Newly developed spontaneous echocardiographic contrast as a potential marker of intracardiac thrombus formation after a transcatheter edge-to-edge mitral valve repair.

Case description

A 76-year-old man with idiopathic dilated cardiomyopathy, severe chronic kidney disease, and permanent atrial fibrillation (AF) presented with congestive heart failure secondary to severe functional mitral regurgitation (MR) and a low left ventricular ejection fraction of 20%. Atrial fibrillation had been managed previously by administering an oral anticoagulant (OAC, warfarin); because he was at a high risk of bleeding, the dose was adjusted to achieve a prothrombin time-international normalized ratio (PT-INR) of 1.6–2.0 (therapeutic range of PT-INR as per Japanese guidelines: 1.6–2.6).[1] Thereafter, transcatheter edge-to-edge repair (TEER) of the mitral valve (MV) was performed because the patient was at a high surgical risk. A MitraClip XT (Abbott, IL, USA) was successfully implanted at the A2–P2 segment of the MV, and the MR improved to a mild status ( and Supplementary material online, ). However, a spontaneous echocardiographic contrast (SEC) and a newly developed sludge in the left atrium (LA) were observed incrementally, even after controlling the activated clotting time within the recommended range of 300–350 s ( and Supplementary material online, ). The post-operative MV area (2.1 mm²) and the mean transmitral pressure gradient (2.7 mmHg) were acceptable; however, a blunted pulmonary venous flow persisted, and the mean LA pressure increased from 13 mmHg to 18 mmHg. This suggested relative mitral stenosis (MS; see Supplementary material online, ). Although thrombus formation in the LA was not observed immediately after the procedure, transthoracic echocardiography (TTE) performed 5 days after the TEER confirmed a large thrombus attached to an iatrogenic atrial septal defect (ASD; and Supplementary material online, ). The patient was initiated on a strengthened anticoagulation therapy with continuous intravenous infusion of unfractionated heparin and subsequent increasing OAC (target therapeutic PT-INR: 2.6–3.0). The thrombus disappeared 1 week later (D). The patient was discharged without any neurological abnormalities.

(A–B) Comparison of transoesophageal echocardiography findings obtained before and after the transcatheter edge-to-edge mitral valve repair: (A) mitral regurgitation and (B) left atrial appendage. Asterisks indicate the implanted clip. Arrows show a newly developed sludge in the left atrial appendage. (C) Transoesophageal echocardiography reveals a newly developed, large, mobile thrombus (arrows) attached to an iatrogenic atrial septal defect. (D) Transthoracic echocardiography focused on the iatrogenic atrial septal defect on post-operative Days 1, 5, and 12. Arrows indicate the thrombus. LA, left atrium; LV, left ventricle; RA, right atrium.

SEC, observed in cases with LA dysfunction or MS, is a known thrombotic predictor.[2] A newly developed post-TEER SEC suggests an improvement in MR because a reduced MR jet can induce blood-flow stasis; however, the clinical impact of post-TEER SEC remains unclear. In this case, although the post-TEER mean transmitral pressure gradient and the MV area did not meet the conventional MS criteria, the increased LA pressure suggested relative iatrogenic MS. Moreover, an injury site caused by a large-bore steering-guiding catheter could become a thrombogenic nidus.[3] To our knowledge, this is the first report to describe a temporary post-TEER SEC in relative iatrogenic MS, which may have been associated with a sub-acute thrombus attached to an iatrogenic ASD. A newly developed post-TEER SEC could be a potential marker of intracardiac thrombus formation. Careful management of antithrombotic therapy for preventing thrombogenic events and thorough evaluation of neurological abnormalities should be performed in such settings.

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