B50-15 Double Trouble at the Apex - Cardiac Computed Tomography Confirmed Left Ventricular Thrombi and Newly Diagnosed Factor V Leiden Following Nstemi

Abstract Chest pain that can fit into one of two diagnosis channels that have a majority overlap with pulmonary embolism (PE) and acute coronary syndrome (ACS) is a common dilemma in the emergency department. The case began as a PE case but ultimately revealed two LV apical thrombi and a new diagnosis of a Factor V Leiden mutation. A 64-year-old woman with a past medical history of hypertension, diabetes, and hyperlipidemia presented with sudden, severe left-sided chest pain after exertion, as well as cramping in her left leg after prolonged sitting at work, leading to concern for a possible PE. An ECG showed evolving inferior and anterior T wave changes, and bedside cardiac ultrasound showed normal right-ventricular function; however, given her symptoms, she was ultimately taken to a CT pulmonary angiogram (CTPA). CTPA was negative for PE or aortic dissection; however, it did show calcified coronary arteries.As the patient remained in pain and persistent ECG changes, urgent coronary angiography was performed, which demonstrated a severe ramus intermedius lesion that was successfully treated with a drug-eluting stent and identification of distal circumflex thrombotic occlusion. After the procedure, echocardiography determined satisfactory LV function but demonstrated a mobile mass at the apex, suspicious for thrombus.Due to the persistence of her pain and ECG changes, she had urgent coronary angiography that demonstrated a severe ramus intermedius lesion treated with a drug-eluting stent, in addition to a thrombotic occlusion in the distal circumflex. Subsequent echocardiogram analysis revealed mildly reduced left ventricular (LV) function and a mobile apical massDelayed cardiac CT was even more definitive in resolving the apical mass into two discrete LV apical thrombi with no association with her atrium. Hypercoagulable workup revealed a previously unknown Factor V Leiden mutation. The patient was eventually transitioned from heparin to apixaban and from ticagrelor to clopidogrel, with a short course of aspirin. The patient did well and was discharged with close follow-up from cardiology and hematology.This case emphasizes that a negative CT pulmonary angiogram does not mark the end of the diagnostic workup. Careful stepwise evaluation in the context of multiple imaging modalities helped better understand the underlying cause of her symptoms and reveal a previously unanticipated thrombophilia. The cardiac CT was beneficial when the echocardiogram results were questionable. Identifying the Factor V Leiden mutation is particularly important for future management, justifying continued management with anticoagulation therapy with closer follow-up. This abstract is funded by: None