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Background: Branch atheromatous disease (BAD) is a primary cause of early neurological deterioration (END) in penetrating artery occlusion, leading to poor functional outcomes. While it has been proposed to classify BAD under large artery atherosclerosis, uncertainty exists regarding the optimal treatment strategy, including cholesterol-lowering targets. Objectives: We aimed to assess the clinical implications and temporal changes of atherosclerotic plaques before and after high-intensity statin treatment. Design: This is a high-resolution vessel-wall imaging sub-analysis of the trial of Statin and Dual Antiplatelet Therapy in Preventing Early Neurological Deterioration in Branch Atheromatous Disease (SATBRAD). Methods: In this prospective, single-group cohort study, participants in the treatment arm of the SATBRAD trial received early dual antiplatelet therapy and high-intensity statin treatment. The majority of these participants subsequently underwent high-resolution vessel-wall magnetic resonance imaging (MRI). Those with atheromatous plaques in the parent artery continued high-intensity statin treatment for 6 months, followed by a repeat MRI to monitor plaque changes. Results: There were 57 patients who underwent vessel-wall imaging and 24 exhibited contrast-enhanced plaques. Patients with contrast-enhanced plaques showed higher rates of END (29.2% vs 6.1%, p = 0.027), perfusion defects (62.5% vs 24.2%, p = 0.004), and lower rates of good outcomes at 3 months (50.0% vs 81.8%, p = 0.011). After adjusting for confounding factors, contrast-enhanced plaque had a negative impact on achieving a good outcome at 3 months (adjusted odds ratio = 0.04; 95% confidence interval = <0.01–0.60). Following high-intensity statin treatment in 36 patients, there was a notable reduction in stenosis (33.7% vs 29.3%, p = 0.005) and contrast-enhanced plaque volume (16.3 vs 11.6 mm3, p = 0.015). Conclusion: The study highlighted the association between contrast-enhanced atherosclerotic plaques, END, and poor functional outcomes, with high-intensity treatment leading to plaque volume reduction. These results underscore the shared pathology between BAD and intracranial atherosclerosis, emphasizing the necessity for further research and tailored treatment strategies for BAD. Trial registration: ClinicalTrials.gov; Identifier: NCT04824911 (https://clinicaltrials.gov/study/NCT04824911). Plain language summary: Changes in atherosclerosis and its impact on health after statin treatment: what we learned from detailed vessel imaging in the SATBRAD trial Branch atheromatous disease (BAD) is a major cause of early worsening of stroke symptoms, leading to poor recovery. While some experts believe BAD should be treated like large artery disease, the best treatment approach, including cholesterol-lowering targets, remains unclear. This study aimed to assess how high-intensity statin treatment affects atherosclerotic plaques over time and its impact on patient health. Analyzing detailed vessel images from the SATBRAD trial, where patients received high-intensity statins and magnetic resonance imaging, revealed that 24 out of 57 patients had plaques that showed up clearly with contrast enhancement. These patients were more likely to experience early worsening of stroke symptoms and perfusion compromise and had poorer outcomes. After six months of high-intensity statin treatment, there was a significant reduction in plaque size and vessel narrowing. The study concluded that contrast-enhanced plaques are linked to worse early stroke symptoms and poor recovery, but high-intensity statin treatment can reduce plaque size, suggesting that BAD may share similarities with larger artery disease and highlighting the need for further research and tailored treatments for BAD. [ABSTRACT FROM AUTHOR]

Acute ischemic stroke (AIS) is one of the leading causes of morbidity worldwide, thus, early recognition is essential to accelerate treatment. The only definite way to diagnose AIS is radiological imaging, which is limited to hospitals. However, two serum neuromarkers, glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1), have been proven as indicators of brain trauma and AIS. We aimed to investigate the potential utility of these markers in distinguishing between large vessel occlusion (LVO) and small vessel occlusion (SVO), considering differences in treatment. Sixty-nine AIS patients were included in our study and divided into LVO and SVO groups based on radiological imaging. Control group consisted of 22 participants without history of neurological disorders. Results showed differences in serum levels of both GFAP and UHC-L1 between all groups; control vs. SVO vs. LVO (GFAP: 30.19 pg/mL vs. 58.6 pg/mL vs. 321.3 pg/mL; UCH-L1: 117.7 pg/mL vs. 251.8 pg/mL vs. 573.1 pg/mL; p < 0.0001), with LVO having the highest values. Other prognostic factors of stroke severity were analyzed and did not correlate with serum biomarkers. In conclusion, a combination of GFAP and UCH-L1 could potentially be a valuable diagnostic tool for differentiating LVO and SVO in AIS patients. [ABSTRACT FROM AUTHOR]

