Inversão total do fluxo em artéria carótida interna direita em paciente com estenose grave do tronco braquiocefálico / Total reversal of internal carotid blood flow in a patient with severe stenosis of the brachiocephalic trunk

RESUMO As estenoses graves e oclusões do tronco braquiocefálico (artéria inominada) são raras, e apresentam uma grande variedade de manifestações clínicas, com alterações relacionadas a isquemia cerebral hemisférica, vertebrobasilar e de membro superior direito. A causa mais comum é a aterosclerose. A ultrassonografia vascular com Doppler pode revelar inversão de fluxo na artéria vertebral direita, hipofluxo na subclávia, e vários tipos de alterações no fluxo da carótida direita, incluindo hipofluxo, inversão parcial do fluxo durante o ciclo cardíaco, e até mesmo inversão completa do fluxo na carótida interna, achado este bastante raro. Os autores descrevem o caso de paciente do sexo feminino, tabagista, com estenose grave do tronco braquiocefálico e crises de lipotimia. Além do roubo de artéria subclávia e do fluxo parcialmente invertido na carótida comum direita, a paciente apresentava exuberante fluxo invertido na carótida interna durante todo o ciclo cardíaco, achado este não encontrado na literatura em tamanha magnitude.

ABSTRACT Occlusions and severe stenoses of the innominate artery (brachiocephalic trunk) are rare and present with a wide variety of clinical manifestations, with hemispheric, vertebrobasilar and right upper limb ischemic symptoms. The most common cause is atherosclerosis. Duplex scanning may show right vertebral artery flow reversal, diminished subclavian flow, and several patterns of right carotid flow disturbance, including slow flow, partial flow reversal during the cardiac cycle and even complete reversal of flow in the internal carotid artery, which is a very uncommon finding. Herein, the authors describe the case of a female patient who was a heavy smoker, had severe stenosis of the brachiocephalic trunk, and had episodes of collapse. Besides the subclavian steal and partial flow reversal in the common carotid artery, duplex scanning also showed high-velocity reversed flow in the internal carotid artery during the entire cardiac cycle, a finding that is not reported in the literature at this magnitude.

Analysis of Caspase-9 protein and microRNAs miR-21, miR-126 and miR-155 related to the apoptosis mechanism in the cerebellum of rats submitted to focal cerebral ischemia associated with an alcoholism model / Análise da proteína Caspase-9 e dos microRNAs miR-21, miR-126 e miR-155 relacionados ao mecanismo de apoptose no cerebelo de ratos submetidos à isquemia cerebral focal associada ao modelo de alcoolismo

ABSTRACT This study aimed to analyze the cerebellum of rats submitted to an experimental focal cerebral ischemia, by middle cerebral artery occlusion for 90 minutes, followed by reperfusion for 48 hours, associated with an alcoholism model. Methods Fifty adult Wistar rats were used, subdivided into five experimental groups: control group (C): animals submitted to anesthesia only; sham group (S): animals submitted to complete simulation of the surgical procedure; ischemic group (I): animals submitted to focal cerebral ischemia for 90 minutes followed by reperfusion for 48 hours; alcoholic group (A): animals that received daily absolute ethanol diluted 20% in water for four weeks; and, ischemic and alcoholic group (I + A): animals receiving the same treatment as group A and, after four weeks, submitted to focal cerebral ischemia for 90 minutes, followed by reperfusion for 48 hours. The cerebellum samples were collected and immunohistochemical analysis of Caspase-9 protein and serum analysis by RT-PCR of microRNAs miR-21, miR-126 and miR155 were performed. Results The expression of Caspase-9 was higher in groups I, A and I + A. In the microRNAs analyses, miR-126 was higher in groups A and I + A, miR-155 was higher in groups I and I + A. Conclusions We conclude that apoptosis occurs in the cerebellar cortex, even if it is distant from the ischemic focus, and that microRNAs 126 and 155 show a correlation with cellular apoptosis in ischemic rats and those submitted to the chronic alcohol model.

