Intracranial Embolism

In patients with acute cardiogenic cerebral embolism, a residual thrombus may still be present in the cardiac cavity even after reperfusion therapy. We aimed to investigate the occurrence of a residual cardiac thrombus in cardioembolic stroke after reperfusion therapy and analyze its impact on clinical outcome.

We enrolled patients with cardioembolic stroke from our prospectively collected database who underwent 2-phase cardiac computed tomography within 7 days after reperfusion therapy. Residual cardiac thrombus was defined as a filling defect on both early- and late-phase images, whereas circulatory stasis was defined as a filling defect only on the early-phase images in the left atrial appendage. The primary outcome was a poor clinical outcome (modified Rankin Scale score, 3-6) at 90 days. The secondary outcome was a composite end point event (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke) at 90 days. A total of 303 patients were included, of whom 94 (31.0%) had a residual cardiac thrombus. Binary logistic regression analysis showed that the presence of a residual cardiac thrombus was associated with a poor clinical outcome (odds ratio, 1.951 [95% CI, 1.027-3.707]; P=0.041) but not circulatory stasis in the left atrial appendage (odds ratio, 1.096 [95% CI, 0.542-2.217]; P=0.798). Furthermore, there was no correlation between a residual cardiac thrombus and the composite end point event (30.0% versus 31.1%; P=1.000).

Residual cardiac thrombus occurs in approximately one-third of patients with cardioembolic stroke after reperfusion therapy and is often indicative of a poor clinical outcome.

A 71-year-old man with hypertension and diabetes mellitus presented to our hospital because he felt lightheaded. Diffusion-weighted images (DWI) on brain MRI showed high signal lesions in the left cerebellar hemisphere and the right pons. The diagnosis of cerebellar infarction was made, but he refused treatment. One month later, he came to our hospital because his body leaned to the left. Neurological examination revealed dysarthria and cerebellar truncal ataxia. An electrocardiogram showed atrial fibrillation. DWI on brain MRI showed high signal lesions in the bilateral cerebellar hemispheres and middle cerebellar peduncles (MCP). Dabigatran 300 ‍mg/day was administered for cardiogenic cerebral embolism. On the 12th day of onset, he was transferred to a rehabilitation hospital. At 72 years old, T₂*-weighted images on brain MRI showed hot cross bun sign (HCBs) in the pons. We considered that HCBs were caused by antegrade or retrograde degeneration (or both) of pontine infarcts and bilateral MCP infarcts in the pontine cerebellar tract. It seemed preferable to use T₂*-weighted images or proton density-weighted images rather than T₂-weighted images to detect HCBs. When HCBs is detected, it should be noted that HCBs can be caused by bilateral MCP infarcts in addition to multiple system atrophy.