Background: Ischemic stroke account for about 87% of all stroke cases. This study will focus on ischemic stroke due to small vessel occlusion as one of the subtypes based on TOAST (trial of ORG 10172 in acute stroke treatment). Objective: To determine the characteristics of ischemic stroke patients caused by small vessel occlusion and are expected to be used as a basis for further research. Methods: A descriptive observational retrospective study regarding the characteristics of acute ischemic stroke patients due to small vessel occlusion at Sanglah Hospital. Secondary data were obtained from patient medical records. Results: The total number of cases of small vessel occlusion was 338. The majority of the sample were men (64.5%) between 40-60 years old (53.6%). Most of the samples were patients who had experienced an ischemic stroke for the first time (75.1%) with NIHSS (National Institute of Health Stroke Scale) scores showing mild (48.2%) and moderate (51.5%) symptoms. Around half of them had a history of hypertension (60.1%), dyslipidemia (59.5%), and diabetes mellitus (44.1%). The most common location of infarction was in the anterior circulation (77.5%) with almost the same ratio of right and left hemisphere locations. Conclusion: Ischemic stroke due to occlusion of small vessels at Sanglah Hospital Denpasar for 3 years was 35.2% of the total ischemic stroke cases. Half of the total sample had classic vascular risk factors. Further research is needed to determine another effective treatment strategy other than just secondary prevention such as life style moderation to prevent recurrency.

Acute ischemic stroke (AIS) is one of the leading causes of morbidity worldwide, thus, early recognition is essential to accelerate treatment. The only definite way to diagnose AIS is radiological imaging, which is limited to hospitals. However, two serum neuromarkers, glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1), have been proven as indicators of brain trauma and AIS. We aimed to investigate the potential utility of these markers in distinguishing between large vessel occlusion (LVO) and small vessel occlusion (SVO), considering differences in treatment. Sixty-nine AIS patients were included in our study and divided into LVO and SVO groups based on radiological imaging. Control group consisted of 22 participants without history of neurological disorders. Results showed differences in serum levels of both GFAP and UHC-L1 between all groups; control vs. SVO vs. LVO (GFAP: 30.19 pg/mL vs. 58.6 pg/mL vs. 321.3 pg/mL; UCH-L1: 117.7 pg/mL vs. 251.8 pg/mL vs. 573.1 pg/mL; p < 0.0001), with LVO having the highest values. Other prognostic factors of stroke severity were analyzed and did not correlate with serum biomarkers. In conclusion, a combination of GFAP and UCH-L1 could potentially be a valuable diagnostic tool for differentiating LVO and SVO in AIS patients.

Abstract Background Triglyceride-glucose (TyG) index is a simple and reliable surrogate marker of insulin resistance. Elevated TyG index was related to stroke recurrence. This study aimed to explore the associations between TyG index with ischemic stroke recurrence in nondiabetic patients with small vessel occlusion. Methods From November 1, 2016 to February 28, 2021, consecutive acute ischemic stroke patients admitted within 1 week after onset were screened. The stroke mechanism was determined based on medical history, laboratory examinations, cardiac examinations, vascular examinations and neuroimaging. Nondiabetic patients with small vessel occlusion were enrolled and followed up for 1 year. The primary outcome was ischemic stroke recurrence. Logistic regression and Kaplan–Meier survival curve were used to analyze the association of the TyG index and stroke recurrence. Results A total of 6100 acute ischemic stroke patients were screened, with 1970 nondiabetic patients with small vessel occlusion included and divided into 4 groups according to the TyG index quartiles (Q1: 8.92). There were significant differences in age, body mass index, systolic blood pression, diastolic blood pressure, lipid-lowering agents, infarct location, fasting blood glucose, total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, uric acid, and stroke recurrence among the 4 groups. In the multi-adjusted models, compared to Q1 of the TyG index, the odds ratio for Q4 of the TyG index for stroke recurrence was 3.100 (1.366–8.019). The Kaplan–Meier survival (ischemic stroke-free) curves by quartiles of the TyG index also showed statistically significant differences (log-rank test, P = 0.004). Conclusions Our findings suggested that the TyG index was associated with ischemic stroke recurrence in nondiabetic patients with small vessel occlusion, and it could be a valuable biomarker for assessing the risk of ischemic stroke recurrence in these patients.

