|Year : 2014 | Volume
| Issue : 2 | Page : 64-65
Thrombophilia-related complications in the treatment of a left atrial appendage thrombus: A case report
Vito Maurizio Parato, Michele Scarano, Benedetto Labanti
Cardiology Unit and Echo-Lab of Emergency Department, Madonna del Soccorso Hospital, San Benedetto del Tronto, Italy
|Date of Web Publication||1-Jul-2014|
Vito Maurizio Parato
Department of Cardiology Unit of Emergency, Madonna del Soccorso Hospital, 3-7 via Manara, 63074 San Benedetto del Tronto, Marche
Source of Support: None, Conflict of Interest: None
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 2020 Apr 10];24:64-5. Available from: http://www.jcecho.org/text.asp?2014/24/2/64/135621
| Introduction|| |
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. ,,
| Case report|| |
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.  International normalized ratio (INR) at presentation was 1.95.
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.  Patient refused transcatheter closure of the LAA and was chronically treated with Novel Oral AntiCoagulant (NOAC), specifically with rivaroxaban, 20 mg OD.
| Discussion|| |
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. , 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. , 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. 
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[Figure 1], [Figure 2]