Ischemic Stroke In Type Research Articles

Associations of onset age, diabetes duration and glycated hemoglobin level with ischemic stroke risk in type 2 diabetes patients: a prospective cohort study

Objective: To investigate the associations of onset age, diabetes duration, and glycated hemoglobin (HbA1c) levels with ischemic stroke risk in type 2 diabetes patients. Methods: The participants were from Comprehensive Research on the Prevention and Control of the Diabetes in Jiangsu Province. The study used data from baseline survey from December 2013 to January 2014 and follow-up until December 31, 2021. After excluding the participants who had been diagnosed with stroke at baseline survey and those with incomplete information on onset age, diabetes duration, and HbA1c level, a total of 17 576 type 2 diabetes patients were included. Cox proportional hazard model was used to calculate the hazard ratio (HR) and 95%CI of onset age, diabetes duration, and HbA1c level for ischemic stroke. Results: During the median follow-up time of 8.02 years, 2 622 ischemic stroke cases were registered. Multivariate Cox proportional risk regression model showed that a 5-year increase in type 2 diabetes onset age was significantly associated with a 5% decreased risk for ischemic stroke (HR=0.95, 95%CI: 0.92-0.99). A 5-year increase in diabetes duration was associated with a 5% increased risk for ischemic stroke (HR=1.05, 95%CI: 1.02-1.10). Higher HbA1c (per 1 standard deviation increase:HR=1.17, 95%CI: 1.13-1.21) was associated with an increased risk for ischemic stroke. Conclusion: The earlier onset age of diabetes, longer diabetes duration, and high levels of HbA1c are associated with an increased risk for ischemic stroke in type 2 diabetes patients.

Abstract TP193: The Protective Effects Of Exercise On Cerebral Ischemia Injury In Diabetes

Ischemic stroke (IS) causes neurological dysfunction due to a loss of cerebral blood flow with exaggerated cerebral damage in diabetes. Exercise has shown beneficial effects on the vascular system and diabetes by mediating inter-organ communications. However, whether and how exercise contributes preventatively to the brain after IS in type 2 diabetes (T2D) is undefined. Here, we aimed to determine the effects of exercise on the metabolism, cerebral injury, neurological function, and protein expression in the brain after IS. T2D diabetic mice (db/db, 7-8 wks), and age/sex-matched controls (db/c) were subjected to exercise (10 m/min, 5 days/wk for 8-wks) or sedentary. Body weight and blood glucose were recorded once a week. One day after exercise, middle cerebral artery occlusion surgery was performed to induce IS. Sensorimotor deficits were assessed by the adhesive removal and corner tests two days after surgery. Afterward, the brain samples were collected for measuring the infarct size by cresyl violet staining. The proteins from the ipsilateral and contralateral brain were used for Western Blot to measure the levels of endothelial nitric oxide synthase (eNOS), neuronal NOS, NADPH oxidase (Nox2), Nox4, nuclear factor-kappa B (NF-κB), NF-κ light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα). We found: 1) exercise could stabilize the blood glucose in male db/db mice and have effects on preventing blood glucose increase at the early age of female db/db mice; 2) exercise could improve sensorimotor deficits by reducing tape contact and removal time and balancing the corner turning times (p< 0.05); 3) the infarct size is decreased in exercised group in both db/c (18.5 ± 2.2% and 22.2 ± 2.5%), and db/db mice (25.6 ± 3.1% and 35.6 ± 3.8%, exercise vs. sedentary, p< 0.05); 4) proteins related to oxidative stress and inflammation were downregulated in the brain of exercised diabetic IS mice. In conclusion, exercise could provide protective effects on stabilizing metabolism, improving neurological function, and reducing brain injury by downregulating the protein expression related to inflammation and oxidative stress in the brain.

Risk of stroke and retinopathy during GLP-1 receptor agonist cardiovascular outcome trials: An eight RCTs meta-analysis.

