Background: Decreased glomerular filtration rate (GFR) can increase the risk of bleeding tendency and hemorrhagic stroke. However, the relationship between the levels of GFR and hemorrhagic transformation (HT) after acute ischemic stroke is largely unknown. The aim of this study was to assess whether GFR level is associated with HT in acute ischemic stroke. Methods: We reviewed 770 consecutive patients with acute ischemic stroke within 7 days from September 2007 to February 2012 in a prospective stroke registry database. We calculated the patient’s GFR using the Cockcroft-Gault equation, and divided them into 3 groups: ≥60, 30–59 and <30 ml/min/1.73 m². HTs were identified by follow-up computed tomography (CT) or magnetic resonance imaging, and were defined as (1) any degree of high density within the area of low attenuation of vascular territory on noncontrast brain CT, or (2) low-signal intensity area in gradient echo within high-signal intensity meaning acute infarct on diffusion-weighted imaging. Multivariable logistic regression analyses were used to estimate the risk of GFR for HT. Stratification analyses were done according to the presence of HT high risk factors: atrial fibrillation (AF), thrombolysis and large size infarction. Additional logistic regression model for symptomatic HTs was established with the same variables. Results: HTs were noted in 131 patients (17.0%) and symptomatic HTs in 63 patients (8.2%). In univariate analysis, HTs were more frequent in patients with AF (51.9 vs. 16.7%, p < 0.001) and large-size infarction (42.0 vs. 5.3%, p < 0.001). The risk of HT was associated with decreased GFR among 3 subgroups classified according to the value of estimated GFR: 49/394 (12.4%) in the GFR ≥60 group, 66/312 (21.2%) in the 30≤ GFR <59 group and 16/64 (25.0%) in the GFR <30 group (p = 0.002). We found a significant association between the GFR <30 group and HTs in acute ischemic stroke (OR 2.90; 95% CI 1.26–6.68, p = 0.012) after adjusting for other risk factors. Moreover, the incidence of HTs was higher in the subgroups without thrombolysis (OR 3.49; 95% CI 1.44–8.46) and without AF (OR 3.44; 95% CI 1.10–10.76). Decreased GFR also had a tendency of increasing symptomatic HTs (OR 2.39; 95% CI 0.72–7.94, p = 0.154). Conclusions: Low levels of GFR are associated with a high risk of HT after acute ischemic stroke. Further studies are needed to elucidate whether HT in the patients with renal insufficiency are related to a worse outcome after acute ischemic stroke.

Background and Purpose— Left ventricular diastolic dysfunction (LVDD) is a predictor for atrial fibrillation (AF). This study was aimed to investigate whether LVDD in cryptogenic ischemic stroke (CS) could be a clue to stroke mechanism. Methods— The clinical and echocardiographic findings of 1589 consecutive patients with acute ischemic stroke or transient ischemic attack between 2004 and 2013 were reviewed. LVDDs among stroke subtypes were graded by transthoracic echocardiography into 4 groups by severity: normal, abnormal relaxation (grade I), pseudonormal (grade II), and restrictive diastolic filling (grade III), whereas severe LVDD was defined as grade III. We classified the lesion pattern of CS into cardioembolism-mimic or non–cardioembolism-mimic and determined whether cardioembolism-mimic lesions were associated with severe LVDD. Results— The fraction of severe LVDD in CS was not different from that of stroke with AF (27.3% versus 37.1%; P =0.173) but was significantly higher than that of stroke without AF (27.3% versus 13.4%; P =0.008). Cardioembolism-mimic CS had more severe LVDD than non–cardioembolism-mimic CS (41.4% versus 11.5%; P =0.013). LVDD of grade II (odds ratio, 4.37; 95% confidence interval, 2.99–6.41) and grade III (odds ratio, 5.60; 95% confidence interval, 3.42–9.17) were independently related to stroke with AF after adjusting covariates. Conclusions— The severe LVDD could be a predictor of stroke with AF, and its frequency was similar between CS and stroke with AF. Cardioembolism-mimic CS had significantly more severe LVDD than non–cardioembolism-mimic CS. LVDD could be helpful to discriminate the stroke mechanism in the patients with acute CS.

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Hypertensive brainstem encephalopathy (HBE) is a variant of hypertensive encephalopathy characterized by brainstem and cerebellar involvement. Simultaneous supratentorial involvement in HBE is rarely reported as a vasogenic edema in subcortex and/ or periventricular white matter. A 36-year-old woman visited hospital due to headache lasting 7 days before admission. Initial blood pressure was 270/170mmHg. T2-weighted and fluid-attenuated inversion recovery magnetic resonance imaging revealed multifocal high signal intensity lesions in upper medulla, pons, midbrain and cerebellar hemisphere. Especially, atypical periventricular lesions were shown as perpendicular fingers to the lateral ventricle like multiple sclerosis. Her clinical symptoms and radiological lesions were subsided with lowering blood pressure. We herein report a HBE with unusual supratentorial involvement mimicking multiple sclerosis.