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Do the Occluders deserve blame? Two cases of severe thrombosis in the left atrium in patients with bioprosthetic mitral valves and percutaneously implanted occluders
Natalia Jurzak-Myśliwy

Department of Cardiology, 1st Military Clinical Hospital with the Outpatient Clinic, Lublin, Poland,

Correspondence to Author: Natalia Jurzak-Myśliwy
Abstract:

We discuss two clinical instances of patients in the case report that follow valvular intervention and percutaneous occluder implantation into the left atrium.

A 68-year-old male who was admitted to the department of cardiology with a non-ST-elevation myocardial infarction is the first patient (NSTEMI). He had a history of severe secondary mitral regurgitation, paroxysmal atrial fibrillation, and biological mitral prosthesis implantation. The patient had percutaneous closure of the left atrium appendage due to contraindications to the long-term use of anticoagulants. A guy in his 80s with a history of persistent atrial fibrillation is the second case. The patient had an Amplatzer occluder and percutaneous Atrial Septal Defect type II (ASD II) closure eight years ago.

Due to multivessel coronary disease and significant mitral regurgitation a year later, the patient had Coronary Artery Bypass Graft (CABG) and biological mitral valve implantation. Transthoracic echocardiography (TTE) on both patients revealed severe left atrial thrombosis.

Introduction:

When anticoagulant medication is contraindicated for atrial fibrillation patients, left atrial appendage closure (LAAC) is a commonly utilised technique to avoid stroke [1]. Thrombotic incidents after LAAC are very uncommon. Device-Related Thrombosis (DRT) is thought to contribute between 1.6% to 16% of all thromboses, according to recent research [2-5]. In the case of DRT following percutaneous repair of the atrial septal defect, a similar circumstance applies (ASD). Recent Meta-analyses have estimated DRT to be 1% [6]. Following valvular intervention and percutaneous implantation of an extra device into the left atrium, we provide two clinical instances of patients in the study that follows.

Case Presentation:

A 68-year-old male who was admitted to the department of cardiology with NSTEMI is the first patient. The patient had a myocardial infarction with ST segment elevation three years prior, which was treated with coronary angioplasty and the placement of a drug-eluting stent (DES).

The patient also had ulcerative colitis, paroxysmal atrial fibrillation, type 2 diabetes, hypertension, and obesity. Three years ago, the patient underwent biological mitral prosthesis implantation due to the patient's substantial primary mitral regurgitation. The patient had left atrial appendage closure with the Amplatzer occluder a year after cardiac surgery due to the presence of contraindications to the use of anticoagulants (recurrent gastrointestinal bleeding of unclear aetiology). Using coronary angiography, the multivessel disease was shown.

Elevated gradients via the mitral bioprosthesis were visible on the TTE (PG max 30 mmHg, PG mean 14 mmHg). It was possible to see additional echostructure, which indicated the presence of a thrombus in the left atrium.The presence of a significant thrombus, with a maximum thickness of 30 mm linked to the implanted occluder, was confirmed by transesophageal echocardiography (TEE). PG mean was measured at 13 mmHg, and the bioprosthesis cusps moved normally. Additional factors like EOA (Effective Orifice Area) of 1.6 cm2 and EOAi of 0.75 cm2/m2 led us to believe that there may be a PPM (Prosthesis-Patient Mismatch).

The second patient is an 80-year-old male who has a history of chronic obstructive pulmonary disease, hypertension, bladder malignancy, and persistent atrial fibrillation. The patient had percutaneous closure of ASD II with the Amplatzer occluder eight years prior. A biological mitral valve was implanted due to severe secondary mitral regurgitation during the patient's CABG procedure for multivessel coronary disease a year later. Due to poor adherence, the patient on chronic warfarin therapy has labile International Normalized Ratio (INR) levels. Due to an aggravation of chronic heart failure, the patient was recently hospitalised to the department of cardiology. The interventricular septum and the anteroseptal wall also displayed akinesia, and TTE revealed a reduced ejection fraction of up to 30%.

The mitral prosthetic has the necessary gradients. It was possible to see that the left atrium contained a sizable thrombus. The wall of the left atrium was covered in a sizable thrombus that was mostly connected to the occluder. Additionally, the left atrium appendage had a thrombus. Views from several angles revealed that there was a leak near the occluder.

Discussion:

There is currently no established standard for echocardiographic control in patients with biological mitral valve and percutaneous occluder. There are yet no known instances of percutaneous occluders and mitral bioprostheses-related severe left atrial thrombosis in humans. Patients who have biological valve prostheses, percutaneous occluders, and thrombosis risk factors ought to have routine TTE once a year. However, this necessitates additional research and defined protocols. Whether patients with implanted biological valve prosthesis should be candidates for occluder implantation is still an open subject. Research is necessary for anticoagulant therapy as well. Should patients suspected with PPM always be treated with Vitamin K Antagonists (VKAs) or Non-Vitamin K Antagonist Oral Anti-Coagulation Agents (NOACs).

Conclusion:

Early device-related thrombosis is quite uncommon. Patients who have a biological mitral prosthetic are similarly affected. A thrombotic problem was discovered several years after the heart surgery in the cases mentioned above. Percutaneous occluders placed in the left atrium were a common feature among these patients. The thrombus's primary mass was on the occluder in both instances. Is it a coincidence or a "thrombogenic duo" caused by the valve prosthesis and the extra device in the left atrium?.

References:

1. Tzikas A, Gafoor S, Meerkin D, Freixa X, Cruz-Gonzalez I, Lewalter T,et al. Left atrial appendage occlusion with the AMPLATZER Amulet device: An expert consensus step-by-step approach. Euro Intervention. 2016;11(13):1512-21.

2. Lempereur M, Aminian A, Saw J, Freixa X, Gafoor S, Kefer J, et al.Rebuttal with regards to. Device associated thrombus formation after left atrial appendage occlusion: A systematic review of events reported with the Watchman, the Amplatzer Cardiac Plug and the Amulet. Catheter Cardiovasc Interv. 2017;90(5):E111-E21.

3. Fauchier L, Cinaud A, Brigadeau F, Lepillier A, Pierre B, Abbey S, etal. Device-related thrombosis after percutaneous left atrial appendage occlusion for atrial fibrillation. J Am Coll Cardiol. 2018,71(14):1528-36.

4. Hildick-Smith D, Landmesser U, Camm AJ, Diener HC, Paul V, SchmidtB, et al. Left atrial appendage occlusion with the Amplatzer™ device: Full results of the prospective global observational study. Eur Heart J. 2020;41(30):2894-901.

5. Cochet H, Iriart X, Sridi S, Camaioni C, Corneloup O, Montaudon M, et al. Left atrial appendage patency and device-related thrombus after percutaneous left atrial appendage occlusion: A computed tomography study. Eur Heart J Cardiovasc Imaging. 2018;19(12):1351-61.

6. Abaci A, Unlu S, Alsancak Y, Kaya U, Sezenoz B. Short and long term complications of device closure of atrial septal defect and patent foramen ovale: Meta-analysis of 28,142 patients from 203 studies. Catheter Cardiovasc Interv. 2013;82(7):1123-38.

Citation:

Natalia Jurzak-Myśliwy. Do the Occluders deserve blame? Two cases of severe thrombosis in the left atrium in patients with bioprosthetic mitral valves and percutaneously implanted occluders. Insights of Clinical and Medical Images 2022.