Lisda Amalia Department of Neurology, The First Affiliated Hospital of Faculty of Medicine, Universitas Padjadjaran/RSUP dr. Hasan Sadikin, Bandung, IndonesiaCorrespondence: Lisda Amalia Jl.Pasteur 38, Bandung, 40161, IndonesiaEmail dr.lisda@gmail.comIntroduction: Blockage of the cerebral arteries due to thrombosis and embolism resulting in decreased blood flow to the brain, reduced oxygen supply to the brain, resulting in neuronal damage and causes astrocyte cells to secrete glial fibrillary acidic protein (GFAP). The objective of this study was to determine the correlation between GFAP levels serum and clinical outcome in patients with acute ischemic stroke.Methods: This was observational with a cross-sectional design on acute ischemic stroke patients confirmed by CT scans and divided into large vessel occlusion and small-vessel occlusion. Clinical outcome was measured using the National Institutional Health Stroke Scale (NIHSS) tool. Statistical analysis uses Spearman’s rank correlation test and Mann Whitney’s test, significant if p < 0.05.Results: After collecting 33 research subjects, we found 16 people with large vessel occlusion and 17 people with small vessel occlusion. Serum GFAP levels were 0.2– 1.9 ng/mL, 9.1% with a mild neurological deficit, 45.45% were moderate neurological deficits, and 45.45% were severe neurological deficits. There was a significant positive correlation (r = 0.522; p = 0.002) between serum GFAP levels and the degree of neurological deficit in ischemic stroke patients. There was a statistically significant difference between serum GFAP levels in ischemic stroke patients with CT scan results of large artery occlusion compared to small artery occlusion (0.7 vs 0.4ng/mL; p = 0.001).Conclusion: There was a positive correlation between GFAP level serum and NIHSS score on acute ischemic stroke. The higher the value of GFAP serum level, the higher the value for NIHSS and correlated with stroke severity and the extent of brain damage in ischemic stroke patients.Keywords: GFAP, clinical outcome, acute ischemic stroke, small vessel occlusion, large vessel occlusion

Background: Triglyceride-glucose (TyG) index is a simple and reliable surrogate marker of insulin resistance. Elevated TyG index was related to stroke recurrence. This study aimed to explore the associations between TyG index with ischemic stroke recurrence in nondiabetic patients with small vessel occlusion. Methods: From November 1, 2016 to February 28, 2021, consecutive acute ischemic stroke patients admitted within 1 week after onset were screened. The stroke mechanism was determined based on medical history, laboratory examinations, cardiac examinations, vascular examinations and neuroimaging. Nondiabetic patients with small vessel occlusion were enrolled and followed up for 1 year. The primary outcome was ischemic stroke recurrence. Logistic regression and Kaplan–Meier survival curve were used to analyze the association of the TyG index and stroke recurrence. Results: A total of 6100 acute ischemic stroke patients were screened, with 1970 nondiabetic patients with small vessel occlusion included and divided into 4 groups according to the TyG index quartiles (Q1: < 8.20; Q2: 8.20–8.53; Q3: 8.54–8.92; Q4: > 8.92). There were significant differences in age, body mass index, systolic blood pression, diastolic blood pressure, lipid-lowering agents, infarct location, fasting blood glucose, total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, uric acid, and stroke recurrence among the 4 groups. In the multi-adjusted models, compared to Q1 of the TyG index, the odds ratio for Q4 of the TyG index for stroke recurrence was 3.100 (1.366–8.019). The Kaplan–Meier survival (ischemic stroke-free) curves by quartiles of the TyG index also showed statistically significant differences (log-rank test, P = 0.004). Conclusions: Our findings suggested that the TyG index was associated with ischemic stroke recurrence in nondiabetic patients with small vessel occlusion, and it could be a valuable biomarker for assessing the risk of ischemic stroke recurrence in these patients. [ABSTRACT FROM AUTHOR]

