pulmonary embolism (PE). For this reason she was taking warfarin at time of our evaluation. A nonvalvular atrial fibrillation (AF) with HR 96/m was found. At clinical examination there were signs of heart failure (rales and peripheral edema), functional NYHA class III and high BP (170/110).

Because of a previous pulmonary embolism in her clinical history a trans-esophageal echocardiography (TEE) was performed. TEE revealed a left atrial appendage (LAA) roundish mass, sizing 1.2 × 1.2 cm that seemed a thrombus [Figure 1]. Regarding echocardiographic features, the mass was hyperechogenic and calcified, suggesting it was an old formation, consistent with an organized thrombus. Dense left atrial spontaneous echo-contrast (SEC) was found. Left atrium was dilated and LVEF% was normal. [4] International normalized ratio (INR) at presentation was 1.95.
Figure 1: TEE image of the LAA thrombus at time of fi rst evaluation

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Together with heart failure treatment, intravenous anticoagulation with unfractionated heparin was initiated. The value of aPTT during treatment was 1.9 times. Treatment was complicated by an additional right lower limb embolic event treated by Fogarty arterial embolectomy catheter. In addition, after 7 days of therapy, the LAA thrombus remained unchanged [Figure 2].
Figure 2: TEE image of the LAA thrombus after 7 days of treatment with intravenous unfractionated heparin

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A previous testing revealed heterozygosity for both the factor V Leiden and the methylenetetrahydrofolate reductase C677T mutations inducing resistance activated protein C. The test was performed 5 years before and after PE event. The combination of these thrombophilic factors can probably explain the poor anticoagulant response, additional embolic events and the failure of resolution of the LAA thrombus. [5] Patient refused transcatheter closure of the LAA and was chronically treated with Novel Oral AntiCoagulant (NOAC), specifically with rivaroxaban, 20 mg OD.


  Discussion Top


AF is epidemiologically the most common cardiac arrhythmia, and it is responsible for 15% to 20% of all ischemic strokes and 26% of all embolic events. [1],[6] It is assumed that >90% of clinically apparent embolisms in AF originate from the LAA.

The case-study emphasizes the importance of the high risk of thrombo-embolism with inherited thrombophilic factors. [7],[8] Besides this thrombophilic status may lead to a resistance to anticoagulation treatment.

For patients with resistance to chronic oral anticoagulation, new therapeutic approaches have been developed. Transcatheter closure of the left atrial appendage (LAA) is becoming more common as an interventional therapy to prevent thromboembolic complications in patients with atrial fibrillation (AF) and contraindications or resistance to chronic oral anticoagulation. [6]

 
  References Top

1.Bungard TJ, Ackman Ml, Ho G, Tsuyuki RT. Adequacy of anticoagulation in patient with atrial fibrillation coming to a hospital. Pharmacotherapy 2000;20:1060-5.  Back to cited text no. 1
    
2.Martinelli I, Passamonti SM, Bucciarelli P. Thrombophilic states. Handb Clin Neurol 2014;120:1061-71.  Back to cited text no. 2
    
3.Lino FL, Traina E, Barreto JA, Moron AF, Mattar R. Thrombophilic mutations and polymorphisms, alone or in combination, and recurrent spontaneous abortion. Clin Appl Thromb Hemost 2014.  Back to cited text no. 3
    
4.Nakagawa M, Saikawa T. Echocardiogram in atrial fibrillation. Nihon Rinsho 2013;71:49-53.  Back to cited text no. 4
    
5.Cohoon KP, Heit JA. Inherited and secondary thrombophilia. Circulation 2014;129:254-7.  Back to cited text no. 5
    
6.Cruz-Gonzalez I, Yan BP, Lam YY. Left atrial appendage exclusion: State-of-the-art. Cathet Cardiovasc Interv 2010;75:806-13.  Back to cited text no. 6
    
7.Sakurai K, Hirai T, Nakagawa K, Kameyama T, Nozawa T, Asanoi H, et al. Left atrial appendage function and abnormal hypercoagulability in patients with atrial flutter. Chest 2003;124:1670-4.  Back to cited text no. 7
    
8.Jalouli I, Mrad M, Fekih-Mrissa N, Hajjej Z, Lebbi A, Labbene I, et al. Inherited thrombophilia-related complications in the treatment of a biatrial thrombus. Blood Coagul Fibrinolysis 2013;24:205-7.  Back to cited text no. 8
    


    Figures

  [Figure 1], [Figure 2]


This article has been cited by
1 Non-vitamin K antagonist oral anticoagulants for the treatment of intracardiac thrombosis
Eiman Ghaffarpasand,Maneli D. Tehrani,Jolanta Marszalek,Gerald Chi
Journal of Thrombosis and Thrombolysis. 2018;
[Pubmed] | [DOI]



 

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