PURPOSE: Cigarette smoking (CS) is one of the major risk factors of cerebral atherosclerotic disease, however, its level of contribution to extracranial and intracranial atherosclerotic stenosis (ECAS and ICAS) was not fully revealed yet. The purpose of our study was to assess the association of CS to cerebral atherosclerosis along with other risk factors. MATERIALS AND METHODS: All consecutive patients who were angiographically confirmed with severe symptomatic cerebral atherosclerotic disease between January 2002 and December 2012 were included in this study. Multivariate logistic regression analyses were performed to identify risk factors for ECAS and ICAS. Thereafter, CS group were compared to non-CS group in the entire study population and in a propensity-score matched population with two different age-subgroups. RESULTS: Of 1709 enrolled patients, 794 (46.5%) had extracranial (EC) lesions and the other 915 (53.5%) had intracranial (IC) lesions. CS group had more EC lesions (55.8% vs. 35.3%, P<0.001) whereas young age group (<50 years) had more IC lesion (84.5% vs. 47.6%, P<0.001). In multivariate analysis, seven variables including CS, male, old age, coronary heart disease, higher erythrocyte sedimentation rate, multiple lesions, and anterior lesion were independently associated with ECAS. In the propensity-score matched CS group had significant more EC lesion compared to non-CS group (65.7% vs. 47.9%) only in the old age subgroup. CONCLUSION: In contrast to a significant association between CS and severe symptomatic ECAS shown in old population, young patients did not show this association and showed relatively higher preference of ICAS.
Atherosclerosis ; Blood Sedimentation ; Cerebrovascular Circulation ; Constriction, Pathologic ; Coronary Disease ; Humans ; Intracranial Arteriosclerosis ; Logistic Models ; Male ; Multivariate Analysis ; Risk Factors ; Smoking ; Tobacco Products

PURPOSE: Complete removal of air bubbles from balloons for neurovascular angioplasty is cumbersome. We compared the preparation difficulty, air removal efficiency, and air collection pattern of six different balloon catheter preparation methods to propose a better preparation method for both initial and second balloon uses, especially for small-profile angioplasty balloon catheters. MATERIALS AND METHODS: A total of 18 neurovascular angioplasty balloon catheters with nominal diameters of 2 mm were prepared to test six different preparation methods: the instruction for use method (method A), simplified method using a syringe (method B) and four newly devised preparation methods using inflating devices (methods C–F). Serial radiographs were obtained while the balloons were gradually inflated. We measured the time for each preparation and the bubble number, analyzed their distribution in the balloon, and calculated the contrast filling ratio (contrast filling area/total balloon area) for initial and second ballooning. The whole process was repeated three times. RESULTS: The preparation time varied widely (11.5 seconds [method D] to 73.3 seconds [method A]). On initial inflation, the contrast filling ratio at 8 atm was the highest (100%) with methods A and F. On second inflation, the ratio was again highest with method A (99.5%), followed by method F (99.2%). Initial ballooning tended to show a uniform pattern of single bubble in the distal segment of the balloon; in contrast, second ballooning showed varying patterns in which the bubbles were multiple and randomly distributed. CONCLUSION: None of the six methods were able to completely exclude air bubbles from the balloon catheters including the second ballooning; however, the method of repeating aspiration with high-volume inflating device (method F) could be a practical option considering the simplicity and efficiency of preparation.
Angioplasty ; Angioplasty, Balloon ; Catheters ; Clothing ; Embolism, Air ; Equipment Failure ; Inflation, Economic ; Intracranial Arteriosclerosis ; Methods ; Syringes