To explore the risk of stroke (including ischemic and hemorrhagic stroke) in type 2 diabetes mellitus treated with glucagon-like peptide 1 receptor agonist (GLP-1RA) medication according to data from the Cardiovascular Outcome Trials(CVOT). Randomized controlled trials (RCT) on GLP-1RA therapy and cardiovascular outcomes in type 2 diabetics published in full-text journal databases such as Medline (via PubMed), Embase, Clinical Trials.gov, and the Cochrane Library from establishment to May 1, 2022 were searched. We assess the quality of individual studies by using the Cochrane risk of bias algorithm. RevMan 5.4.1 software was use for calculating meta- analysis. A total of 60,081 randomized participants were included in the data of these 8 GLP-1RA cardiovascular outcomes trials. Pooled analysis reported statistically significant effect on total stroke risk[RR=0.83, 95%CI(0.73, 0.95), p=0.005], and its subtypes such as ischemic Stroke [RR=0.83, 95%CI(0.73, 0.95), p=0.008] from treatment with GLP-1RA versus placebo, and have no significant effect on the risk of hemorrhagic stroke[RR=0.83, 95%CI(0.57, 1.20), p=0.31] and retinopathy [RR=1.54, 95%CI(0.74, 3.23), p=0.25]. GLP-1RA significantly reduces the risk of ischemic stroke in type 2 diabetics with cardiovascular risk factors.

Preoperative hyperglycemia is associated with elevated risk of perioperative ischemic stroke in type 2 diabetic patients undergoing non-cardiovascular surgery: A retrospective cohort study.

Diabetes mellitus (DM) has been reported to be associated with perioperative stroke, but the effects of preoperative hyperglycemia on the risk of perioperative stroke in diabetic patients undergoing non-cardiovascular surgery remain unclear. This study investigated the association between preoperative hyperglycemia and the risk of perioperative ischemic stroke in type 2 diabetic patients undergoing non-cardiovascular surgery. This retrospective cohort study screened 27,002 patients with type 2 DM undergoing non-cardiovascular surgery with general anesthesia between January 2008 and August 2019 at The First Medical Center of Chinese People's Liberation Army (PLA) General Hospital. The exposure of interest was preoperative hyperglycemia, defined as a fasting plasma glucose (FPG) ≥ 7 mmol/L. The outcome of interest was a new diagnosis of perioperative ischemic stroke within 30 days after surgery. Residual confounding was minimized by controlling for observable patient and intraoperative factors. Logistic regression was conducted in the total and propensity score matched cohorts. In addition, we stratified patients into six subgroups to investigate whether the association between preoperative hyperglycemia and perioperative ischemic stroke differs in these subgroups. The overall incidence of perioperative ischemic stroke was 0.53% (n = 144) in the current cohort. The odds of perioperative ischemic stroke were significantly increased for patients with preoperative hyperglycemia after adjusting for patient- related variables (OR: 1.95; 95% CI: 1.39-2.75; p < 0.001), surgery-related variables (OR: 2.1; 95% CI: 1.51-2.94; p < 0.001), and all confounding variables (OR: 1.78; 95% CI: 1.26-2.53; p < 0.001). The risk of perioperative stroke was significantly increased in patients with preoperative hyperglycemia (OR: 2.51; 95% CI: 1.66-3.9; p < 0.001) in the propensity score matched cohort. Preoperative hyperglycemia was associated with the outcome for all the subgroups except for patients undergoing neurosurgery. Preoperative hyperglycemia is associated with an elevated risk of perioperative stroke in patients with type 2 DM undergoing non-cardiovascular surgery. The effect could be eliminated for patients undergoing neurosurgery, during which specific risk factors should be considered.

Potential Biomarkers to Predict Acute Ischemic Stroke in Type 2 Diabetes.

Background and Purpose: Patients with type 2 diabetes (T2D) have increased risk of cardiovascular disease (CVD), encompassing myocardial infarction, stroke, and peripheral vascular disease. We hypothesized that those biomarkers indicative of acute ischemic stroke (AIS) seen in large vessel occlusion (LVO) may also be elevated in T2D and further enhanced by stress conditions; therefore, these proteins represent potentially predictive biomarkers for those T2D patients at high risk of AIS. Methods: We performed an exploratory proteomic analysis in control subjects (n = 23) versus those with type 2 diabetes (T2D) (n = 23) who underwent a hyperinsulinemic clamp study to transient severe hypoglycemia [blood glucose <2.0 mmol/L (36 mg/dl)] in a prospective case-control study. We compared these proteins described as diagnostic and prognostic biomarkers for AIS due to LVO: lymphatic vessel endothelial hyaluronic acid receptor-1 (LYVE1), thrombospondin-1 (THBS1), pro-platelet basic protein (PPBP), and cadherin 1 (CDH1). Results: At baseline (BL), PPBP (p < 0.05), THBS1 (p < 0.05), and CDH1 (p < 0.01) were elevated in T2D; LYVE1 was not different between controls and T2D subjects at BL or at subsequent timepoints. PPBP and THBS1 tended to increase at hypoglycemia in both cohorts, though reached significance only in controls (p < 0.05), returning to BL levels post-hypoglycemia. CDH1 levels were higher in T2D at BL, at hypoglycemia and up to 2-h posthypoglycemia, thereafter reverting to BL levels. Conclusion: Elevated levels of PPBP, THBS1, and CDH1, circulatory proteins suggested as biomarkers of AIS due to LVO, may, in T2D patients, be prognostically indicative of a cohort of T2D patients at increased risk of ischaemic stroke. Prospective studies are needed to determine if this reflects future clinical risk.Clinical trial reg. no: NCT03102801.

