ObjectivesThis study sought to report technical details and clinical results of the first series of endovascular recanalization for cervical internal carotid artery (ICA) occlusion.

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Cerebral hyperperfusion syndrome (CHS) is a clinical syndrome following a revascularization procedure. In the past decade, neurointerventional surgery has become a standard procedure to treat stenotic or occluded cerebral vessels in both acute and chronic settings, as well as endovascular thrombectomy in acute ischemic stroke. This review aims to summarize relevant recent studies regarding the epidemiology, diagnosis, and management of CHS as well as to highlight areas of uncertainty. Extracranial and intracranial cerebrovascular diseases in acute and chronic conditions are considered. The definition and diagnostic criteria of CHS are diverse. Although impaired cerebrovascular autoregulation plays a major role in the pathophysiology of CHS, the underlying mechanism is still not fully understood. Its clinical characteristics vary in different patients. The current findings on clinical and radiological presentation, pathophysiology, incidence, and risk factors are based predominantly on carotid angioplasty and stenting studies. Hemodynamic assessment using imaging modalities is the main form of diagnosis although the criteria are distinct, but it is helpful for patient selection before an elective revascularization procedure is conducted. After endovascular thrombectomy, a diagnosis of CHS is even more complex, and physicians should consider concomitant reperfusion injury. Management and preventative measures, including intensive blood pressure control before, during, and after revascularization procedures and staged angioplasty, are discussed in detail.

Background and Purpose: Contrast-induced encephalopathy (CIE) is a rare and underrecognized complication after endovascular thrombectomy (EVT) for acute ischemic stroke. This study investigated the incidence and risk factors of CIE in patients who underwent EVT. Methods: Consecutive patients with acute ischemic stroke who received EVT between September 2014 and December 2019 at 2 medical centers were included. CIE was diagnosed on clinical criteria of neurological deterioration or delayed improvement within 24 hours after the procedure that was unexplained by the infarct or hemorrhagic transformation and radiological criterion of edematous change extending beyond the infarct core accompanied by contrast staining. Results: Of 421 patients with acute ischemic stroke who received EVT, 7 (1.7%) developed CIE. The manifestations included worsening of focal neurological signs, coma, and seizure. Patients with CIE were more likely to experience contrast-induced acute kidney injury than were those without CIE, but the volume of contrast medium was comparable between the two groups. The independent risk factors for CIE included renal dysfunction (defined as an estimated glomerular filtration rate <45 mL/min per 1.73 m 2 ; odds ratio, 5.77 [95% CI, 1.37–24.3]; P =0.02) and history of stroke (odds ratio, 4.96 [95% CI, 1.15–21.3]; P =0.03). Patients with CIE were less likely to achieve favorable functional outcomes (odds ratio, 0.09 [95% CI, 0.01–0.87]; P =0.04). Conclusions: CIE should be suspected in patients with clinical worsening after EVT accompanied by imaging evidence of contrast staining and edematous changes, especially in patients with renal dysfunction or history of stroke.

Background and Purpose: We aim to investigate whether histopathologic examination of thrombi retrieved from acute ischemic stroke patients undergoing endovascular treatment could distinguish cancer-related stroke from other etiologies. Methods: Thrombi from patients undergoing endovascular treatment were analyzed. The etiology of stroke was divided into cardioembolism, large artery atherosclerosis, and active cancer groups. All selected thrombi were subjected to hematoxylin and eosin staining. The percentages of fibrin/platelets, red blood cells, and white blood cells within a thrombus were quantified. Results: One-hundred fifty-two patients (active cancer, 19; cardioembolism, 107; large artery atherosclerosis, 26) were included. Thrombi from the active cancer group exhibited a higher fibrin/platelet composition than did those from the cardioembolism and large artery atherosclerosis groups (median, 85.7% versus 43.9% and 42.5%; P <0.001). Fibrin/platelet composition was the only independent factor (odds ratio, 1.05 [95% CI, 1.02–1.08]) in differentiating cancer-related stroke from stroke caused by cardioembolism and large artery atherosclerosis. A fibrin/platelet proportion of ≥65% accurately predicted cancer-related stroke (area under the curve, 0.84; P <0.001). Conclusions: In thrombi retrieved from patients undergoing endovascular treatment, a high fibrin/platelet composition was a probable indicator of cancer-related stroke.

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Two-dimensional (2D) arrays of gold nanoparticles with sulfur-containing fullerene nanoparticles were self-assembled through the formation of Au-S covalent bonds. Disulfide functional groups were introduced into the C60 molecule by reacting propyl 2-aminoethyl disulfide with C60. The 2D arrays were formed at the interface of the aqueous phase of gold particles and organic phase of fullerene particles as a blue transparent film. Transmission electronic microscope images showed that the fullerene spacing between adjacent Au (∼10 nm) particles was about 2.1 ( 0.4 nm, which was consistent with the result of 2.18 nm by molecular molding calculations (MM + ). The UV-visible spectrum of this film showed a red shift and increased bandwidth due to the small spacing between gold nanoparticles. The arrays were deposited on the top of pairs of gold electrodes to form 2D colloidal single electron devices. The electrode pairs were made by electron beam lithographic techniques, and the separation between tips of the two electrodes in a pair was about 100 nm. Electron transport measurements at low temperatures exhibited Coulomb blockade type current-voltage characteristics due to the charge effects. The assembled arrays have potential applications as nanoelectronics.

Background: Delayed postpancreatectomy hemorrhage (PPH) is a fatal complication caused by arterial erosion. This study reports a single-center experience of managing delayed PPH with different endovascular treatment approaches.Methods: We reviewed the data of patients who had delayed PPH due to hepatic artery or gastroduodenal artery stump perforation and underwent endovascular treatment between 2003 and 2018. We categorized endovascular treatment approaches involving hepatic artery sacrifice, superselective pseudoaneurysm embolization with hepatic artery preservation, and covered stent placement. Technical success rates, hemorrhage recurrence rates, major and minor hepatic complication rates, and 30-day and 1-year mortality rates were assessed.Results: A total of 18 patients were reviewed; 11 (61%), 4 (22%), and 3 (17%) delayed PPH cases were managed through hepatic artery sacrifice, superselective pseudoaneurysm embolization, and hepatic artery stenting, respectively. Multidetector computed tomography was performed in 14 (78%) patients. The technical success rate was 100%. The overall hemorrhage recurrence rate was 39%, with superselective pseudoaneurysm embolization having a 100% hemorrhage recurrence rate-much higher than that of hepatic artery sacrifice or stent graft placement. The overall major and minor hepatic complication rates were 56% and 83%, respectively. The overall 30day and 1-year mortality rates were 11% and 25%, respectively. The 30-day and 1-year mortality rates and minor and major hepatic complication rates were similar in each group. Conclusion: Hepatic artery sacrifice is more effective than superselective pseudoaneurysm embolization in the management of delayed PPH. Covered stent placement may be a reasonable alternative treatment to hepatic artery sacrifice.