Thrombus formation on the stump of a resected left atrial appendage in a case with a history of left atrial appendage thrombus owing to left atrial ischaemia: a follow-up case report

Abstract

Case recap We previously reported a 64-year-old male patient with a complicated left atrial appendage (LAA) thrombus due to left atrial ischaemia. 1 The patient developed total occlusion of both the right coronary artery (RCA) and left circumflex artery (LCX), which supply blood to the left atrium and the thrombus formed in the LAA despite the sinus rhythm. The patient underwent surgical revascularization of the coronary arteries with LAA resection. In the present report, we describe further interesting findings regarding the case that occurred after the surgery. Further follow-up Given the diagnosis of multivessel coronary artery disease (RCA segment 1:100%, LCX segment 11:100%, and left anterior descending artery segment 7:90%) with LAA thrombus, the patient underwent coronary artery bypass grafting (CABG) with LAA resection. Transoesophageal echocardiography just before the closure of the thoracotomy showed that the thrombus was completely resolved (see Supplementary material online, Video S1 ). Generally, he recovered well, although he complicated ventricular tachycardia, which required electrical cardioversion on post-operative day (POD) 4. He was started on acetylsalicylic acid 100 mg daily with clopidogrel 75 mg daily as an antiplatelet therapy after CABG. Anticoagulation therapy was not initiated because the sinus rhythm persisted, and he had no evidence of complications such as atrial fibrillation (AF). However, the left atrium was moderately dilated (left atrial volume index of 44 mL/m2). The patient underwent a cardiac rehabilitation program and had an uneventful clinical course. The left atrial contraction seemed to recover because the A wave of the transmitral flow on echocardiography increased over time ( Figure 1A–C ). Left ventricular ejection fraction remained severely impaired (around 30%). There were no signs suggesting mitral annulus calcifications or significant mitral regurgitation. On POD 24, cardiac computed tomography (CCT), which was performed to evaluate the patency of the bypassed grafts, accidentally detected a thrombus at the right atrial appendage (RAA) and stump of the resected LAA ( Figure 2A ). We switched from acetylsalicylic acid to edoxaban 30 mg daily as an anticoagulation therapy. We selected the reduced dose of edoxaban because he fulfilled two of the criteria (47 kg body weight and 32 mL/min creatinine clearance). We continued the clopidogrel with edoxaban regimen after discharge. Three months later, repeat CCT confirmed a complete resolution of the thrombus in both atria ( Figure 2B ). Echocardiography performed contemporarily showed that the contraction of the left atrium remained acceptable ( Figure 1D ). Although he underwent remote electrocardiogram monitoring through a wearable cardioverter defibrillator (until 3 months after discharge) and transvenous implantable cardioverter defibrillator (from 3 months after discharge), atrial arrhythmia had never been documented. Although we proposed that the patient discontinue the anticoagulation therapy because follow-up echocardiography suggested atrial contractile function recovered, he refused for fear of thrombosis recurrence. Thus, anticoagulation therapy was continued in the outpatient setting. Figure 1 (A–D) Transmitral flow of echocardiography before surgery (A), the 6th post-operative day (B), 21st post-operative day (C), and 3 months after surgery (D). Arrows indicate A wave. The velocity of A wave in each period was 20 m/s (A), 38 m/s (B), 44 m/s (C), and 48 m/s (D), respectively. POD, post-operative day. Figure. 2 (A) Cardiac computed tomography on the 25th post-operative day (POD). Thrombus in the right atrial appendage (asterisk) and the stump of resected left atrial appendage (arrow). (B) Cardiac computed tomography at 3 months after the surgery. The thrombi were completely resolved. Discussion The mechanism for thrombus formation in the left atrium, as postulated, is ascribed to blood stasis, hypercoagulability, and endomyocardial dysfunction of the left atrial wall. 2 Of these, blood stasis and endomyocardial impairment, which are attributed to left atrial ischaemia, played a key role in thrombus formation for the first event of our case. 1 As for the present clinical course, we believe that blood stasis originating from the stunning of the left atrial myocardium could have contributed to the thrombus formation after LAA resection because it took several weeks for atrial contractile function to recover, as shown in Figure 1 . As for the thrombus in the RAA, our patient developed an occlusion in the RCA that had branches perfusing RAA, and we infer that the thrombus in the RAA was also formed by a similar mechanism. It is a well-known phenomenon that in patients with AF, electrical cardioversion results in a transient impairment of the left atrial and LAA function (referred to as atrial stunning), thereby increasing the risk of thrombus formation just after the restoration of sinus rhythm. 3 Therefore, the current guideline recommends that anticoagulation therapy be maintained after cardioversion for 4 weeks in patients with AF of a duration greater than 48 h, even if they had a low thromboembolic risk. 4 In addition, it has been reported that physiological response to highly invasive surgeries, such as CABG, promotes temporal hypercoagulability during the post-operative period. 5 Hence, we postulate that thrombi may have been formed in the early phase after surgery when the patient had comorbid impaired atrial contractile function with hypercoagulation. Although, fortunately, we detected the thrombi before the patient developed thromboembolic events, anticoagulation therapy in the early days after surgery might prevent the formation of thrombi. Our case also underscores the importance of anticoagulation therapy for patients who develop thrombus due to an atrial ischaemic mechanism. In particular, we highlighted the efficacy of direct oral anticoagulants (DOACs) for thrombi originating from atrial ischaemia. Although DOACs can be safe and easy to use, the data regarding efficacy for left atrial thrombus formed by the rare mechanism remain scarce compared to warfarin. Further reports of cases with similar aetiology are warranted. As for implications to find out similar cases, we speculate that focusing on the findings of the slow flow of the atrial branches from coronary angiography with a quite low velocity of A wave on the transmitral flow on echocardiography can be useful. If clinicians detect such findings, attempts to search for atrial thrombi, such as CCT, can be a feasible option. As for another implication for practice, our case stresses that the thrombus may be formed before the atrial function is restored, even if the patients undergo complete revascularization. On the other hand, it remains unclear how long such patients should keep anticoagulation therapy. We infer that discontinuation would be reasonable if atrial contractile function recovered during the chronic period. However, our case preferred to keep anticoagulants in fear of thrombi recurrence. It is difficult to consider how to manage anticoagulants in such cases. Clinicians should decide by balancing several aspects, such as patients’ preferences and the risk/benefit of keeping anticoagulants. Supplementary Material ytad157_Supplementary_Data Click here for additional data file.