Background and purpose: This study aimed to examine the association of polyvascular disease and clinical outcomes in patients with lacunar stroke.Methods: Data of patients with recent lacunar stroke were collected from The Third China National Stroke Registry. Polyvascular disease is defined as the existence of atherosclerosis across two or more vascular beds. For the present study, polyvascular disease patients were grouped as follows: coronary heart disease (CHD) and lacunar stroke, peripheral arterial disease (PAD) and lacunar stroke, and CHD/PAD and lacunar stroke. The major clinical outcome was recurrence, and the secondary clinical outcome was major adverse cardiovascular events (MACEs). A Cox proportional multivariable hazards regression model was applied to estimate the association between polyvascular disease and outcomes.Results: Among 3,165 patients with recent lacunar stroke, CHD was present in 375 (11.8%) and peripheral arterial disease in 168 (5.3%). The hazard ratio (HR) for stroke recurrence was 0.98 (95% confidence interval [CI], 0.65–1.46; p = 0.91) for patients with CHD and lacunar stroke, 1.07 (95% CI, 0.61–1.87; p = 0.82) for patients with PAD and lacunar stroke, and 0.95 (95% CI, 0.66–1.35; p = 0.75) for patients with CHD/PAD and lacunar stroke compared with patients with isolated lacunar stroke. The HR for MACEs was 1.01 (95% CI, 0.69–1.49; p = 0.94) for patients with CHD and lacunar stroke, 1.11 (95% CI, 0.65–1.90; p = 0.71) for patients with PAD and lacunar stroke, and 0.99 (95% CI, 0.70–1.40; p = 0.95) for patients with CHD/PAD and lacunar stroke.Conclusion: Polyvascular disease is not associated with recurrence of stroke and MACEs in patients with recent lacunar stroke at 1 year.

Background and purpose: This study aimed to examine the association of polyvascular disease and clinical outcomes in patients with lacunar stroke. Methods: Data of patients with recent lacunar stroke were collected from The Third China National Stroke Registry. Polyvascular disease is defined as the existence of atherosclerosis across two or more vascular beds. For the present study, polyvascular disease patients were grouped as follows: coronary heart disease (CHD) and lacunar stroke, peripheral arterial disease (PAD) and lacunar stroke, and CHD/PAD and lacunar stroke. The major clinical outcome was recurrence, and the secondary clinical outcome was major adverse cardiovascular events (MACEs). A Cox proportional multivariable hazards regression model was applied to estimate the association between polyvascular disease and outcomes. Results: Among 3,165 patients with recent lacunar stroke, CHD was present in 375 (11.8%) and peripheral arterial disease in 168 (5.3%). The hazard ratio (HR) for stroke recurrence was 0.98 (95% confidence interval [CI], 0.65–1.46; p = 0.91) for patients with CHD and lacunar stroke, 1.07 (95% CI, 0.61–1.87; p = 0.82) for patients with PAD and lacunar stroke, and 0.95 (95% CI, 0.66–1.35; p = 0.75) for patients with CHD/PAD and lacunar stroke compared with patients with isolated lacunar stroke. The HR for MACEs was 1.01 (95% CI, 0.69–1.49; p = 0.94) for patients with CHD and lacunar stroke, 1.11 (95% CI, 0.65–1.90; p = 0.71) for patients with PAD and lacunar stroke, and 0.99 (95% CI, 0.70–1.40; p = 0.95) for patients with CHD/PAD and lacunar stroke. Conclusion: Polyvascular disease is not associated with recurrence of stroke and MACEs in patients with recent lacunar stroke at 1 year. [ABSTRACT FROM AUTHOR]

