Thrombolytic Therapy in Severe Cardioembolic Stroke After Reversal of Dabigatran with Idarucizumab: Case Report and Literature Review.

Whether idarucizumab, an antidote of dabigatran, can be used effectively and safely before thrombolytic therapy with recombinant tissue plasminogen activator (rt-PA) in patients with stroke undergoing treatment with dabigatran remains unknown. We herein describe a 57-year-old man who developed severe cardioembolic stroke with a National Institutes of Health Stroke Scale score of 22 in the left middle cerebral artery territory while undergoing treatment with dabigatran for nonvalvular atrial fibrillation and who was treated with rt-PA after the reversal of dabigatran with idarucizumab. The thrombolytic therapy following the use of idarucizumab significantly improved the patient's neurological symptoms without hemorrhagic complications, although acute arterial occlusion of the right lower limb was found during the clinical course.

Early Reperfusion After Brain Ischemia Has Beneficial Effects Beyond Rescuing Neurons.

BACKGROUND AND PURPOSE: Recent studies show that successful endovascular thrombectomy 6 to 12 hours after stroke onset enhances functional outcomes 3 months later. In this study, we investigated the effects of reperfusion after ischemia on repair processes in the ischemic areas, as well as on functional recovery, using mouse stroke models. METHODS: We examined time-dependent histological changes and functional recovery after transient middle cerebral artery occlusion of different durations, including permanent middle cerebral artery occlusion, using the CB-17 (CB-17/lcr-+/+Jcl) mouse strain, which has poor pial collateral blood flow. RESULTS: Large microtubule-associated protein 2-negative areas of neuronal death were produced in mice subjected to ≥60 minutes of ischemia followed by reperfusion on day 1, while restricted microtubule-associated protein 2-negative regions were observed in mice subjected to a 45-minute period of ischemia. A substantial reduction in microtubule-associated protein 2-negative areas was observed on day 7 in mice given early reperfusion and was associated with better functional recovery. Klüver-Barrera staining demonstrated that white matter injury on day 1 was significantly lesser in mice with reperfusion. Immunohistochemistry and electron microscopy revealed that a greater number of endothelial cells were present in the infarct areas in mice with earlier reperfusion and were associated with a more rapid recruitment of platelet-derived growth factor receptor ß-positive pericytes and subsequent intrainfarct fibrosis. Early reperfusion also resulted in a greater accumulation of glial fibrillary acidic protein-positive astrocytes in peri-infarct areas. Peri-infarct astrogliosis was attenuated in platelet-derived growth factor receptor ß heterozygous knockout mice. CONCLUSIONS: Early reperfusion after ischemia enhances the survival of endothelial cells and pericytes within ischemic areas even after the infarct is established, resulting in efficient intrainfarct fibrosis and peri-infarct astrogliosis. These effects might be associated with efficient peri-infarct reorganization and functional recovery.

Influence of Statin Pretreatment on Initial Neurological Severity and Short-Term Functional Outcome in Acute Ischemic Stroke Patients: The Fukuoka Stroke Registry.

BACKGROUND: Statins have neuroprotective effects against ischemic stroke. However, associations between pre-stroke statin treatment and initial stroke severity and between the treatment and functional outcome remain controversial. This study aimed at determining these associations in ischemic stroke patients. METHODS: Among patients registered in the Fukuoka Stroke Registry from June 2007 to October 2014, 3,848 patients with ischemic stroke within 24 h of onset, who had been functionally independent before onset, were enrolled in this study. Ischemic stroke was classified as cardioembolic or non-cardioembolic infarction. Primary and secondary study outcomes were mild neurological symptoms defined as a National Institutes of Health Stroke Scale score of ≤4 on admission and favorable functional outcome defined as a modified Rankin Scale score of ≤2 at discharge, respectively. Multivariable logistic regression models were used to quantify associations between pre-stroke statin treatment and study outcomes. RESULTS: Of all 3,848 participants, 697 (18.1%) were taking statins prior to the stroke. The frequency of mild neurological symptoms was significantly higher in patients with pre-stroke statin treatment (64.1%) than in those without the treatment (58.3%, p < 0.01). Multivariable analysis showed that pre-stroke statin treatment was significantly associated with mild neurological symptoms (OR 1.31; 95% CI 1.04-1.65; p < 0.01). Sensitivity analysis in patients with dyslipidemia (n = 1,998) also showed the same trend between pre-stroke statin treatment and mild neurological symptoms (multivariable-adjusted OR 1.26; 95% CI 0.99-1.62; p = 0.06). In contrast, the frequency of favorable functional outcome was not different between patients with (67.0%) and without (65.3%) the treatment (p = 0.40). Multivariable analysis also showed no significant association between pre-stroke statin treatment and favorable functional outcome (OR 1.21; 95% CI 0.91-1.60; p = 0.19). Continuation of statin treatment, however, was significantly associated with favorable functional outcome among patients with pre-stroke statin treatment (multivariable-adjusted OR 2.17; 95% CI 1.16-4.00; p = 0.02). CONCLUSIONS: Pre-stroke statin treatment in ischemic stroke patients was significantly associated with mild neurological symptoms within 24 h of onset. Pre-stroke statin treatment per se did not significantly influence the short-term functional outcome; however, continuation of statin treatment during the acute stage of stroke seems to relate with favorable functional outcome for patients with pre-stroke statin treatment.