Clinical profile of acute ischemic stroke in type 2 diabetes mellitus

Stroke is the second leading causes of death worldwide and approximately 80% of strokes are due to ischemic cerebral infarction and 20% due to brain haemorrhage. Diabetes Mellitus is a very common metabolic disorder and it is an independent risk factor for stroke. Glucose intolerance in a stroke patient may or may not reflect glycemia prior to the event. This study is to assess the clinical profile of Acute Ischemic stroke in type 2 Diabetes Mellitus.To evaluate the clinical profile of acute ischemic stroke in type 2 Diabetes Mellitus. This a cross sectional descriptive study. This is an cross sectional study including 64 patients.Maximum number of patients were in the age group of 60 – 69 years, with mean age of 63.59±12.59 years.The male to female of 1.37:1. There were 25 patients (39.1%) well controlled Diabetes patients, 16(25.0%) fairly controlled and 23 (35.9%) were poorly controlled Diabetic patient. The common risk factors were Diabetes mellitus, hypertension, smoking, dyslipidemia, Rheumatic heart disease and Retroviral disease.HbA1c should be considered as an independent risk factor for poor clinical outcome and worse prognosis.Early diagnosis and treatment of diabetes including lifestyle modification and periodic monitoring of HbA1c levels may reduce the development of stroke and morbidity and mortality associated with it. Commonest clinical presentation was motor weakness (100%), cranial nerve dysfunction(45.3%), altered sensorium (29.7%), language disturbances (45.3%), sensory impairment(26.6%).

Altered Jagged1-Notch1 Signaling in Enhanced Dysfunctional Neovascularization and Delayed Angiogenesis After Ischemic Stroke in HFD/STZ Induced Type 2 Diabetes Rats.

Diabetes exacerbates brain damage in cerebral ischemic stroke. Our previous study has demonstrated that after cerebral ischemia, type 2 diabetes rats displayed worse neurological outcomes, larger cerebral infarction and severer blood-brain barrier disruption. However, our knowledge of the mechanisms of how diabetes impacts the cerebrovascular repair process is limited. This study was aimed to characterize structural alterations and potential mechanisms in brain microvessels before and after ischemic stroke in type 2 diabetic rats treated with high-fat diet and streptozotocin (HFD/STZ). Furtherly, we tested our hypothesis that dysregulated intercellular Jagged1-Notch1 signaling was involved in the dysfunctional cerebral neovascularization both before and after ischemic stroke in HFD/STZ rats. In our study, we found increased yet dysfunctional neovascularization with activated Jagged1-Notch1 signaling in the cerebrovasculature before cerebral ischemia in HFD/STZ rats compared with non-diabetic rats. Furthermore, we observed delayed angiogenesis as well as suppressed Jagged1-Notch1 signaling after ischemic stroke. Our results elucidate the potential mechanisms underlying diabetes-related cerebral microvasculature dysfunction after ischemic stroke.

Abstract TMP32: Transcriptome Changes of Brain Myeloid Cells After Ischemic Stroke in Type 2 Diabetic Mice

