Abstract

Case Presentation: A 76-year-old female with history of amyloid light chain (AL) cardiac amyloidosis and prior stroke presented with acute bilateral leg weakness. MRI of the brain revealed subacute infarcts in the right basal ganglia and precentral gyrus as well as chronic left cerebellar infarctions. CT angiogram of the head and neck did not show any significant intracranial or carotid artery disease. All current and previous admission ECGs and telemetry showed sinus rhythm with no atrial arrhythmias. Transthoracic echocardiogram with bubble study noted LV ejection fraction of 62%, normal left atrial size and no evidence of an intracardiac shunt. Despite the lack of traditional indicators, a cardioembolic source was feared given the high risk of intracardiac thrombi in AL amyloid patients. A TEE was performed and confirmed a large left atrial appendage (LAA) thrombus with severely reduced velocities and spontaneous echo contrast (Figure 1). The patient was started on apixaban for secondary stroke prevention. Discussion: Amyloid proteins deposit throughout heart tissue, distorting mechanical function and electric conduction resulting in reduced blood flow and a high risk of intracardiac thrombi that is 10 times that of nonamyloid patients. Patients with cardiac amyloidosis have a high prevalence of atrial arrhythmias, particularly atrial fibrillation, but remain at significant risk of thrombi even in the absence of these arrhythmias, ranging from 3-20%. Risk factors for clot include AL type amyloid and features of worsened hemodynamics such as LV systolic and diastolic dysfunction, elevated heart rates and lower systolic blood pressure. This case demonstrates the importance of aggressively “hunting” for intracardiac thrombi in amyloid patients presenting with stroke even without perceived risk factors, especially given the protective effect of starting anticoagulation.

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