Possible involvement of basic FGF in the upregulation of PDGFRß in pericytes after ischemic stroke.

Central nervous system (CNS) pericytes have been recognized as an indispensable component of the neurovascular unit. The expression of platelet-derived growth factor receptor ß (PDGFRß) is markedly increased in CNS pericytes after brain ischemia. It has been elucidated that PDGFRß, expressed in pericytes and pericyte-derived fibroblast-like cells, plays important roles in the maintenance of the blood-brain barrier (BBB) and in the repair process in infarct areas. The aim of this study was to uncover how the PDGFRß expression is regulated in pericytes after brain ischemia. We found that basic fibroblast growth factor (bFGF), but neither hypoxia at 1% O2 nor acidification at pH 6.5, significantly upregulated the PDGFRß expression in human cultured CNS pericytes. SU5402, an inhibitor of FGF receptor (FGFR), and inhibitors of its downstream effectors Akt and Erk abolished the bFGF-induced upregulation of PDGFRß. On the other hand, acidification significantly upregulated the expression of bFGF, while hypoxia upregulated the expression of FGFR1 in the pericytes. The expression of bFGF and FGFR1 was markedly induced in the ischemic hemisphere after ischemic insult in a middle cerebral artery occlusion stroke model. Immunofluorescent double labeling demonstrated that the expression of bFGF and FGFR1 was co-localized with PDGFRß-positive cells in peri-infarct areas. Moreover, treatment with bFGF enhanced cell growth and the PDGF-BB-induced migratory activity of cultured pericytes, which were significantly suppressed by SU5402 or Sunitinib, an inhibitor of PDGFR. These data suggested that increased bFGF upregulates the expression of PDGFRß and may enhance PDGFRß-mediated pericyte functions after brain ischemia.

Involvement of platelet-derived growth factor receptor ß in fibrosis through extracellular matrix protein production after ischemic stroke.

Fibrosis is concomitant with repair processes following injuries in the central nervous system (CNS). Pericytes are considered as an origin of fibrosis-forming cells in the CNS. Here, we examined whether platelet-derived growth factor receptor ß (PDGFRß), a well-known indispensable molecule for migration, proliferation, and survival of pericytes, was involved in the production of extracellular matrix proteins, fibronectin and collagen type I, which is crucial for fibrosis after ischemic stroke. Immunohistochemistry demonstrated induction of PDGFRß expression in vascular cells of peri-infarct areas at 3-7days in a mouse stroke model. The PDGFRß-expressing cells extended from peri-infarct areas toward the ischemic core after day 7 while expressing fibronectin and collagen type I in the infarct areas. In contrast, desmin and α-smooth muscle actin, markers of pericytes, were only expressed in vascular cells. In PDGFRß heterozygous knockout mice, the expression of fibronectin and collagen type I was attenuated at both mRNA and protein levels with an enlargement of the infarct volume after ischemic stroke compared with that in wild-type littermates. In cultured brain pericytes, the expression of PDGF-B, PDGFRß, fibronectin, and collagen type I, but not desmin, was significantly increased by serum depletion (SD). The SD-induced upregulation of fibronectin and collagen type I was suppressed by SU11652, an inhibitor of PDGFRß, while PDGF-B further increased the SD-induced upregulation. In conclusion, the expression level of PDGFRß may be a crucial determinant of fibrosis after ischemic stroke. Moreover, PDGFRß signaling participates in the production of fibronectin and collagen type I after ischemic stroke.

Features of brain magnetic resonance imaging diffusion-weighted images of aortogenic embolic stroke.