BACKGROUND AND PURPOSE: We investigated whether the intracranial arterial calcification status reflects the overall cerebral atherosclerosis burden. METHODS: Patients with acute cerebral infarction who were admitted to a single university hospital stroke center and underwent brain computed tomography angiography (CTA) between May 2011 and December 2015 were included. We reviewed their demographic, clinical, and imaging data. Cerebral artery calcification was assessed from the cavernous portion of both internal carotid arteries, and patients were categorized into three groups according to the calcification status. The cerebral atherosclerosis score was calculated as the sum of the degree of stenosis of the major intracranial and extracranial arteries on brain CTA. RESULTS: In total, 1,161 patients were included (age=67±13 years, mean±standard deviation), of which 517 were female. Intracranial arterial calcification and atherosclerosis were detected in 921 patients. The cerebral atherosclerosis score tended to increase with the calcification status (no calcification=2.0±3.0, mild=3.8±3.8, severe=6.5±4.8; p < 0.001 in analysis of variance followed by the Bonferroni test). Multivariable logistic regression analysis including age, sex, vascular risk factors, body mass index, estimated glomerular filtration rate, high-sensitivity C-reactive protein, and calcification status showed that intracranial calcification was independently associated with an advanced cerebral atherosclerosis burden in a dose-dependent manner (compared to no calcification: odds ratio=2.0 and 95% confidence interval=1.1–3.4 for mild calcification, and odds ratio=4.7 and 95% confidence interval=2.7–8.3 for severe calcification). CONCLUSIONS: This study found that the calcification status of the cavernous portion of an internal carotid artery can reflect the overall cerebral atherosclerosis burden.
Angiography ; Arteries ; Atherosclerosis ; Body Mass Index ; Brain ; C-Reactive Protein ; Carotid Artery, Internal ; Cerebral Arteries ; Cerebral Infarction ; Constriction, Pathologic ; Female ; Glomerular Filtration Rate ; Humans ; Intracranial Arteriosclerosis* ; Logistic Models ; Risk Factors ; Stroke ; Vascular Calcification

No abstract available.
Cerebral Infarction ; Humans ; Intracranial Arteriosclerosis ; Subarachnoid Hemorrhage

BACKGROUND: The patients with familial hypercholesterolemia (FH) suffer from early onset atherosclerotic vascular disease due to high level of cholesterol and subsequent vascular inflammation, especially in the form of coronary artery disease. We investigated the clinical characteristics of FH associated cerebral infarction and its possible mechanism. METHODS: Between January 2014 and May 2017, acute cerebral infarction patients who admitted to Chung-Ang University Hospital were reviewed from stroke registry and the diagnosis of FH was made based on the Dutch Lipid Clinic Network Diagnostic Criteria for FH. We reviewed their initial laboratory and brain imaging information, prescribed medication and followed lipid profile after discharge. Stroke mechanism was determined based on Trial of ORG 10172 in Acute Stroke Treatment classification. RESULTS: Among 1,401 acute cerebral infarction or transient ischemic attack patients, one probable and three possible FH stroke patients were detected. All the patients denied of previous coronary artery disease history and initial lipid panel revealed high levels of total cholesterol (378±75 mg/dL) and low-density lipoprotein-cholesterol (238±56 mg/dL). Stroke mechanisms were heterogeneous, including one atherosclerotic, two vertebral artery dissection cases and one coagulation disorder. All the patients were combined with noticeable degree of intracranial atherosclerosis and were maintained with statin treatment. CONCLUSIONS: This study illustrates diverse stroke mechanism among stroke patients with FH. Further research is required to disclose exact incidence of FH among stroke population and effective treatment strategy.
Atherosclerosis ; Cerebral Infarction ; Cholesterol ; Classification ; Coronary Artery Disease ; Diagnosis ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Hyperlipoproteinemia Type II ; Incidence ; Inflammation ; Intracranial Arteriosclerosis ; Ischemic Attack, Transient ; Neuroimaging ; Stroke ; Vascular Diseases ; Vertebral Artery Dissection

No abstract available.
Arteries ; Intracranial Arteriosclerosis

Intracranial large artery disease (ILAD) is the major cause of stroke worldwide. With the application of recently introduced diagnostic techniques, the prevalence of non-atherosclerotic ILAD is expected to increase. Herein, we reviewed recent reports and summarized progress in the diagnosis and clinical impact of differentiation between ILAD of atherosclerotic and non-atherosclerotic origin. Our review of the literature suggests that more careful consideration of non-atherosclerotic causes and the application of appropriate diagnostic techniques in patients with ILAD may not only provide better results in the treatment of patients, but it may also lead to more successful clinical trials for the treatment of intracranial atherosclerosis.
Arteries* ; Atherosclerosis ; Constriction, Pathologic ; Diagnosis ; Humans ; Intracranial Arteriosclerosis ; Magnetic Resonance Imaging ; Prevalence ; Stroke

