Left Atrial Appendage Thrombus When Least Expected: Look Before You Shock, Evaluate Before You Ablate

Adel Mina, MD, FACC and Nicholas Warnecke, PA-C, UnityPoint Health Methodist, Peoria, Illinois
Adel Mina, MD, FACC and Nicholas Warnecke, PA-C, UnityPoint Health Methodist, Peoria, Illinois


Atrial fibrillation (AF) has rapidly become one of the most common arrhythmias, with its prevalence affecting over 4 percent of the population above the age of 60.1,2 Often associated with AF is the occurrence of thromboemobolic events such as stroke. This embolic phenomena accounts for approximately 16.6% of embolic strokes in the United States today.3 The risk of stroke is not only associated with AF, but can also accompany a number of the treatments for this arrhythmia. The options for the management of AF range from simple rate control with rate-limiting agents to rhythm control with antiarrhythmics; however, both require implementation of long-term anticoagulation for the prevention of thromboemobolic events. 

There are also a number of procedures that can be used in the treatment of AF, the most common of which is direct current cardioversion. Catheter ablation is recognized as an alternate option for patients with symptomatic AF who have failed or were intolerant to antiarrhythmic drug therapy.4 A potential complication associated with catheter ablation and direct current cardioversion is stroke. The incidence of thromboembolism is variable, with reports ranging from 0% to 7%.5 One of the mechanisms of thromboembolism is thought to be the dislodgement of a left atrial clot that was present before the procedure. 

Generally, many steps have been implemented to reduce the risk of stroke. These steps often include the patient being anticoagulated to achieve an international normalized ratio (INR) of 2 to 3, for 3 weeks before direct current cardioversion.6 The use of transesophageal echocardiography (TEE) to exclude a left atrial thrombus before the procedure is sometimes used to confirm absence of a left atrial clot. Even with these pre-emptive measures at reducing the risk of stroke prior to these procedures, there are still instances in which a thrombus is still evident within the left atrial appendage (LAA). 

Historically, the threshold for a TEE before an AF ablation has been low, because a stroke is a potentially devastating complication that can be avoided.5 Generally, there are a number of factors that must be considered prior to TEE. Factors often considered include the risk to the patient, cost of the procedure, overall experience from a patient perspective, alternatives to a TEE to identify a LAA clot, and the likelihood that a clot will actually be found.

In this paper we hope to highlight that every case must be individualized when it comes to stroke risk reduction prior to pursuing direct current cardioversion and/or ablation. Five case studies will highlight certain instances in which simply following current medical guidelines may not be enough to sufficiently reduce the risk of stroke. 

Case #1

A 76-year-old male with a history of long-lasting persistent AF, a myocardial infarction in 2001 for which a stent was placed in the left anterior descending artery, ischemic cardiomyopathy, hyperlipidemia, hypertension, diabetes, and obesity, presented with symptoms of fatigue, low energy and shortness of breath with mild exertion. The symptoms were attributed to his chronic AF. His AF has been managed with a rate control strategy and long-term anticoagulation with coumadin, as his CHADS2 score was 3 (hypertension, age >75 and diabetes). The patient’s INR has been therapeutic for the 2-3 months prior to contemplating cardioversion. His transesophageal echocardiogram showed severe left atrial enlargement, mild LV dysfunction with an ejection fraction (EF) of 45%, no LAA thrombus, and moderate mitral insufficiency. He was cardioverted to sinus bradycardia after his second shock. He was also started on sotalol.

Unfortunately, he presented to the office with atrial flutter 4 months after his original cardioversion. His sotalol was changed to amiodarone, and a second cardioversion was pursued. Transesophageal echocardiogram prior to the second cardioversion showed no thrombus, and he was successfully cardioverted to sinus rhythm. Shortly thereafter, he went back into atrial flutter and was therefore scheduled for atrial flutter ablation. He continued to maintain a therapeutic INR for 10 weeks prior to the ablation. Prior to his ablation a transesophageal echocardiogram was performed that showed spontaneous echo contrast and a thrombus in the LAA (Figure 1), resulting in cancellation of his procedure. He was given enoxaparin for 10 days, and his coumadin dose was consequently increased to maintain an INR of 2.5–3.5. 