Background: Recent prospective registration studies of transient ischemic attack in Western countries demonstrated that large artery atherosclerosis is the highest risk etiology for early stroke recurrence under urgent evaluation and treatment. On the other hand, some limited transient ischemic attack studies from East Asian countries showed transient ischemic attack patients due to small vessel occlusion were at a higher early stroke risk. Aims: We aimed to assess the risk for early stroke in small vessel occlusion-transient ischemic attack patients in a Japanese large transient ischemic attack registry. Methods: We analyzed the data of a prospective Japanese transient ischemic attack registry including 1320 transient ischemic attack patients within seven days after onset. Small vessel occlusion-transient ischemic attack was defined as the presence of lacunar transient ischemic attack syndrome, without other etiologies. The outcome measure was recurrent stroke within 30 days after transient ischemic attack. The predictors of 30-day recurrent stroke were estimated using the Cox proportional hazards model. Results: The study population had a mean age of 69 ± 12 years and 470 were women. Recurrent stroke was observed in 61 patients (4.6%), and the highest rate was observed with small vessel occlusion-transient ischemic attack (7.8%), followed by large artery atherosclerosis (5.4%). In multivariate analysis, recurrent stroke was independently associated with small vessel occlusion-transient ischemic attack (hazard ratio (HR): 2.01, 95% confidence interval (CI): 1.19–3.35), higher systolic blood pressure (HR: 1.18, 95% CI: 1.08–1.28), and presentation within 3 h after onset (HR: 2.21, 95% CI: 1.27–4.04). Furthermore, small vessel occlusion-transient ischemic attack with acute small deep infarct on diffusion-weighted imaging was a stronger predictor of recurrent stroke (HR: 4.87, 95% CI: 2.09–10.0). Conclusion: Small vessel occlusion-transient ischemic attack, especially with acute small deep infarct, had a higher early stroke risk compared with other etiologies in Japanese transient ischemic attack patients who received early management. [ABSTRACT FROM AUTHOR]

• In acute SVO patients, IV-TPA within 4.5 h improved functional outcome. • IV-TPA within 4.5 h showed a low SICH risk in patients due to SVO. • IV-TPA was more effective in patients aged ≥80. Intravenous tissue-plasminogen activator (IV-TPA) treatment in acute ischemic stroke (AIS) patients due to small vessel occlusion (SVO) has been debated because of its small expected benefit and symptomatic intracranial hemorrhage (SICH) risk. Furthermore, data on subgroups of SVO patients are limited. From a prospective multicenter stroke registry database, AIS patients due to SVO within 24 h from onset were selected. Efficacy outcomes were 3-month modified Rankin Scale (mRS) score 0–1 proportion and mRS score distribution. Additionally, subgroup analyses were conducted by age, sex, initial National Institute Health Stroke Scale (NIHSS) score, and presenting limb paresis. This study included 2482 patients: 193 in the IV-TPA group and 2289 in the control group. After adjusting covariates, IV-TPA treatment was associated with an increased mRS 0-1 outcome (adjusted OR [95% CI], 1.56 [1.06–2.29]; P = 0.0249), but was not significantly associated with a favorable mRS shift (1.33 [0.98–1.81]; P = 0.0709). SICH and 3-month death occurred in three (1.6%) and none in the IV-TPA group versus one (0.04%) and 16 (0.7%) in the control group. In subgroup analyses, the IV-TPA effect appeared significantly greater in patients aged ≥80 versus <80 for mRS score distribution (P interaction = 0.012). This study showed that, in SVO patients, IV-TPA within 4.5 h may improve functional outcome with a low SICH risk. The benefit appeared more substantial in patients aged ≥80. [ABSTRACT FROM AUTHOR]

Our objective was to investigate the effect of cilostazol in acute therapy for small vessel stroke patients. The neurologic deficits in some patients of small vessel brain infarction will progress even if a patient takes immediate medical treatments including aspirin or other antiplatelet drugs. In Japan, cilostazol, presenting not only the antiplatelet effect but also the arteriole dilation, is used for treatment of ischemic stroke. In this study, acute stroke patients with small vessel occlusion were treated with cilostazol instead of aspirin in the conventional medication after 2010. Therefore, patients between April 2007 and March 2009 were classified into the conventional group (group-con, n = 220), and patients between April 2010 and March 2012 were classified into the cilostazol group (group-cilo, n = 230). Enrolled patients were classified into lacunar infarction (LI) and branch atheromatous disease. Progressing stroke was defined as the increase of National Institutes of Health Stroke Scale score of 2 or more within 48 hours. The clinical outcome was assessed by the modified Rankin Scale (mRS) score at 1 month. As the result, the significant reduction in progressing stroke was dominant in the LI of brainstem (P = .01). The length of hospital stay was significantly shorter in the group-cilo compared with the group-con (18.6 and 21.2 days, P = .03). Moreover, mRS score at 1 month was significantly lower in the group-cilo than the group-con (1.9 and 2.3, P = .03). In conclusion, cilostazol reduced the risk of early neurologic deterioration of patients with small vessel brain infarction. It is eagerly desired to conduct a large randomized control trial. [Copyright &y& Elsevier]