Introduction: Type 2 diabetes mellitus (T2DM) is associated with poor outcome after stroke. Brain myeloid cells are considered to play a pivotal role in modulating brain damage and recovery after stroke, but how myeloid response to stroke under diabetic condition is largely unclear. We used single-cell RNA sequencing (scRNA seq) to determine the transcriptome profiles of brain myeloid cells under diabetic and ischemic conditions using T2DM mouse model. Hypothesis: The altered gene expression in the brain myeloid cells under diabetic condition leads to the aggravation of ischemic brain injury. Methods: We performed scRNA seq in Percoll gradient-isolated brain mononuclear cells from middle-aged db/db and db/+ mice three days after direct middle cerebral artery occlusion (MCAO) or sham-operation. Clusters of brain myeloid cells were predominantly annotated as macrophages (mp) or microglia (mg) according to the expression of marker genes in each cell type. We identified DM-unique differentially expressed genes (DEGs) and stroke-unique DEGs, and assessed the biological role of these DEGs by enrichment analysis. Results: Myeloid cell population was increased in DM ( db/db without MCAO; mp 37.3% mg 10.6%) and stroke ( db/+ with MCAO; mp 26.2% mg 33.2%) group compared to control ( db/+ without MCAO; mp 3.4% mg 0.8%) group. In macrophages, 91 DM-unique (64 up- and 27 down-regulated) and 464 stroke-unique (458 up- and 6 down-regulated) DEGs were identified, whereas 258 stroke-unique (254 up- and 4 down-regulated) DEGs were identified in microglia. Enrichment analysis revealed that DM-unique down-regulated DEGs in macrophages were related to MHC class II antigen processing involved in Staphylococcus aureus infection pathway, indicating a possible relationship between immunosuppression and stroke aggravation in diabetes. DM-unique and stroke-unique up-regulated DEGs were related to oxidative phosphorylation, phagocytosis, and protein metabolism. Conclusions: The present study demonstrated altered gene expression profile and molecular network of brain myeloid cells in response to diabetic and ischemic conditions by scRNA seq, providing a clue to the underlying mechanism of the adverse effect of T2DM on stroke.

Association of hemoglobin glycation index with outcomes of acute ischemic stroke in type 2 diabetic patients

ABSTRACTObjective This study aimed to investigate the association between the hemoglobin glycation index (HGI) and the prognosis of diabetic patients with ischemic stroke.Methods Data were derived from the Abnormal Glucose Regulation in Patients with Acute Stroke across China (ACROSS-China) registry. Diabetic patients with ischemic stroke were included. HGI was calculated by subtracting the predicted HbA1c based on fasting plasma glucose from the observed HbA1c, and then classified into three groups by the tertiles: low HGI (<−0.62), moderate HGI (−0.62 to 0.35) and high HGI (≥0.36). Outcomes included stroke recurrence, all-cause death and poor outcome at 12 months.Results A total of 976 diabetic patients were included. Low HGI was associated with an increased risk of stroke recurrence and poor outcome (adj.hazard ratio 1.53, 95% confidence intervals (CIs) 1.11–2.12, p = 0.01; and adj.odds ratio 1.64, 95% CI 1.13–2.38, p = 0.01, respectively), and high HGI was associated with an increased risk of poor outcome (adj.odds ratio 1.54, 95% CI 1.06–2.24, p = 0.02), compared with moderate HGI. We found a U-shaped association between HGI and the prognosis.Conclusion Both low HGI and high HGI was associated with an increased risk of poor prognosis in diabetic patients with ischemic stroke, compared with moderate HGI.

Early Increased Bradykinin 1 Receptor Contributes to Hemorrhagic Transformation After Ischemic Stroke in Type 1 Diabetic Rats.

Hemorrhagic transformation (HT) is a major complication of ischemic stroke and further deteriorates neurological outcomes. Bradykinin 1 receptor (B1R) has been proven to mediate vasculo-toxicity in various experimental models. However, its role in the development of HT after stroke remains unclear. We detected the B1R expression in brain tissues with or without HT in a rat model of cerebral ischemia/reperfusion (I/R) with type 1 diabetes, showing higher B1R expression in the hemorrhagic areas than the ischemic tissues. Then, B1R agonist or antagonist was administrated intravenously just before reperfusion to investigate its effect on HT and the underlying molecular mechanism. Administration of low (300nmol/kg) or high (1μmol/kg) dose of B1R antagonist mitigated hemorrhage, improved neurobehavioral deficits, and preserved blood-brain-barrier (BBB) integrity after reperfusion for 8h whereas the 300nmol/kg of B1R agonist aggravated these outcomes, though only the high does of B1R antagonist affected the infarction volume. Extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation was increased by B1R activation but decreased by B1R inhibition, which mediated B1R toxicity on BBB disruption and ischemia-related HT. Furthermore, B1R activation facilitated the mRNA and protein expressions of MMP-9 in the hemorrhagic tissues, and these increases were blocked by both ERK inhibitor U0126 and NF-κB inhibitor PDTC. U0126 also remarkably decreased the B1R-induced NF-κB/p65 activation. We concluded that upregulated B1R may contribute to early HT after I/R in type 1 diabetic rats via ERK1/2/NF-κB/MMP-9 pathway. B1R inhibition could be an encouraging therapeutic strategy to withstand HT after ischemic stroke in diabetic patients.

