Case Presentation: A 34-year-old Caucasian lady with metabolic syndrome and hypertension presented with a sudden onset 10/10 right lower extremity pain associated with numbness and inability to ambulate. Vital signs were stable. On examination, her right lower extremity was pale, cold and pulseless. Her laboratory tests including hypercoagulable workup were normal. A CT aortogram with runoff revealed thrombosis of the right common, external iliac and proximal portions of the internal iliac arteries. She underwent a right common iliac embolectomy and was started on heparin drip and warfarin. Transthoracic echocardiography to evaluate for a source of emboli revealed a 3 x 1 cm nonhomogeneous mobile mass adherent to distal inferior LV wall with an EF of 55-60%. Transesophageal echocardiography showed a 2.8 x 1.5 cm mobile mass in the left ventricular apex inferiorly with a moderate sized apical thrombus. Coronary angiogram was normal. The LV mass was suspected to be either a myxoma or fibroelastoma and was surgically excised. Biopsy revealed fragments of cardiac muscle with organizing thrombus. She was subsequently discharged home on warfarin with INR goal of 2 – 3.
Discussion: LV thrombus is a well-known complication of acute myocardial infarction with an incidence of 5-15%. LV thrombus in the absence of akientic or dyskinetic apex is extremely rare and can be attributed to hypercoagulable state or undetectable disorders of the endocardium. LV thrombus formation has been associated with antiphospholipid antibody syndrome, hypereosinophilic syndrome, G1691A mutation of factor V gene, G20210A mutation of prothrombin gene, protein C & S deficiencies, SLE and Adamantiades-Bechet’s disease. Large doses of alpha epoetin administration has been reported to cause LV thrombus formation by sudden and rapid increase in the blood viscosity. 1.3% of patients with Takotsubo’s cardiomyopathy are shown to develop LV thrombus. Transient myocardial ischemia from coronary spasm or patchy fibrosis from diffuse small coronary vessel disease have been postulated to cause LV thrombus formation in the absence of an obvious cardiac disease. Imaging modalities like echocardiography and cardiac MRI play a key role in establishing the diagnosis and differentiating between a thrombus and a tumor. The role of endomyocardial biopsy to diagnose small coronary vessel disease is unclear. Approximately, 60% of the LV thrombi are at risk to embolize. Regardless of the etiology, patients with LV thrombus should be adequately anticoagulated with heparin and warfarin with a goal INR of 2-3 for at least 3-6 months.
Conclusions: In the absence of structural heart diseases or hypercoagulable state, mobile pedunculated LV mass is either a thrombus or a tumor. Evaluation of the mass using cardiac MRI will help differentiate between a thrombus and a tumor. Anticoagulation remains the mainstay of treating LV thrombus regardless of the etiology.