Background: Cyclooxygenase-2 (COX-2) catalyzes the formation of prostaglandins that contribute to the inflammation in atherosclerosis. The aim of the present study was to investigate the relationship between two polymorphisms (−1195G>A and -765G>C) in the COX-2 gene and subtypes of ischemic stroke in a Chinese population. Methods: Genomic DNA of 224 patients with large artery atherosclerosis (LAA), 329 patients with small vessel occlusion (SVO), and 450 controls were genotyped for the COX-2 1195G>A (rs689466) and -765G>C (rs20417) polymorphisms using polymerase chain reaction-restriction fragment length polymorphism. Chi-square test and logistic regression analysis were performed for association analysis. Results: The frequencies of variant allele with -1195G>A and -765G>C polymorphisms were 0.46 and 0.22, respectively. The -1195GA genotype and 1195A allele carriers were identified independently to be related with ischemic stroke (adjusted OR = 1.51, 95 % CI: 1.09-2.10, P = 0.02; OR = 1.45, 95 % CI: 1.06-1.97, P = 0.02) and SVO (adjusted OR = 1.57, 95 % CI: 1.07-2.30, P = 0.02; OR = 1.50, 95 % CI: 1.05-2.16, P = 0.03). In contrast, the 1195G>A polymorphism was not associated with LAA. No relationship between the -765G>C polymorphism and risk of either ischemic stroke was observed. The linkage disequilibrium analysis showed that -1195G>A and -765G>C SNPs are moderate linkage disequilibrium in this study population ( D′ = 0.72, r = 0.16). Compared with G-1195-G-765 haplotype, the haplotype of A-1195-G-765 showed significant increased risk of ischemic stroke (OR = 1.27, 95 % CI: 1.05-1.54, P = 0.02) and SVO (OR = 1.27, 95 % CI: 1.02-1.58, P = 0.03) but not LAA. Conclusions: In conclusion, we found that -1195G>A polymorphism and A-1195-G-765 haplotype of COX-2 were associated with susceptibility to ischemic stroke in a Chinese population. The effects were confined to SVO among the stroke subtypes rather than to LAA. [ABSTRACT FROM AUTHOR]

Background: Small deep infarcts might be classified into 2 types: lacunar and branchatheromatous infarcts. However, since their initial description, small deep infarcts were still regarded as the same category of the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification, small vessel occlusion (SVO). We hypothesized that the 2 types of small deep infarcts would be distinct clinical entities. This study was conducted to investigate the clinical characteristics in the 2 groups of patients according to lesion pattern and combined atherosclerotic diseases. Methods: We included patients with small deep infarcts in the subcortical area. The patients were divided into 2 groups: (1) island lesions and (2) linear lesions on coronal diffusion weighted imaging. The status of the relevant artery was categorized as no stenosis, non-significant (<50% of luminal narrowing) and significant (>50% of luminal narrowing). We compared the clinical and imaging characteristics of two lesion types according to various arterial status. Results: This study analyzed a total of 248 patients. Independent factors for island lesions on coronal DWI were male, severe leukoaraiosis, microbleeds, abnormal glycated hemoglobin (HbA1C), and abnormal estimated glomerular filtration ratio (eGFR) adjusted by age, sex, and inititial National Institutes of Health Stroke Scale. In addition, in patients without significant relevant arterial stenosis, island lesion patterns were more frequently associated with severe periventricular white matter hyperintensity, diabetes mellitus, abnormal eGFR and abnormal HbA1C than linear lesion patterns. Conclusion: This study demonstrated that SVO of TOAST classifications had different imaging and clinical characteristics according to the lesion patterns of coronal imaging. It suggests that two types of SVO should be regarded as the different categories of stroke classification. [ABSTRACT FROM AUTHOR]