Case #2

A 58-year-old male presented with a past medical history significant for aortic valve replacement with a mechanical valve on long-term coumadin therapy, history of coronary artery disease with prior coronary artery bypass graft surgery, chronic kidney disease, and diabetes. He was seen in the hospital for acute onset of congestive heart failure symptoms. At that time his INR was noted to be supratherapeutic. A transthoracic echo revealed a worsening EF of 25%, down from 45% within 48 hours of onset of atrial flutter. The calculated CHADS2 score was 2 (congestive heart failure, diabetes). He became hemodynamically intolerant to the atrial flutter, warranting a direct current cardioversion. Prior to the cardioversion, a TEE was done to evaluate the LAA for clot formation. The TEE in fact did demonstrate a thrombus (Figure 2), resulting in cancellation of the cardioversion and further aggressive medical management of the atrial flutter. 

Case #3

A 73-year-old male presented with a past medical history of AF and nonischemic cardiomyopathy. His CHADS2 score was 1 (congestive heart failure). He presented in the hospital in April 2013 with florid congestive heart failure. His evaluation showed that he was in AF with rapid ventricular response. He underwent further evaluation with transesophageal echocardiogram, which revealed a large thrombus in the LAA (Figure 3A). He was then started on full-dose rivaroxaban and continued with a rate control strategy. The patient was then re-evaluated for direct current cardioversion 10 weeks later, after initiation of rivaroxaban, with a transesophageal echocardiogram. (Figure 3B.) Results of the test revealed most of the clot had dissolved; however, there were still remnants of his LAA clot. The procedure was cancelled, and the patient was continued on rate control and anticoagulation with rivaroxaban.

Case #4

A 66-year-old male presented for evaluation of atrial flutter. He has a prior history of AF and atrial flutter. He had 2 direct current cardioversions in the past at an outside facility and was put on amiodarone 200 mg daily. He presented with recurrence of his atrial flutter, confirmed with an EKG showing atrial flutter with 2:1 AV block. He has been anticoagulated on coumadin for more than 4 years, with multiple therapeutic INRs before his ablations. INRs ranged from 2.6–3.1, with weekly checks for 2 consecutive months. His CHADS2 score was 2 (congestive heart failure and hypertension). He has a history of cardiomyopathy, but his current echo showed he had a close to normal EF with moderate left atrial enlargement. He also has a history of chronic obstructive pulmonary disease, end stage renal disease, and mild cor pulmonale. 

Transesophageal echo done prior to atrial flutter ablation showed significant worsening of his heart function, with a left ventricular ejection fraction of 30% and a right ventricular ejection fraction of 5%. He was found to be in AF, with rapid ventricular response and worsening of his cardiomyopathy. He was also found to have LAA thrombus and large mobile thrombus in the right atrium (Figure 4). The procedure was cancelled, and the patient was given concomitant heparin and coumadin for 3 days. He was sent home with follow-up monitoring of the INR (to maintain INR of 2.5–3.5). 

Case #5

An 88-year-old female presented with a history of sick sinus syndrome and paroxysmal AF. She had received prior direct current cardioversions a couple of times in the past, with significant improvement of her symptoms. She has a history of severe mitral and tricuspid insufficiency, for which she had mitral valve repair using a 32 mm annuloplasty ring and tricuspid valve repair using a 32 mm Edwards tricuspid annuloplasty ring in 2011. 

She was seen in the office for progressive shortness of breath due to atrial flutter with rapid ventricular response, despite being on a high dose of beta blockers and calcium channel blockers. She was feeling extremely fatigued and short of breath with minimal exertion, which affected her quality of life. Therefore, she was scheduled for ablation. Her CHADS2 score was 2 (congestive heart failure and age). She was on coumadin for 8 years and had weekly therapeutic INRs (range 2.0–3.5) for 1 month prior to the planned ablation.