Relationship between serum uric acid and ischemic stroke in a large type 2 diabetes population in China: A cross-sectional study

ObjectiveTo investigate the relationship of serum UA and ischemic stroke in type 2 diabetes patients in China. MethodWe examined the above relationship using the data of the project “Comprehensive Research on the Prevention and Control of the Diabetes” (CRPCD) study. A total of 19,442 participants were enrolled in the cross-sectional study. The enrolled participants were divided into quintiles of the serum UA levels with cut off values for two age groups (<60 versus ≥60years). Binary logistic regression analyses were used to evaluate whether the levels of serum UA were independently associated with ischemic stroke in type 2 diabetes. ResultsThe serum UA levels were significantly higher in the participants with age≥60years than those with age<60years (P=0.000). In the age group of <60years, the odds ratio for ischemic stroke with type 2 diabetes in quintile 5 over quintile 1 was 2.420 (95% CI, 1.566–3.470) in the unadjusted model and 1.765 (95% CI, 1.097–2.840) after controlling potential confounders. However, the reverse results were observed in the age group of ≥60years. The odds ratio in quintile 4 over quintile 1 in model 3 and model 4 were 0.767 (95% CI, 0.630–0.934) and 0.782 (95% CI, 0.640–0.957). ConclusionOur results indicated that serum UA levels were independently positively associated with ischemic stroke in patients aged <60years, but the association was U-shaped in patients aged ≥60years.

Long-term evaluation of neurological impairment scales after ischemic stroke in type 2 diabetic Caucasians

Long-term evaluation of neurological impairment scales after ischemic stroke in type 2 diabetic Caucasians

Clinical Profile of Ischemic Stroke in Type 2 Diabetic Patients: Experience in a Tertiary Care Hospital

Background: Stroke is the third highest cause of morbidity and mortality in the world. Diabetes mellitus increases risk of ischemic stroke. Stroke in diabetic patients is different from stroke in non-diabetics in several perspectives. This cross-sectional study was carried out to observe clinical profile of ischemic stroke in Type 2 diabetic patients.Materials and Methods: This cross-sectional observational study was done in the Department of Neurology, BIRDEM General Hospital from April to September, 2010. Non-probability purposive sampling was used.Results: A total number of 50 subjects were included, all were hospitalized ischemic stroke with type- 2 diabetic patient. Maximum number (36.0%) of the patients was in between 61 to 70 years age group with mean age 59.9 ±13.9 years. There was male predominance and male-female ratio was1.5: 1. Majority of the patient (50%) noticed features of stroke at morning (6 am-12.00 noon).Regarding risk factor profile, 35(70%) had uncontrolled DM, 35(70%) used to lead sedentary lifestyle, 30(60%) had history of tobacco use, 20(40%) had Obesity and 42(84%) were hypertensive. A Few cases 5 (10%) were alcoholic. Most (90%) of the patients admitted with weakness at either half of body. Some had difficulties in speech (80%), altered consciousness (24%), difficulties in swallowing (4%); rest of the patients had facial weakness (4%) and others (2%). 94.0% patient had regular pulse, 6% had irregular pulse. 80.0% had high blood pressure on admission. Mean systolic and diastolic blood pressure was 153± 5.3 mm of Hg and 97±4.4 mm of Hg respectively. 40.0% patient had abnormal fundoscopy (Diabetic and/or hypertensive retinopathy). Carotid bruit was found in 2% case but one had sign of dyslipidaemia. 76% was conscious and oriented, 24%altered conscious level, 90% had hemiplegia or hemiparesis, 72% had dysarthria, 4% had dysphasia and 16% others.Conclusion: Elderly and male people are more prone to develop ischemic stroke. Hemiparesis or hemiplegia, dysarthria is the major clinical presentation and high blood pressure is an important risk factor for ischemic stroke. Further study can be done to compare the clinical profile between diabetic and non-diabetic populations.Birdem Med J 2015; 5(2): 88-91

Sitagliptin After Ischemic Stroke in Type 2 Diabetic Patients: A Nationwide Cohort Study.

