Cerebral Microbleeds With Atrial Fibrillation After Ablation Therapy.

BACKGROUND: The prevalence of cerebral microbleeds (CMBs) is significantly higher in patients with atrial fibrillation (AF) than in those without AF. CMBs in patients with AF have been reported to be primarily of the lobar type, but the exact cause of this remains unknown. We investigated the possibility that hemorrhagic transformation of embolic microinfarction can account for de novo lobar CMBs. METHODS: A total of 101 patients who underwent ablation therapy for AF were prospectively registered, and 72 patients completed the assessment with MRI 6 months after catheter ablation. Brain MRI, including diffusion-weighted imaging (DWI) and susceptibility-weighted imaging (SWI), were examined at 1-3 days (baseline) and 6 months after catheter ablation. We quantitatively evaluated the spatial and temporal distribution of embolic microinfarctions and de novo CMBs. RESULTS: Of the 101 patients, 68 were enrolled in this study. Fifty-nine patients (86.8%) showed embolic microinfarctions on baseline DWI immediately after catheter ablation. There were 137 CMBs in SWI, and 96 CMBs were of the lobar type. Six months later, there were 208 CMBs, including 71 de novo CMBs, and 60 of 71 (84.5%) were of the lobar type. Of the 71 de novo CMBs, 56 (78.9%) corresponded to the location of previous embolic microinfarctions found on baseline DWI. The platelet count was significantly lower and hematocrit/hemoglobin and Fazekas score were higher in the group with de novo CMBs than in the group without de novo CMBs. CONCLUSION: De novo CMBs frequently appeared after catheter ablation therapy. Our results suggest that embolic microinfarction can cause lobar CMBs.

Hyperemic myocardial blood flow in patients with atrial fibrillation before and after catheter ablation: A dynamic stress CT perfusion study.

BACKGROUND: Atrial fibrillation (AF) patients without coronary artery stenosis often show clinical evidence of ischemia. However myocardial perfusion in AF patients has been poorly studied. The purposes of this study were to investigate altered hyperemic myocardial blood flow (MBF) in patients with AF compared with risk-matched controls in sinus rhythm (SR), and to evaluate hyperemic MBF before and after catheter ablation using dynamic CT perfusion. METHODS: Hyperemic MBF was quantified in 87 patients with AF (44 paroxysmal, 43 persistent) scheduled for catheter ablation using dynamic CT perfusion, and compared with hyperemic MBF in 87 risk-matched controls in SR. Follow-up CT after ablation was performed in 49 AF patients. RESULTS: Prior to ablation, hyperemic MBF of patients in AF during the CT (1.29 ± 0.34 ml/mg/min) was significantly lower than in patients in SR (1.49 ± 0.26 ml/g/min, p = 0.002) or matched controls (1.65 ± 0.32 ml/g/min, p < 0.001); no significant difference was seen between patients in SR during the CT and matched controls (vs. 1.50 ± 0.31 ml/g/min, p = 0.815). In patients in AF during the pre-ablation CT (n = 24), hyperemic MBF significantly increased after ablation from 1.30 ± 0.35 to 1.53 ± 0.17 ml/g/min (p = 0.004); whereas in patients in SR during the pre-ablation CT (n = 25), hyperemic MBF did not change significantly after ablation (from 1.46 ± 0.26 to 1.49 ± 0.27 ml/g/min, p = 0.499). CONCLUSION: In the current study using stress perfusion CT, hyperemic MBF in patients with AF during pre-ablation CT was significantly lower than that in risk-matched controls, and improved significantly after restoration of SR by catheter ablation, indicating that MBF abnormalities in AF patients are caused primarily by AF itself.

Brain magnetic resonance imaging and cognitive alterations after ablation in patients with atrial fibrillation.

Catheter ablation is an important non-pharmacological intervention for atrial fibrillation (AF), but its effect on the incidence of asymptomatic cerebral emboli and long-term effects on cognitive function remain unknown. We prospectively enrolled 101 patients who underwent AF ablation. Brain magnetic resonance imaging (MRI) (72 patients) and neuropsychological assessments (66 patients) were performed 1-3 days (baseline) and 6 months after ablation. Immediately after ablation, diffusion-weighted MRI and 3-dimensional double inversion recovery (3D-DIR) detected embolic microinfarctions in 63 patients (87.5%) and 62 patients (86.1%), respectively. After 6 months, DIR lesions disappeared in 41 patients. Microbleeds (MBs) increased by 17%, and 65% of the de novo MBs were exactly at the same location as the microinfarctions. Average Mini-Mental State Examination scores improved from 27.9 ± 2.4 to 28.5 ± 1.7 (p = 0.037), and detailed neuropsychological assessment scores showed improvement in memory, constructional, and frontal lobe functions. Ejection fraction, left atrial volume index and brain natriuretic peptide level improved from baseline to 3-6 months after ablation. Despite incidental microemboli, cognitive function was preserved 6 months after ablation.

Cerebral Embolism Associated with Calcified Amorphous Tumor: A Review of Cerebral Infarction Cases.

Calcified amorphous tumor (CAT) is a non-neoplastic tumor composed of calcified nodules consisting of amorphous fibrous material, and it may eventually cause cerebral infarction (CI). We experienced a 67-year-old woman with CAT who had recurrent CI. After excision of the CAT, the CI did not show recurrence. A review of previous papers on CI due to CAT in Pubmed revealed that 7 of 13 studies originated in Japan and that CI can occur even with small CAT. Surgical treatment is recommended to prevent CI recurrence, especially when CAT is accompanied by mitral annular calcification or has marked mobility.