TEE prior to ablation showed severe biatrial enlargement. Thrombus visualized in the LAA, a second thrombus was seen in the right atrial appendage, and a third thrombus was seen in the subtricuspid valvular area at the base of the right ventricle (Figures 5A and 5B). Normal left ventricular function, moderate right ventricular hypokinesia, mild mitral insufficiency, and moderate tricuspid insufficiency were also seen.

We performed an independent case review by another cardiologist who is certified by the National Board of Echocardiography (ASCeXAM Certificate). The cardiologist was blinded to patient identity and outcome; this was done to validate the integrity of the report and to avoid over or under diagnosis of the presence of thrombi. His report confirmed that all cases had at least one thrombus that was highly probable or definitely present, and that cardioversion or ablation should not be done based on the images he reviewed for each case (Table 1).


In all the cases discussed here, we were able to demonstrate the presence or high likelihood of the presence of atrial thrombi despite having therapeutic oral anticoagulation. For example, in case #1 we were able to demonstrate a de novo atrial thrombus despite the patient being on anticoagulation with a therapeutic INR. Even more interesting is that in case #2 we were able to demonstrate the development of a left atrial thrombus despite supratherapeutic INR and time duration of less than 48 hours for atrial flutter. In case #3 we were able to show the persistence of LAA thrombus in a patient with a relatively low risk for thromboembolus based on a CHADS2 score of 1 and on therapeutic dosing of rivaroxaban for greater than 10 weeks.

Four of the five cases had low EF; this highlights the associated hypercoagulable state seen in cardiomyopathy patients. In all five cases, patients were appropriately managed with oral anticoagulation, yet thrombus development occurred. These cases help to emphasize the importance of thorough evaluation for the presence of atrial thrombus prior to direct current cardioversion and/or ablation, especially in patients with a low EF, as this may represent an advanced hypercoagulable state. 

According to the ACC guidelines, it is inappropriate to perform TEE for stable patients with therapeutic anticoagulation >3 weeks.7 Also, it is inappropriate to perform TEE for AF <48 hours, including patients with no history of AF and who were in AF for less than 48 hours. It was believed that there was not enough time for a thrombus to form, and therefore, TEE was not useful.6 If guidelines alone had been used in the management of these 5 patients, potentially serious and life-altering complications such as stroke might have been possible. 

Other authors also concur with our viewpoint. A study from the Cleveland Clinic examined the results of over 1,000 TEEs performed immediately before a catheter ablation procedure for AF.8 The degree of blood stasis was categorized as thrombus, sludge, and spontaneous echo contrast. They found that left atrial thrombus and sludge were present in only 0.6% and 1.5% of patients, but that the prevalence of left atrial/left atrial appendage thrombus sludge increased with ascending CHADS2 score (scores 0 [0%], 1 [2%], 2 [5%], 3 [9%], and 4 to 6 [11%], p < 0.01).5

However, these results from the Cleveland Clinic study show that there is a 1% risk of finding a thrombus or sludge even in patients who present for their ablation procedure in sinus rhythm when the CHADS2 score is >1. Therefore, although there are some additional risks, inconveniences, and costs, it seems that the only patients who do not need a TEE before an AF ablation are those who present for the procedure in sinus rhythm and have a CHADS2 score of 0. 

It is important to thoroughly evaluate patients undergoing direct current cardioversion or ablation for structural heart disease. In our experience, a TEE may be lifesaving from potentially morbid complications in patients with structural heart disease including cardiomyopathy, congestive heart failure, valvular heart disease, severe left atrial enlargement, prior heart valve surgery or prior atrial thrombi even if patients are hemodynamically stable. Also, a TEE may be considered for patients with a CHADS2 score >1. Both frequent therapeutic INR measurements and new oral anticoagulants may still have limitations in ensuring the absence of thrombus formation despite length of therapy >3 weeks.

Disclosures: The authors have no conflicts of interest to report regarding the article herein. 


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