The cerebrovascular safety and efficacy of sitagliptin, a dipeptidyl peptidase-4 inhibitor, in patients with type 2 diabetes mellitus (T2DM) with ischemic stroke remains uncertain. The aim of this study was to assess the efficacy and safety of sitagliptin in patients with T2DM with recent ischemic stroke. We analyzed data from the Taiwan National Health Insurance Research Database between March 1, 2009, and December 31, 2011. Ischemic stroke patients were identified from individuals with T2DM. Patients who received sitagliptin were compared with those who did not to evaluate the cardiovascular safety and efficacy of sitagliptin. The primary outcome was a composite of ischemic stroke, myocardial infarction, or cardiovascular death. A total of 5145 type 2 diabetic patients with ischemic stroke met our inclusion criteria and were followed for up to 2.83 years (mean, 1.17 years). Overall, 1715 patients (33.3%) received sitagliptin and 3430 patients (66.7%) did not. The primary composite outcome occurred in 190 patients in the sitagliptin group (11.1%) and in 370 patients in the comparison group (10.8%) (hazard ratio [HR] = 1.02; 95% confidence interval [CI], 0.85-1.21). Patients treated with sitagliptin had a similar risk of ischemic stroke, hemorrhagic stroke, and all-cause mortality with an HR of 0.95 (95% CI, 0.78-1.16, P = 0.612), 1.07 (95% CI, 0.55-2.11, P = 0.834), and 1.00 (95% CI, 0.82-1.22, P = 0.989), respectively, compared with patients not treated with sitagliptin. Treatment with sitagliptin in type 2 diabetic patients with recent ischemic stroke was not associated with increased or decreased risks of adverse cerebrovascular outcomes.

Poor Outcome of Experimental Ischemic Stroke in Type 2 Diabetic Rats: Impaired Circulating Endothelial Progenitor Cells Mobilization

It is well accepted that type 2 diabetic mellitus (T2DM) results in the poor outcome of ischemic stroke. However, the mechanisms by which T2DM causes aggravated cerebral ischemic/reperfusion (I/R) injury are not clear. Recently, endothelial progenitor cells (EPCs) are considered to be related with the outcome of ischemic stroke. More importantly, T2DM can affect the function of circulating EPCs. This study tried to investigate whether T2DM worsens the cerebral I/R injury via affecting circulating EPCs. We used high-fat diet-fed and low-dose streptozotocin-treated male rats receiving middle cerebral artery occlusion surgery as animal model of focal cerebral I/R injury with T2DM (diabetic operated). And the rats were divided into 4 groups: normal sham, diabetic sham, normal operated, and diabetic operated. We measured the circulating EPCs counts and the levels of vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) in peripheral plasma of 4 groups. We found that diabetic rats subjected to I/R exhibited significantly severe deterioration in neurologic deficits compared with nondiabetic counterparts, which manifested higher infarct volume and cell apoptosis as well as lower neurologic defective score. There was no significant difference on the plasma glucose of groups before cerebral I/R injury compared with that of the groups posterior to cerebral I/R injury despite cerebral I/R injury had the tendency to increase the plasma glucose no matter in the presence or the absence of T2DM. In addition, there were the marked downregulation of circulating EPCs counts and the levels of VEGF and eNOS in diabetic rats before the cerebral I/R injury. Despite I/R injury without T2DM, there was a significant increase in the circulating EPCs counts, the circulating EPCs counts in I/R injury with T2DM group were significantly decreased compared with those in the other 3 groups. We also observed that the level of eNOS was significantly improved by I/R injury without considering the presence of T2DM. Thus, our present study suggested that it might be the impaired EPCs mobilization into theblood that contributed to the worse outcome of cerebral I/R injury with T2DM.

Visit-to-visit variability of fasting plasma glucose as predictor of ischemic stroke: competing risk analysis in a national cohort of Taiwan Diabetes Study.

BackgroundGlycemic variation as an independent predictor of ischemic stroke in type 2 diabetic patients remains unclear. This study examined visit-to-visit variations in fasting plasma glucose (FPG), as represented by the coefficient of variation (CV), for predicting ischemic stroke independently, regardless of glycated hemoglobin (HbA1c) and other conventional risk factors in such patients.MethodsType 2 diabetic patients enrolled in the National Diabetes Care Management Program, ≥30 years old and free of ischemic stroke (n = 28,354) in 2002 to 2004 were included, and related factors were analyzed with extended Cox proportional hazards regression models of competing risk data on stroke incidence.ResultsAfter an average 7.5 years of follow-up, there were 2,250 incident cases of ischemic stroke, giving a crude incidence rate of 10.56/1,000 person-years (11.64 for men, 9.63 for women). After multivariate adjustment, hazard ratios for the second, third and fourth versus first FPG-CV quartile were 1.11 (0.98, 1.25), 1.22 (1.08, 1.38) and 1.27 (1.12, 1.43), respectively, without considering HbA1c, and 1.09 (0.96, 1.23), 1.16 (1.03, 1.31) and 1.17 (1.03, 1.32), respectively, after considering HbA1c.ConclusionsBesides HbA1c, FPG-CV was a potent predictor of ischemic stroke in type 2 diabetic patients, suggesting that different therapeutic strategies now in use be rated for their potential to (1) minimize glucose fluctuations and (2) reduce HbA1c level in type 2 diabetic patients to prevent ischemic stroke.