BACKGROUND AND PURPOSE: Vasa vasorum (VV) have been believed to be rare or non-existent in small-caliber intracranial arteries. In a series of human cerebral artery specimens, we identified and examined the distribution of VV in association with co-existing intracranial atherosclerosis. METHODS: We obtained cerebral artery specimens from 32 consecutive autopsies of subjects aged 45 years or above. We scrutinized middle cerebral artery (MCA), vertebral artery (VA), and basilar artery (BA) for the presence of adventitial VV. We described the distribution of VV, and the characteristics of co-existing atherosclerotic lesions. RESULTS: Among 157 intracranial arteries, adventitial VV were present in 74 of the 157 specimens (47%), involving MCA (n=13, 18%), BA (n=14, 19%), and VA (n=47, 64%). Although qualitatively these 74 adventitial VV distributed similarly in arteries with or without atherosclerotic lesions (disease-free arteries n=4/8; arteries of pre-atherosclerosis n=17/42; and arteries of progressive atherosclerosis n=53/107), the presence of adventitial VV in intracranial VA was associated with a heavier plaque load (1.72±1.66 mm2 vs. 0.40±0.32 mm2, P < 0.001), severer luminal stenosis (25%±21% vs. 12%±9%, P=0.002), higher rate of concentric lesions (79% vs. 36%, P=0.002), and denser intraplaque calcification (44% vs. 0%, P=0.003). Histologically, intracranial VA with VV had a larger diameter (3.40±0.79 mm vs. 2.34±0.58 mm, P < 0.001), thicker arterial wall (0.31±0.13 mm vs. 0.23±0.06 mm, P=0.002), and a larger intima-media (0.19±0.09 mm vs. 0.13± 0.04 mm, P=0.003) than VA without VV. CONCLUSIONS: Our study demonstrated the distribution of adventitial VV within brain vasculature and association between vertebral VV and progressive atherosclerotic lesions with a heavier plaque load and denser intraplaque calcification.
Arteries ; Atherosclerosis ; Autopsy ; Basilar Artery ; Brain ; Cerebral Arteries ; Constriction, Pathologic ; Humans ; Intracranial Arteriosclerosis* ; Middle Cerebral Artery ; Phenobarbital ; Vasa Vasorum* ; Vertebral Artery

Although there is an intuitive appeal to treat symptomatic stenotic intracranial arteries with endovascular therapies such as angioplasty and stenting, current data from randomized trials show intensive medical therapy is far superior for preventing stroke. This is in large part due to the high risk of peri-procedural stroke from angioplasty and stenting. If angioplasty and stenting is to emerge as a proven treatment for intracranial stenosis, endovascular techniques will need to become much safer, identification of patients with intracranial stenosis who are at particularly high risk of stroke despite intensive medical therapy will need to be targeted, and well-designed randomized trials will be necessary to show endovascular therapy is superior to medical therapy in these high-risk patients.
Angioplasty* ; Arteries* ; Constriction, Pathologic* ; Endovascular Procedures ; Humans ; Intracranial Arteriosclerosis ; Stents* ; Stroke

For patients with symptomatic intracranial atherosclerosis (ICAS), antithrombotic agents are the mainstay of therapy. Anticoagulation (warfarin) is not widely used since it is not more effective than aspirin and carries a high risk of bleeding. New oral anticoagulants are showing promise, but their use has not been investigated in appropriate clinical trials. Since the recurrent stroke risk is high with aspirin monotherapy, dual antiplatelets are considered in the early stage of symptomatic ICAS. Based on the Clopidogrel in High-Risk Patients with Acute Nondisabling Cerebrovascular Events (CHANCE) and Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) results, aspirin plus clopidogrel has been recommended. However, this combination was not superior to aspirin monotherapy in patients with ICAS in the CHANCE substudy. Progression of ICAS is common, and it is associated with recurrent strokes. In the Trial of Cilostazol in Symptomatic Intracranial Arterial Stenosis (TOSS) study, aspirin plus cilostazol was more effective than aspirin monotherapy in preventing progression. The TOSS II trial showed that the overall change in stenosis was better with aspirin plus cilostazol than with aspirin plus clopidogrel. Aside from antithrombotic therapy, risk factor management is critical for secondary prevention, and high blood pressure is clearly linked to recurrent stroke. However, blood pressure may have to be cautiously managed in the early stage of stroke. Considering that ICAS is the major cause of stroke worldwide, further investigations are needed to establish optimal management strategies for patients with ICAS.
Anticoagulants ; Aspirin ; Blood Pressure ; Constriction, Pathologic ; Fibrinolytic Agents ; Hemorrhage ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Hypertension ; Intracranial Arteriosclerosis* ; Risk Factors ; Secondary Prevention ; Stents ; Stroke