Abstract 4359800: Acute Left Ventricular Thrombosis and Systemic Embolism Following Testosterone Therapy

Introduction: Testosterone replacement therapy (TRT) is linked to venous thromboembolism (VTE) and cardiovascular risks, but intracardiac thrombus formation has not been reported. This case highlights rapid left ventricular (LV) thrombus development and thromboembolic events in a patient on TRT, with no traditional hypercoagulable risk factors. Case Presentation: A 48-year-old male with tobacco use and daily alcohol intake presented with progressive dyspnea. Transthoracic echocardiography (TTE) revealed reduced ejection fraction (24%) and left ventricular dilatation (LVIDD 6 cm). There was no thrombus visualized in the left ventricle. Coronary angiography showed no obstructive disease. Guideline-directed medical therapy (GDMT) was initiated. He returned within 24 hours of discharge with dizziness and aphasia. Computed tomography angiography (CTA) identified a partially occluding embolus in the left middle cerebral artery (MCA), confirmed by MRI as an acute left frontoparietal infarct. Repeat TTE (5 days from prior TTE) demonstrated a large, mobile apical septal LV thrombus. CT imaging also revealed pulmonary embolism and splenic infarction. Hypercoagulable workup (prothrombin mutation, Factor V Leiden, cardiolipin antibodies) was negative. The patient disclosed scheduled testosterone injections for hypogonadism, with a total testosterone level of 1,081 ng/dL (reference: 300–1,000 ng/dL). Discussion: This case illustrates rapid LV thrombus formation and thromboembolism temporally linked to TRT. Despite guideline-based heart failure management, thrombus developed within 5 days of prior TTE. Prior studies associate TRT with VTE and stroke, but this is the first report of acute LV thrombus and multi-organ emboli in the absence of traditional hypercoagulable states. Proposed mechanisms include TRT-induced erythrocytosis, platelet activation, and endothelial dysfunction [1–4]. Conclusion: TRT may precipitate intracardiac thrombosis and thromboembolic events even without classical risk factors. Clinicians should consider TRT cessation and anticoagulation in similar cases, emphasizing cautious patient selection and monitoring. Further research is needed to clarify TRT’s role in hypercoagulability and cardiac remodeling.