RESUMO O objetivo deste estudo foi analisar o cerebelo de ratos submetidos à isquemia cerebral focal experimental, por oclusão da artéria cerebral média por 90 minutos, seguida de reperfusão por 48 horas, associada a um modelo de alcoolismo. Métodos Foram utilizados 50 ratos Wistar adultos, subdivididos em cinco grupos experimentais: grupo controle (C): animais submetidos apenas à anestesia; grupo sham (S): animais submetidos à simulação completa do procedimento cirúrgico; grupo isquêmico (I): animais submetidos à isquemia cerebral focal por 90 minutos, seguidos de reperfusão por 48 horas; grupo alcoólico (A): animais que receberam etanol absoluto diário diluído em 20% em água por quatro semanas; e grupo isquêmico e alcoólico (I + A): animais que recebem o mesmo tratamento do grupo A e, após quatro semanas, submetidos à isquemia cerebral focal por 90 minutos, seguidos de reperfusão por 48 horas. As amostras de cerebelo foram coletadas e a análise imuno-histoquímica da proteína Caspase-9 e a análise sérica por RT-PCR dos microRNAs miR-21, miR-126 e miR155 foram realizadas. Resultados A expressão de Caspase-9 foi maior nos grupos I, A e I + A. Nas análises de microRNAs, o miR-126 foi maior nos grupos A e I + A, o miR-155 foi maior nos grupos I e I + A. Conclusões Concluímos que a apoptose ocorre no córtex cerebelar, mesmo distante do foco isquêmico, e que os microRNAs 126 e 155 mostram uma correlação com a apoptose celular em ratos isquêmicos e submetidos ao modelo crônico de álcool.

Hypothermia treatment ameliorated cyclin-dependent kinase 5-mediated inflammation in ischemic stroke and improved outcomes in ischemic stroke patients

OBJECTIVES: The inflammatory response is a key mechanism of neuronal damage and loss during acute ischemic stroke. Hypothermia has shown promise as a treatment for ischemic stroke. In this study, we investigated the molecular signaling pathways in ischemic stroke after hypothermia treatment. METHODS: Cyclin-dependent kinase 5 (CDK5) was overexpressed or silenced in cultured cells. Nuclear transcription factor-κB (NF-κB) activity was assessed by measurement of the luciferase reporter gene. An ischemic stroke model was established in Sprague-Dawley (SD) rats using the suture-occluded method. Animals were assigned to three groups: sham operation control, ischemic stroke, and ischemic stroke + hypothermia treatment groups. Interleukin 1β (IL-1β) levels in the culture supernatant and blood samples were assessed by ELISA. Protein expression was measured by Western blotting. RESULTS: In HEK293 cells and primary cortical neuronal cultures exposed to hypothermia, CDK5 overexpression was associated with increased IL-1β, caspase 1, and NF-κB levels. In both a murine model of stroke and in patients, increased IL-1β levels were observed after stroke, and hypothermia treatment was associated with lower IL-1β levels. Furthermore, hypothermia-treated patients showed significant improvement in neurophysiological functional outcome. CONCLUSIONS: Overall, hypothermia offers clinical benefit, most likely through its effects on the inflammatory response.

Mecobalamin and early functional outcomes of ischemic stroke patients with H-type hypertension

SUMMARY OBJECTIVE To analyze the effect of mecobalamin on the early-functional outcomes of patients with ischemic stroke and H-type hypertension. METHODS From October of 2014 to October of 2016, 224 cases of ischemic stroke and H-type hypertension were selected. The patients were randomly divided into treatment control groups, with 112 patients in each group. The control group was treated with the conventional therapy. The observation group was treated with 500 µg of mecobalamin three times a day in addition to the conventional therapy. We compared serum homocysteine (Hcy), hs-CRP levels, carotid plaques, and NIHSS scores between the two groups on the 2nd day and at 4 weeks, 8 weeks, 3 months, and 6 months. RESULTS After 4 weeks, 8 weeks, 3 months and 6 months, the difference of serum Hcy level between the two groups was statistically significant (t = 4.049, 3.896, 6.052, 6.159, respectively. All P <0.05). After the treatment, at 4 weeks, 8 weeks, 3 months and 6 months, the levels of hs-CRP in the treatment group were significantly lower than those in the control group (t = 37.249, 28.376, 26.454, 20.522, respectively. All P <0.01). After 3 months and 6 months, the carotid artery plaques were significantly reduced in the treatment group compared to those in the control group (t = 2.309 and 2.434. All P <0.05). After 3 months and 6 months, the NIHSS score was significantly higher in the treatment group compared to those in the control group (t = 2.455 and 2.193. All P <0.05). CONCLUSION Mecobalamin can reduce the level of plasma homocysteine, then lead to reductions of levels of plasma inflammatory factors and volume of carotid artery plaques, resulting in more significant functional recovery.