BACKGROUND: The features of acute aortogenic embolic stroke on magnetic resonance diffusion-weighted imaging (DWI) have not been fully elucidated, so we compared patients with acute aortogenic embolic stroke and those with acute cardioembolic stroke. METHODS AND RESULTS: This study included 40 consecutive patients with acute aortogenic embolic stroke, and 40 age- and sex-matched patients with acute cardioembolic stroke. The diagnosis of aortogenic embolic stroke was made when patients met 5 criteria: (1)acute neurologic event lasting >24h; (2) positive signals on DWI; (3) atherosclerotic lesions ≥3.5-mm thick at the aortic arch on transesophageal echocardiography; (4) neuroradiologic features suggesting embolic stroke, such as lesions involving the brain cortex or the re-opening phenomenon of previously occluded vessels on Magnetic Resonance Angiography (MRA); and (5) absence of other embolic sources, including heart disease and carotid stenosis. The number, site, and maximal diameter of the infarct lesions on DWI were compared between the aortogenic and cardiogenic groups. The aortogenic patients more frequently had ≥3 lesions (25.0% vs. 2.5%, P<0.01), lesions with a maximal diameter <30mm (77.5% vs. 20.0%, P< 0.001), and vertebrobasilar system lesions (55.0% vs. 10.0%, P< 0.001) than the cardiogenic patients. CONCLUSIONS: Acute aortogenic embolic stroke is characterized by multiple (≥3) and small lesions, and involvement of the vertebrobasilar system.

Statins and the risks of stroke recurrence and death after ischemic stroke: the Fukuoka Stroke Registry.

BACKGROUND AND PURPOSE: The findings of recent clinical trials suggest that treatment with high-dose statins reduces the risk of stroke recurrence. However, the doses approved in Japan are much lower than those in the previous studies. This study aimed to elucidate whether prescribed doses of statins reduce the risks of cerebrovascular events (CVEs: stroke recurrence or transient ischemic attack) and all-cause mortality in a cohort of Japanese patients with first-ever ischemic stroke. METHODS: The 2822 eligible patients registered in the Fukuoka Stroke Registry with first-ever acute ischemic stroke from June 2007 to February 2011 were classified into statin users (n = 993) and non-users (n = 1829) at discharge, and followed up until March 2012. We assessed the cumulative risks of CVE and all-cause mortality by the Kaplan-Meier method, and calculated hazard ratios (HRs) and 95% confidential intervals (CIs) using the Cox proportional hazards model. RESULTS: During the follow-up time (median, 2.0 years), 305 patients had CVEs and 345 died. The cumulative risks of CVE and death after 4 years were significantly lower in statin users than in non-users (13.8% versus 19.5%, P = 0.005 for CVE; 11.8% versus 21.7%, P < 0.001 for death). After adjusting for multiple confounding factors, statin treatment significantly reduced the risks of CVE (HR, 0.70; 95% CI, 0.53 to 0.92; P = 0.011) and all-cause mortality (HR, 0.67; 95% CI, 0.50 to 0.89; P = 0.006). CONCLUSIONS: Our findings suggest that low-dose statin may reduce the risks of CVE and death in Japanese patients with acute ischemic stroke.

Clinical significance of plasma VEGF value in ischemic stroke - research for biomarkers in ischemic stroke (REBIOS) study.

BACKGROUND: Vascular endothelial growth factor (VEGF) is a well-known molecule mediating neuronal survival and angiogenesis. However, its clinical significance in ischemic stroke is still controversial. The goal of this study was to examine the temporal profile of plasma VEGF value and its clinical significance in ischemic stroke with taking its subtypes into consideration. METHODS: We prospectively enrolled 171 patients with ischemic stroke and age- and gender-matched healthy subjects. The stroke patients were divided into 4 subtypes: atherothrombotic infarction (ATBI, n = 34), lacunar infarction (LAC, n = 45), cardioembolic infarction (CE, n = 49) and other types (OT, n = 43). Plasma VEGF values were measured as a part of multiplex immunoassay (Human MAP v1.6) and we obtained clinical information at 5 time points (days 0, 3, 7, 14 and 90) after the stroke onset. RESULTS: Plasma VEGF values were significantly higher in all stroke subtypes but OT than those in the controls throughout 90 days after stroke onset. There was no significant difference in the average VEGF values among ATBI, LAC, and CE. VEGF values were positively associated with neurological severity in CE patients, while a negative association was found in ATBI patients. After adjustment for possible confounding factors, plasma VEGF value was an independent predictor of poor functional outcome in CE patients. CONCLUSIONS: Although plasma VEGF value increases immediately after the stroke onset equally in all stroke subtypes, its significance in functional outcome may be different among the stroke subtypes.