Increased Risk of Ischemic Stroke after Hyperosmolar Hyperglycemic State: A Population-Based Follow-Up Study

BackgroundAlthough much attention has been focused on the association between chronic hyperglycemia and cerebrovascular diseases in type 2 diabetes mellitus (DM) patients, there is no data regarding the risk of ischemic stroke after a hyperosmolar hyperglycemic state (HHS) attack. The objective of this study was to investigate the risk of ischemic stroke in type 2 DM patients after an HHS attack.MethodsFrom 2004 to 2008, this retrospective observational study was conducted on a large cohort of Taiwanese using Taiwan’s National Health Insurance Research Database (NHIRD). We identified 19,031 type 2 DM patients who were discharged with a diagnosis of HHS and 521,229 type 2 DM patients without an HHS diagnosis. Using the propensity score generated from logistic regression models, conditional on baseline covariates, we matched 19,031 type 2 DM patients with an HHS diagnosis with the same number from the comparison cohort. The one-year cumulative rate for ischemic stroke was estimated using the Kaplan-Meier method. After adjusting covariates, Cox proportional hazard regression was used to compute the adjusted one-year rate of ischemic stroke.ResultsOf the patients sampled, 1,810 (9.5%) of the type 2 DM patients with HHS and 996 (5.2%) of the comparison cohort developed ischemic stroke during the one-year follow-up period. After adjusting for covariates, the adjusted HR for developing ischemic stroke during the one-year follow-up period was 1.8 (95% C.I., 1.67 to 1.95, P<0.001) for type 2 DM patients with HHS compared with those without HHS.ConclusionAlthough DM is a well-recognized risk factor for atherosclerosis, type 2 DM patients that have suffered a HHS attacks are at an increased risk of developing ischemic stroke compared with those without HHS.

Neamine induces neuroprotection after acute ischemic stroke in type one diabetic rats

IntroductionAngiogenin is a member of the ribonuclease superfamily and promotes degradation of the basement membrane and the extracellular matrix. After stroke in type one diabetes (T1DM) rats, Angiogenin is significantly increased and the Angiogenin is inversely correlated with functional outcome. Neamine, an aminoglycoside antibiotic, blocks nuclear translocation of Angiogenin, thereby abolishing the biological activity of Angiogenin. In this study, we therefore investigated the effect and underlying protective mechanisms of Neamine treatment of stroke in T1DM. MethodsT1DM was induced in male Wistar rats by streptozotocin (60mg/kg, ip), and T1DM rats were subjected to embolic middle cerebral artery occlusion (MCAo). Neamine (10mg/kg ip) was administered at 2, 24 and 48h after the induction of embolic MCAo. A battery of functional outcome tests was performed. Blood–brain barrier (BBB) leakage, and lesion volume were evaluated and immunostaining, and Western blot were performed. ResultsNeamine treatment of stroke in T1DM rats significantly decreased BBB leakage and lesion volume as well as improved functional outcome compared to T1DM-control. Neamine also significantly decreased apoptosis and cleaved caspase-3 in the ischemic brain. Using immunostaining, we found that Neamine treatment significantly decreased nuclear Angiogenin, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) activity, advanced glycation endproducts receptor (RAGE) number, the positive area of toll-like receptor 4 (TLR4) and increased Angeopoietin-1 expression compared to T1DM-MCAo control rats. Western blot results are consistent with the immunostaining. ConclusionNeamine treatment of stroke is neuroprotective in T1DM rats. Inhibition of neuroinflammatory factor expression and decrease of BBB leakage may contribute to Neamine-induced neuroprotective effects after stroke in T1DM rats.