RESUMO OBJETIVO Analisar o efeito de mecobalamin sobre os primeiros resultados funcionais de pacientes com AVC isquêmico e hipertensão H-type. MÉTODOS De outubro de 2014 a outubro de 2016, 224 casos de AVC isquêmico e hipertensão H-type foram selecionadas. Os pacientes foram divididos aleatoriamente em grupo de tratamento e grupo controle, com 112 doentes em cada grupo. O grupo controle foi tratado com a terapia de rotina. O grupo de observação foi tratado com 500 µg de mecobalamin três vezes por dia, além da rotina de tratamento. No segundo dia, 4 semanas, 8 semanas, 3 meses e 6 meses, comparamos níveis séricos da homocisteína (Hcy) e de hs-CRP, placas da carótida e pontuações NIHSS entre os dois grupos. RESULTADOS Após 4 semanas, 8 semanas, 3 meses e 6 meses, a diferença dos níveis séricos de Hcy entre os dois grupos foi estatisticamente significativa (t= 4,049, 3,896, 6,052, 6,159, respectivamente. Todos os P<0,05). Após o tratamento de 4 semanas, 8 semanas, 3 meses e 6 meses, os níveis de hs-CRP no grupo de tratamento foram significativamente inferiores aos do grupo controle (t=37,249, 28,376, 26,454, 20,522, respectivamente. Todos os P<0,01). Depois de 3 meses e 6 meses, as placas da artéria carótida foram significativamente reduzidas no tratamento, em comparação com os do grupo controle (t=2,309 e 2,434. Todos os P<0,05). Depois de 3 meses e 6 meses, as pontuações NIHSS foram significativamente mais elevadas no tratamento em comparação com as do grupo controle (t=2,455 e 2,193. Todos os P<0,05). CONCLUSÃO Mecobalamin pode reduzir o nível de homocisteína plasmática, o que conduz à redução dos níveis de plasma inflamatórios e do volume das placas na artéria carótida, resultando em maior recuperação funcional.

Apo B/Apo A-I ratio in central and peripheral arterial diseases

BACKGROUND: The apo B/apo A-I ratio represents the balance between atherogenic particles, rich in apo B, and the antiatherogenic ones, apo A-I rich. This study investigated the association between atherosclerotic diseases in different anatomical sites and apo B/apo A-I ratio. METHODS: Lipids, lipoproteins, and apolipoproteins A-I and B were assessed in 30 subjects with coronary artery disease (CAD), 26 with ischemic stroke (IS), 30 with peripheral arterial obstructive disease (PAOD), and 38 healthy subjects (controls). RESULTS: HDLc and Apo A-I were significantly lower in PAOD and CAD groups, respectively, than in other groups. Significantly higher levels of triglycerides were observed for CAD and PAOD groups than for controls. Apo B was significantly higher in IS group than in control and PAOD groups. The apo B/apo A-I ratio showed significantly higher in CAD and IS groups when compared to control and PAOD groups (p < 0.001). CONCLUSION: The apo B/apo A-I ratio was important for identifying an increased trend for coronary and cerebral atherosclerosis. In spite of the increased trend for apo B/apo A-I ratio in IS and CAD groups, the studied variables cannot be considered in an isolated way, given as those parameters were analyzed together by a binary logistic regression, no association has been demonstrated.

