A left atrial thrombus (LAT) is a collection of clotted blood that develops within the heart’s upper left chamber, the left atrium. The left atrium receives oxygenated blood from the lungs and passes it to the left ventricle, which pumps it to the body. A clot in this chamber is a serious medical finding because it interferes with heart function and creates a risk for complications throughout the circulatory system.
How Left Atrial Thrombi Form
Left atrial thrombi form primarily due to blood stasis, which is sluggish or turbulent blood flow. Normally, the left atrium contracts in a coordinated manner, efficiently propelling blood into the ventricle. When this movement is disrupted, blood pools, increasing the likelihood of clotting factors accumulating and activating.
Atrial Fibrillation (AFib) is the most common cause of pooling, as it causes the left atrium to quiver instead of fully contracting. This ineffective pumping slows blood movement significantly. The Left Atrial Appendage (LAA), a small pouch attached to the atrium, is the most susceptible site for thrombus formation. Its complex structure easily traps stagnant blood, and in patients with non-valvular AFib, over 90% of thrombi are found within the LAA.
Structural heart issues also promote stasis and endocardial damage. Mitral valve diseases, particularly mitral stenosis, impede blood flow out of the left atrium, causing pressure to build up and the chamber to enlarge. This combination slows the blood, facilitating clot organization. Less common factors include severe left ventricular dysfunction or hypercoagulable states.
Detection and Embolic Risk
The most significant danger posed by a left atrial thrombus is systemic embolism, which occurs when a piece of the clot breaks off and travels through the bloodstream. This migrating fragment can lodge in a smaller artery, blocking blood flow to an organ. The most frequent and devastating consequence is an ischemic stroke, where the clot travels to the brain, cutting off the blood supply.
The risk of a thromboembolic event is not uniform, as certain clot characteristics increase its potential to break free. Thrombi that are large (greater than 1.5 centimeters) or those that appear mobile and fragile are associated with a higher rate of embolization. Accurate and timely detection is paramount before any procedure, such as electrical cardioversion, that could dislodge the clot.
Transesophageal Echocardiography (TEE) is considered the gold standard for diagnosing a left atrial thrombus due to its high accuracy. The TEE probe is guided down the esophagus, placing it directly behind the heart. This provides a high-resolution, clear view of the LAA, which is often difficult to visualize with standard ultrasound. TEE allows clinicians to assess the size, shape, and mobility of the clot, informing the urgency and type of treatment required.
Other modalities sometimes complement or substitute for TEE, such as Cardiac Computed Tomography (CT) or Cardiac Magnetic Resonance Imaging (MRI). CT scans detect the clot as a filling defect within the LAA, though differentiating a clot from very slow blood flow can be challenging. Cardiac MRI offers detailed visualization of the heart tissue and is increasingly used to evaluate the structure of the left atrium and LAA, including signs of atrial fibrosis, which is also linked to embolic risk.
Treatment Strategies
Once a left atrial thrombus is confirmed, the immediate priority is to stabilize the clot and facilitate its resolution using anticoagulation therapy. This treatment reduces the clot’s size and prevents it from breaking apart and causing an embolic event. The standard duration for this initial treatment period is typically four to six weeks.
Anticoagulants, commonly called blood thinners, interfere with the blood clotting cascade. Historically, Vitamin K antagonists (VKAs), such as Warfarin, were the primary agents used to treat LAT. Direct Oral Anticoagulants (DOACs), including medications like rivaroxaban and apixaban, are now frequently used and have shown similar or superior efficacy in achieving thrombus resolution.
DOACs offer the advantage of predictable dosing without the frequent blood monitoring required with Warfarin. Following the initial four-to-six-week course of anticoagulation, a repeat TEE is standard practice. This confirms the thrombus has completely dissolved before proceeding with planned interventions, such as restoring a normal heart rhythm. If the clot persists despite optimal medication, switching to a different class of anticoagulant may be considered.
In rare instances where the thrombus is exceptionally large, highly mobile, or if medical therapy fails, surgical removal may be considered. This intervention involves opening the left atrium to physically excise the clot. Long-term management requires addressing the underlying cause, such as optimizing medication to control Atrial Fibrillation. This prevents the blood stasis that allowed the thrombus to form initially.