A 58-year-old female presented with acute arterial insufficiency to her left leg. Following cardiovascular evaluation using multimodality imaging, it was discovered that she had mobile thoracic thrombi overlying a normal descending thoracic aorta which had also caused a splenic infarction. This patient was treated with unfractionated heparin for three days and underwent subsequent thoracic endovascular aortic repair (TEVAR) uneventfully with no subsequent complications at one-year followup. This case highlights the diagnostic and therapeutic challenges in treating patients with this uncommon challenging clinical scenario. 1. Case Scenario A 58-year-old female presented with symptoms and signs compatible with an acutely threatened left leg. Her history revealed that she had no preexisting significant cardiovascular symptoms of note and she had no risk factors for atherosclerosis. There was no family history to suggest any hereditary thrombotic disorders. A computed tomography angiogram (CTA) was performed which confirmed abrupt cutoff of the left mid- to distal tibial artery in the left leg, as well as a recanalized splenic infarction. In addition, as part of her workup before referral, a CTA of the thoracic aorta was performed which revealed a linear filling defect measuring 8？cm which was interpreted as an aortic dissection with an intimal flap (Figures 1(a) and 1(b)). Figure 1: Axial and sagittal images of a computed tomography angiogram demonstrating a serpiginous filling defect in the descending thoracic aorta. The patient was transferred for cardiological assessment where a transthoracic echocardiography revealed hypertensive heart disease with a normal ejection fraction and mild diastolic dysfunction. A transesophageal echo (TEE) revealed a large mobile aortic thrombus in the proximal descending aorta distal to the subclavian artery origin accompanied by two other distal mobile thrombi (Figures 2 and 3, Videos 1, 2, and 3 in see Supplementary material available online at http://dx.doi.org/10.1155/2014/302346.). There were no overt features of either a penetrating aortic ulcer or aortic dissection. The laboratory workup for hereditary and acquired prothrombotic disorders, including vasculitis, was normal. The patient was treated for three days with an intravenous unfractionated heparin infusion and, following extensive cardiothoracic and vascular consultation, thoracic endovascular aortic repair (TEVAR) was successfully performed (Figure 4), whilst the leg ischaemia resolved spontaneously on anticoagulation alone. Following initiation of lifelong
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