INTRODUÇÃO: O índice apo B/apo A-I representa o balanço entre partículas de colesterol potencialmente aterogênicas ricas em apo B e partículas anti-aterogênicas ricas em apo A-I. O objetivo deste estudo foi investigar a associação entre doenças ateroscleróticas em diferentes sítios anatômicos e o índice apo B/apo A-I. MÉTODOS: Lípides, lipoproteínas e apolipoproteínas A-I e B foram quantificados em 30 indivíduos apresentando doença arterial coronariana (DAC), 26 com acidente vascular cerebral (AVC), 34 apresentando doença arterial obstrutiva periférica (DAOP) e 38 indivíduos hígidos (grupo controle). RESULTADOS: HDLc e apo A-I apresentaram-se significativamente mais baixos nos grupos DAOP e DAC, respectivamente, quando comparados com os demais grupos. Níveis de triglicérides foram significativamente mais elevados nos grupos DAC e PAOD quando comparados com o grupo controle. Apo B foi significativamente mais elevada no grupo AVC quando comparado com os grupos controle e DAOP. O índice apo B/apo A-I se mostrou significativamente elevado nos grupos DAC e AVC quando comparados com os demais (p < 0,001). CONCLUSÃO: O índice apo B/apo A-I foi importante para identificar uma tendência aumentada para aterosclerose coronariana e cerebral. No entanto, os parâmetros avaliados não podem ser considerados de forma isolada, considerando que nenhuma associação foi demonstrada quando os dados foram analisados pelo modelo de regressão logística binária.

Plasma homocysteine and ischemic stroke patients in Thailand.

BACKGROUND: Hyperhomocysteinemia was recently found to be a risk factor for stroke; however, the available data from Thailand is scarce. OBJECTIVE: To study plasma homocysteine levels in ischemic stroke and compare it with age-and sex-matched controls, and to identify the association of plasma homocysteine and subtype of stroke. MATERIAL AND METHOD: The authors studied plasma homocysteine levels of ischemic stroke patients with clinical signs and symptoms of stroke as confirmed by CT scan and compared them with control subjects who presented with other diseases and no clinical signs and symptoms of stroke between June 2000- May 2001 in Prasat Neurological institute. Fasting plasma homocysteine was measured by HPLC technique. Abnormal cut off point of plasma homocysteine was identified and associations of plasma homocysteine and stroke were studied by using logistic regression analyses. RESULTS: Two hundred and sixty-eight patients were recruited in the present study (132 controls and 136 ischemic stroke patients). The abnormal cut off point of plasma homocysteine was > 14 micromol/L. The authors found statically significant association of abnormal plasma homocysteine and stroke (p<0.001) with odds ratio of 4.277 (95%CI 2.551-7.171). After adjusting the confounding factor the authors found that high homocysteine was significantly associated with ischemic stroke (p<0.001) with odd ratio of 3.401 (95%CI 1.954-5.922). In the subgroup analyses of type of stroke and abnormal homocysteine, the authors demonstrated that abnormal homocysteine levels were more pronounced in the large vessel subtype than the small group. CONCLUSION: Abnormal homocysteine level is an independent risk factor of ischemic stroke and more correlated with large vessel subtype.

Role of serum fibrinogen in patients of ischemic cerebrovascular disease.

Fibrinogen is an independent risk factor for coronary events in population-based studies and inpatients with coronary heart disease, but there is an uncertainty about its prediction for stroke, particularly in secondary prevention. In view of this uncertainty, study was conducted to establish the role of serum fibrinogen in ischemic stroke. Fifty six patients with acute ischemic stroke of less than 7 days duration were recruited for the study. Fourty two age and sex matched candidates served as control. Baseline characteristics and blood pressure were recorded at admission to hospital. Computer tomography head was done in all patients as per protocol. Sampling took place in the early morning (7-9 AM) using all necessary precaution and serum fibrinogen was measured by method of Clauss. Statiscal analysis was performed using student t test and fisher exact test. In present study, mean plasma fibrinogen in patients group was 326.45 mg/dl, which was significantly higher than control group (202.23 mg/dl) (p<0.001). Mean plasma fibrinogen level in lacunar infarct and non-lacunar infarct did not differ significantly (307.47 mg/dl Vs. 333.19 mg/dl). Smoking was found to be a significant predictor of fibrinogen with 36.7% predictability whereas other parameters (risk factors for ischemic stroke) had little or no predictable value regarding serum fibrinogen. After adjustment for other possible ischemic stroke risk factors; plasma fibrinogen levels was found to be still significantly high in patients as compared to controls (p<0.001). Mean plasma fibrinogen level between patients who survived and who expired does not differ significantly. Present study concluded that fibrinogen is a powerful predictor of ischemic stroke though it does not predict the type and prognosis of stroke.

