A 75-year-old man with no apparent risk factors for cardioembolic stroke was transported presenting with left hemispatial neglect and left complete hemiplegia. MRI revealed a new cerebral infarction in the right middle cerebral artery territory with diffusion-weighted imaging and fluid-attenuated inversion recovery mismatch. The occluded vessel was the right middle cerebral artery (M1 segment). Intravenous rt-PA and mechanical thrombectomy were performed. Pathology of the retrieved thrombus revealed a foreign body granuloma and lipomatous lesion with cholesterol with some calretinin-positive cells. Electrocardiography and transthoracic echocardiography (TTE) showed no abnormalities however, a 4.2mm high-intensity homogeneous plaque in aortic arch and a 14 × 17mm mobile tumor with a stalk were observed in transesophageal echocardiography (TEE). Pathological examination of the tumor revealed a stroma rich in vascular axes and hyaline collagen fibers, with retention of Alcian blue-positive mucinous matrix, leading to a diagnosis of left atrial myxoma. Aortogenic embolism or embolism due to left atrial myxoma was considered. However, since the retrieved thrombus contained calretinin-positive cells, left atrial myxoma was diagnosed as the cause of the embolism. TTE may fail to detect tumors due to factors such as small size. Therefore, TEE is considered necessary in cases of unexplained embolism.

A 91-year-old woman with symptomatic severe aortic stenosis (AS) was admitted for transcatheter aortic valve implantation (TAVI). Preoperative carotid ultrasonography showed no significant stenosis or unstable plaque, but high-intensity transient signals were incidentally detected during pulse Doppler examination. Subsequently, we performed transcranial color-coded sonography (TCCS), which revealed microembolic signals (MES) occurring approximately once per minute in both middle cerebral arteries. Contrast-enhanced CT showed no stenosis in the aortic arch branches or the right common carotid artery origin. Transthoracic echocardiography demonstrated severe AS with significant valve calcification. After the TAVI procedure, we performed TCCS again, and no MES were detected. She has remained free of cerebrovascular events for more than six years following TAVI. MES are known to be detected in patients with carotid artery stenosis, atrial fibrillation, or mechanical valves and are considered a risk factor for stroke. In contrast, we found no previous reports of MES detection in patients with severe AS. Our findings suggest that severe AS can be a source of MES and that TAVI may help eliminate such signals, providing new insights into the pathophysiology of MES.