The risk factors for stroke, a fatal disease, include type two diabetes, hypertension, and genetic influences. Small vessel occlusion (SVO) can be affected by epigenetic alterations, but an association between SVO and the methylation of cytochrome P450 family 26 subfamily C member 1 (CYP26C1) has not been identified. In this study, we measured the level of DNA methylation in the CYP26C1 promoter and the 5′ untranslated region of 115 normal subjects and 56 patients with SVO in Korea. The DNA methylation level of each subject was measured by bisulfite amplicon sequencing, and statistical analysis was performed using the general linear model or Pearson's correlation. The average level of DNA methylation was markedly lower in patients with SVO than in normal subjects (20.4% vs. 17.5%). We found that the methylation of CYP26C1 has a significant positive correlation with blood parameters including white blood cells, hematocrit, lactate dehydrogenase, and Na+ in subjects with SVO. We predicted that binding of RXR-α and RAR-β might be affected by CYP26C1 methylation at CpG sites −246–237 and −294–285. These findings suggest that CYP26C1 methylation in the promoter region may be a predictor of SVO. [ABSTRACT FROM AUTHOR]

Introduction: Recent clinical comparisons of M1 and M2 segment endovascular thrombectomy have reached incongruous results in rates of complication and functional outcomes. This study aims to clarify the controversy surrounding this rapidly advancing technique through literature review and meta-analysis.Methods: A Pubmed search was performed (January 2015-September 2019) using the following keywords: "M2 AND ("stroke" OR "occlusion") AND ("thrombectomy" OR "endovascular")". Safety and clinical outcomes were compared between segments via weighted Student's t-test, Chi-square and odds ratio while study heterogeneity was analyzed using Cochran Q and I2 tests.Results: Pubmed identified 208 articles and eleven studies were included after full-text analysis, comprising 2,548 M1 and 758 M2 mechanical thrombectomy segment cases. Baseline National Institutes of Health Stroke Scale scores were comparatively lower in patients experiencing an M2 occlusion (16 ± 1.25 vs 13.6 ± 0.96, p < 0.01). Patients who underwent M2 mechanical thrombectomy were more likely to experience both good clinical outcomes (modified Rankin Scale 0-2) (48.6% vs 43.5% respectively, OR 1.24; CI 1.05-1.47, p = 0.01) and excellent clinical outcomes (modified Rankin Scale 0-1) (34.7% vs. 26.5%%, OR 1.6; CI 1.28-1.99, p < 0.01) at 90 days compared to M1 mechanical thrombectomy. Neither recanalization rates (75.3% vs 72.8%, OR 0.92, CI 0.75-1.13, p = 0.44) nor symptomatic intracranial hemorrhage rates (5.6% vs 4.9%, OR 0.92; CI 0.61-1.39, p= 0.7) were significantly different between M1 and M2 cohorts. Mortality was less frequent in the M2 cohort compared to M1 (16.3% vs 20.7%, OR 0.73; CI 0.57-0.94, p = 0.01). M1 and M2 cohorts did not differ in symptom onset-to-puncture (238.1 ± 46.7 vs 239.8 ± 43.9 min respectively, p=0.488) nor symptom onset-to recanalization times (318.7 ± 46.6 vs 317.7 ± 71.1 min respectively, p = 0.772), though mean operative duration was shorter in the M2 cohort (61.8 ± 25.5 vs 54.6 ± 24 min, p < 0.01).Conclusions: Patients who underwent M2 mechanical thrombectomy had a higher prevalence of good and excellent clinical outcomes compared to the M1 mechanical thrombectomy cohorts. Additionally, our data suggest lower mortality rates in the M2 cohort and symptomatic intracranial hemorrhage rates that are similar to the M1 cohort. Therefore, M2 segment thrombectomy likely does not pose a significantly elevated operative risk and may have a positive impact on patient outcomes. [ABSTRACT FROM AUTHOR]