Neurotrophin production in brain pericytes during hypoxia: a role of pericytes for neuroprotection.

Neurotrophins are crucial regulators of neuronal survival and death. Evidence suggests that cells comprising the neurovascular unit (NVU) cooperatively mediate neuronal development, survival and regeneration. The aim of this study was to test whether cerebrovascular cells, endothelial cells and pericytes, produce neurotrophins and play neuroprotective roles during hypoxic insults. We examined the expression of neurotrophins and their receptors in cultured human cerebral microvascular endothelial cells and pericytes, astrocytes and the rat neuronal cell line PC12. Differentiated PC12 cells expressed TrkA, the NGF receptor, which was significantly upregulated by hypoxia at 1% O(2) and regulated neuronal survival. Both pericytes and astrocytes expressed three neurotrophins, i.e. NGF, BDNF and NT-3, while TrkB and TrkC, specific receptors for BDNF and NT-3, were expressed in astrocytes, but not pericytes. In response to hypoxia, among the neurotrophins expressed in pericytes and astrocytes only NT-3 expression was significantly upregulated in pericytes. Treatment of astrocytes with NT-3 significantly activated Erk1/2 and increased the expression of NGF both at mRNA and protein levels. The MEK1 inhibitor U0126 or siRNA-mediated knockdown of TrkC abolished the NT-3-induced upregulation of NGF in astrocytes. Taken together, cerebral microvascular pericytes and astrocytes are potent producers of neurotrophins in the NVU. In response to hypoxia, pericytes increase NT-3 production, which induces astrocytes to increase NGF production through the TrkC-Erk1/2 pathway. The interplay between pericytes and astrocytes through neurotrophins in the NVU may play an important role in neuronal survival under hypoxic conditions.

Effect of serum lipid levels on stroke outcome after rt-PA therapy: SAMURAI rt-PA registry.

BACKGROUND: The effects of lipid levels on clinical outcomes after ischemic stroke are controversial. Whether admission lipid levels and prior statin use are associated with early intracerebral hemorrhage (ICH) and long-term functional outcome after recombinant tissue plasminogen activator (rt-PA) therapy for stroke patients was investigated. METHODS: Ischemic stroke patients who received intravenous rt-PA from a multicenter registry were studied. Lipid levels on admission, including total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, and triglyceride levels, as well as prior statin use, were assessed. The primary outcome was favorable outcome at 3 months corresponding to a modified Rankin Scale score ≤1. The secondary outcome was any or symptomatic ICH within the initial 36 h. RESULTS: Of 489 enrolled patients (171 women, 70.8 ± 11.6 years old), 60 used statins prior to stroke, 93 developed ICH (19.0%), and 188 (38.4%) had a favorable 3-month outcome. Of the lipid levels, only the HDL-C level was an independent predictor of favorable outcome after multivariate adjustment for baseline characteristics (OR 1.95, 95% CI 1.10-3.47 per 1 mmol/l; p = 0.023) and after further adjustment for pretreatment radiological findings (OR 2.03, 95% CI 1.07-3.84; p = 0.029). For the 187 stroke patients without cardioembolism, the HDL-C level was more strongly associated with favorable outcome (OR 4.94, 95% CI 1.91-12.76 per 1 mmol/l; p = 0.001). There were no significant associations between ICH and any lipid levels. Prior statin use was not associated with outcomes. CONCLUSIONS: The admission HDL-C level was associated with favorable outcome 3 months after intravenous rt-PA therapy in stroke patients without cardioembolism.

Intravenous recombinant tissue plasminogen activator therapy for stroke patients receiving maintenance hemodialysis: the Stroke Acute Management with Urgent Risk-Factor Assessment and Improvement (SAMURAI) rt-PA registry.