Association of Serum Triglycerides in Patients with Ischaemic Stroke Admitted in Hospital with type-2 Diabetes Patients

Background and Aims: Diabetes mellitus and dyslipidemia, in particular triglyceridemia pose independent risk factors of stroke. Hypertriglyceridemia implicated in the pathogenesis of ischemic stroke by imparting endothelial dysfunction, oxidative stress and lowering fibrinolytic activity. This study was aimed to explore risk incurred by blood triglyceride level for ischemic stroke in type 2 diabetic patients.&#x0D; Materials and Methods: A total number of 80 [50 with acute ischemic stroke and 30 without stroke] type 2 diabetic patients consecutively admitted in the neurology department, during the period of April to September 2012, fulfilling the recruitment criteria were included in the study. Ischemic stroke was confirmed by CT-scan. Informed written consent from the legal attendant of each patient was obtained. Data regarding clinicobiochemical and images studies were retrieved from patient’s record form.&#x0D; Results: Male to female ratio was 1.2:1 of the study subjects. Mean (±SD) age (yrs) was 61.0±10.6 in patients with ischemic stroke (Group I) and 57.0±12.3 in patients without stroke (Group II). Risk factors like BMI, lifestyle, smoking, alcohol intake did not show any statistical significance with incidence of ischemic stroke. Mean (±SD) triglyceride (mg/ dl) was 241±56 and 217±102 in Group I and Group II respectively (p=0.024). Eighty eight percent patients had triglyceride 150 mg/dl in Group I and 70 percent in Group II. Triglyceride level (mean±SD, mg/dl) was significantly higher (335±101) in overweightobese patients (BMI 25 Kg/m2) compared to those (232±68) with normal body weight (BMI&lt;25 Kg/m2). Triglyceride level did not show statistical difference among patients having habit of smoking or not. Mean (±SD) cholesterol (mg/dl, (±SD) was 197±62 and 165±26 in Group I and Group II respectively (p=0.009). Mean (±SD) LDL-c (mg/dl) was 101±45 and 98±42 in Group I (43.8±34.4) compared to Group II (60.2±15.6) (p=0.017). Patients with atherosclerotic changes had significantly higher triglyceride (mean±SD, mg/dl) level (338±155) compared to those without (228±89) (p=0.047).&#x0D; Conclusions: Data concluded that hypertriglyceridemia is relatively common among the diabetic patients even in patients with apparently good glycemic control and possibly incur added risk for ischemic stroke in these patients. However, further studies are needed involving optimum number of patients to substantiate this finding and conclusively comment on the issue and to design effective prevention program to reduce the cerebrovascular morbidity and mortality.&#x0D; Bangladesh Journal of Neuroscience 2013; Vol. 29 (2) : 98-107

Presenting Features of lschaemic Stroke Patients with Type 2 Diabetes during Hospital Admission at BIRDEM

Background &amp; objective: Stroke is the third major cause of morbidity and mortality in the world immediately following ischemic heart disease and malignancy. Diabetes mellitus increases risk of ischemic stroke and mortality and morbidity after stroke. This cross sectional study was carried out to observe clinical profile of ischemic stroke in Type 2 diabetic patient.&#x0D; Materials &amp; Methods: This cross-sectional study was done in the Department of Neurology, Bangladesh Institute of Research and Rehabilitation for Diabetes, Endocrine, and Metabolic Disorders (BIRDEM) Hospital, from April to September 2010. A total of 50 ischemic stroke patients with type-2 diabetes were consecutively recruited. Ischemic stroke was confirmed by clinical examination and CT imaging. Data were analysed using SPSS (Statistical Package for Social Sciences) and were presented as mean ± SD and frequencies with corresponding percentages as appropriate.&#x0D; Results: Of the 50 ischemic patients, over one-third (36%) was in their 6th decades of life. A male preponderance (1.5:1) in the series. Most of the patients presented with weakness on either side of the body (90%) followed by difficulties in speech (80%), altered consciousness (24%) and facial weakness (4%). On examination 76% were conscious and oriented. Other examination findings were hemiparesis (60%), hemiplegia (30%), dysarthria (72%) and dysphagia (4%). The major co-morbid condition was hypertension (86%) with mean systolic and diastolic blood pressures being 153 ± 5 and 97 ± 4 mmHg respectively. On admission 94% had normal pulse and 40% abnormal fundoscopic examination in the form of hypertensive and diabetic retinopathy. Only 2% had carotid bruit.&#x0D; Conclusion: Elderly males are more prone to develop ischemic stroke. Hemiparesis and dysarthria are the major clinical presentation and hypertension might be an important risk factor for ischemic stroke. Further study is recommended to conclusively comment on the clinical features of diabetic ischemic stroke patients and also to compare the clinical profile between diabetic stroke patients.&#x0D; Ibrahim Cardiac Med J 2012; 2(2): 14-18