BACKGROUND: To examine the therapeutic effect of intravenous recombinant tissue plasminogen activator (rt-PA) therapy for stroke patients receiving maintenance hemodialysis (HD). methods: Of 600 stroke patients receiving intravenous rt-PA using 0.6 mg/kg alteplase who were enrolled in a multicenter observational study in Japan, 4 patients (3 men, 64-77 years old) on maintenance HD were studied. RESULTS: The primary kidney disease requiring HD was glomerulonephritis in 2 patients, diabetic nephropathy in 1, and undetermined in 1. The duration of HD ranged between 1.2 and 28 years. Three patients developed stroke on the day of HD, including 1 during HD and another just after HD. All patients had stroke in the carotid arterial territory. Pretreatment NIH Stroke Scale scores ranged between 4 and 20, and decreased by 2-5 points at 7 days. One patient needed intravenous antihypertensive therapy before rt-PA; he developed an ectopic cortical hematoma and intraventricular hemorrhage after rt-PA. The other 3 did not develop hemorrhagic complications. The modified Rankin Scale score at 3 months was 0 in 1 patient, 2 in 2 patients, and 4 in 1 patient. CONCLUSIONS: rt-PA therapy for stroke patients receiving maintenance HD might improve the stroke outcome. Ectopic hematoma was a unique complication in our case series.

[Effects of statin use on intracranial hemorrhage and clinical outcome after intravenous rt-PA for acute ischemic stroke: SAMURAI rt-PA registry].

PURPOSE: We evaluated whether pre- and post-stroke statin use was associated with intracranial hemorrhage (ICH) and clinical outcome at 3 months after intravenous recombinant tissue plasminogen activator (IV rt-PA) for acute ischemic stroke. METHODS: This study enrolled 600 consecutive patients (72 +/- 12 years, woman 37.2%) who received IV rt-PA at ten stroke centers that participated in the SAMURAI rt-PA Registry from October 2005 to July 2008. RESULTS: Statins were used prior to stroke in 112% and within 72 h after IV rt-PA in 10.0% of patients. One hundred nineteen patients (19.8%) developed ICH. Pre-stroke statin use was not an independent factor associated with ICH (OR 1.46; 95% CI 0.76-2.81, p = 0.225). Of 535 patients with a premorbid mRS < or = 1, 199 (37.2%) had a favorable clinical outcome at 3 months (mRS < or = 1). Pre-stroke statin use (OR 1.05; 95% CI 0.55-2.01, p = 0.879), as well as post-stroke statin use (OR 1.31; 95% CI 0.66-2.59, p = 0.440), was not an independent predictor of outcome. CONCLUSIONS: In patients who received IV rt-PA for acute ischemic stroke, statin use did not increase ICH after thrombolysis, nor was it associated with clinical outcome.

Characteristic sonographic findings of early restenosis after carotid endarterectomy.

OBJECTIVE: Restenosis of the carotid artery after carotid endarterectomy (CEA) is a major complication. The frequency, time of occurrence, and tissue characteristics of carotid restenosis were assessed with sonography. METHODS: Two hundred sixteen patients who had CEA for carotid stenosis were studied; follow-up sonography and magnetic resonance angiography were done 2 weeks, 3 months, and then every year after CEA. On sonography, restenosis was defined as an internal carotid artery (ICA) with a peak systolic velocity of 170 cm/s or greater or a maximum area of stenosis of 90% or greater. RESULTS: During 605 artery-years of follow-up, 18 patients (7.5%) were found to have restenosis on sonography: 4 at 3 months, 11 at 1 year, and 3 at 2 years after CEA. At the time that restenosis was detected, in all 18 ICAs the peak systolic velocity exceeded 200 cm/s and had more than doubled since the last measurement (mean +/- SD, 103 +/- 27 to 321 +/-107 cm/s), whereas the area of stenosis exceeded 90% in 6 patients, and magnetic resonance angiography revealed stenosis of 60% or greater in 8 patients. On sonography, all of the restenotic plaques were isoechoic and concentric. The restenosis was asymptomatic in 17 patients. Vascular risk factors or the severity of initial carotid stenosis before CEA were not associated with development of restenosis. Eleven patients had successful endovascular therapy, and the others received medical treatment. CONCLUSIONS: A marked increase in the flow velocity through an operated ICA is a good indication of restenosis. The isoechogenicity and concentricity of the restenotic plaques suggest that the restenosis is primarily the result of intimal hyperplasia.

Carotid artery calcification on multislice detector-row computed tomography.

BACKGROUND: To determine the underlying conditions that affect the degree of calcification of carotid arterial plaques, measured quantitatively using multidetector row computed tomography (MDCT), and to study the association of carotid calcification with clinical symptomatology. METHODS: We measured the calcification volume of stenotic lesions at the carotid bifurcation using MDCT in 84 consecutive patients who were scheduled to undergo carotid revascularization. These results were compared with the clinical and radiological characteristics of the patients. RESULTS: On MDCT, calcification in the carotid plaques was present in 78 patients (93%). Compared to the other patients, patients in the highest quartile of calcification volume (quartile 4) had higher serum creatinine levels (p < 0.001) and tended to have fewer symptomatic ischemic events in the territory of the affected carotid artery in the preceding 6 months (29 vs. 49%, p = 0.099); in particular, there were fewer transient symptoms (5 vs. 27%, p = 0.032) and symptoms possibly occurring due to local embolism (14 vs. 37%, p = 0.045). On ultrasound, plaque ulceration was less prevalent in patients in quartile 4 than in the remaining patients (5 vs. 29%, p = 0.026), although the severity of carotid stenosis was similar among all the quartiles. CONCLUSIONS: Renal dysfunction was associated with enhanced carotid plaque calcification. Patients with severe carotid calcification were found to have a low risk of recent ischemic stroke, presumably due, in part, to a lower prevalence of emboligenic carotid ulceration. MDCT was valuable for the quantitative evaluation of carotid calcification.

Antithrombotic therapy and predilection for cerebellar hemorrhage.

BACKGROUND: With the recent increase in the use of antithrombotic therapy, intracerebral hemorrhage (ICH) has been found to be a common complication. We determined whether the use of oral antithrombotic therapy and the patients' preexisting comorbidities were predictive of cerebellar hemorrhage (CH; previously reported to be associated with anticoagulants) as compared to other ICH, and whether antithrombotic therapy affected the clinical severity of CH. METHODS: A study of 327 consecutive patients hospitalized in our institute within 3 days after the onset of ICH, including 38 patients with a CH. RESULTS: CH accounted for 12% of all ICH, 75% of which occurred in patients on warfarin therapy with an international normalized ratio (INR) for prothrombin time >2.5 (p < 0.0001), and 33% of which occurred in patients on ticlopidine therapy (p = 0.017). Warfarin therapy with an INR >2.5 and high blood glucose on admission were independently predictive of CH as compared to other ICH. In addition, previous ischemic stroke (p = 0.002) and heart diseases (p = 0.018) were more prevalent in patients with CH than in those with other ICH. The number of major arteriosclerotic comorbidities and risk factors was also independently predictive of CH risk. CONCLUSIONS: We confirmed that warfarin therapy with an INR >2.5 is associated with CH. Patients with CH frequently had arteriosclerotic comorbidities requiring antithrombotic therapy that can complicate their acute management.

Superficial temporal artery duplex ultrasonography for improved cerebral hemodynamics after extracranial-intracranial bypass surgery.

BACKGROUND: To investigate the utility of superficial temporal artery (STA) duplex ultrasonography (STDU) for evaluating the improvement of the cerebral hemodynamics after extracranial-intracranial (EC-IC) bypass. METHODS: This study included 40 consecutive patients who underwent EC-IC bypass for occlusive disease of cerebral arteries. STDU was performed to measure the flow velocity, pulsatility index, and diameter of the operated STA before and 14 days after EC-IC bypass. Regional cerebral blood flow (rCBF) and acetazolamide (ACZ) reactivity of the ipsilateral middle cerebral artery (MCA) territory were evaluated by quantitative single-photon emission computed tomography with the ACZ challenge test. We investigated the correlation between STA flow velocity/diameter and rCBF/ACZ reactivity in the ipsilateral MCA territory. RESULTS: Mean flow velocity (MFV; 26.3 +/- 8.8 to 55.3 +/- 16.3 cm/s, p < 0.0001) and diameter (1.57 +/- 0.24 to 2.26 +/- 0.29 mm, p < 0.0001) of the STA, and rCBF (29.1 +/- 3.1 to 35.0 +/- 6.4 ml/100 g/min, p < 0.0001) and ACZ reactivity (-0.02 +/- 0.10 to 0.28 +/- 0.21, p < 0.0001) of the MCA territory increased after EC-IC bypass compared with the baseline values. STA MFV was significantly correlated with the rCBF 14 days after EC-IC bypass (R = 0.70, p < 0.0001). A cutoff value of postsurgical STA MFV greater than 48.5 cm/s yielded the highest diagnostic accuracy (sensitivity 86%; specificity, 82%) for rCBF > or = 32 ml/100 g/min after EC-IC bypass. CONCLUSIONS: STDU was available for evaluating postsurgical patency of the bypass flow and the rCBF of the ipsilateral MCA territory. The mean blood flow velocity of the operated STA is a highly sensitive parameter for predicting rCBF in the ipsilateral MCA territory after EC-IC bypass.