Modelling of increased homocysteine in ischaemic stroke: post-hoc cross-sectional matched case-control analysis in young patients

BACKGROUND & PURPOSE: Hyperhomocysteinaemia has been postulated to participate in pathogenesis of ischaemic stroke (IS). However, especially in young adults, there is possibility of significantly increased IS risk due to increased ænormalÆ homocysteinaemia, i.e., æhiddenÆ (æpathologically dormantÆ) prevalence within a healthy, normally-defined range. We performed a post-hoc modelling investigation on plasma total homocysteinaemia (THCY) in gender- and age-matched young patients in the acute IS phase. We evaluated relationships between THCY and prevalence of other potential risk factors in 41 patients vs. 41 healthy controls. METHOD: We used clinical methods, instrumental and neuroimmaging procedures, risk factors examination, total plasma homocysteine measurements and other laboratory and statistical modelling techniques. RESULTS: IS patients and healthy controls were similar not only for matching variables, but also for smoking, main vitamin status, serum creatinine and lipid profile. Patients with IS, however, had lower vitamin B6 levels and higher THCY, fibrinogen and triglycerides (TGL). At multivariate stepwise logistic regression only increased THCY and TGL were significantly and independently associated with the risk for stroke (72 percent model accuracy, p model=0.001). An increase of THCY with 1.0 æmol/L was associated with 22 percent higher risk of ischaemic stroke [adjusted OR=1.22 (95 percentCI 1.03?1.44)]. In this way, novel lower cut-off value for HCY of 11.58 æmol/L in younger patients has been revealed (ROC AUC= 0.67, 95CI percent 0.55-0.78, p=0.009). CONCLUSION: The new THCY cut-off clearly discriminated between absence and presence of IS (sensitivity>63 percent, specificity>68 percent) irrespectively of age and gender and may be applied to better evaluate and more precisely define, as earlier as possible, the young patients at increased IS risk.

OBJETIVO: Hiperhomocisteinemia tem sido postulada como um dos fatores de risco na patogênese do acidente vascular cerebral isquêmico (AVCI). Todavia, em adultos jovens existe a possibilidade de aumento significativo de risco de AVCI devido a aumento "normal" da homocisteinemia, "oculta" (patologicamente adormecida) dentro de uma variação definida como normal. Neste trabalho foi investigado um modelo post-hoc de dosagem de homocisteina no plasma (HC) em pacientes jovens com AVCI agudo pareados por gênero e idade. Foi avaliado também relações entre HC e prevalência de outros fatores de risco para AVCI em 41 pacientes e 41 controles normais. MÉTODO: Foi utilizado exame clínico, procedimentos instrumentais e de neuroimagem, exame de fatores de risco, dosagem da homocisteína no plasma, outros exames laboratoriais e análise estatística. RESULTADOS: Não foram encontradas diferenças quanto a presença de fumantes, dosagem de vitaminas, creatinina sérica e perfil lipídico entre os pacientes com AVCI e os controles normais. Todavia os pacientes com AVCI apresentaram diminuição de níveis de vitamina B6 e aumento de homocisteína, fibrinogênio e trigliceridios. A análise multivariada de regressão logística mostrou diferenças significativas apenas para HC e trigliceridios independentemente associadas para fatores de risco para AVCI (72 por cento acuracia, p= 0,001). Um aumento de homocisteína de 1,0 æmol/L estava associado com aumento de 22 por cento de risco de AVCI [OR=1,22 (95 por centoIC 1,03-1,44)]. Foi evidenciado portanto um novo valor de cut-off para HC de 11,58 æmol/L em pacientes jovens com AVCI (ROC auc=0,67, 95 por cento IC 0,55-0,78, p= 0,009). CONCLUSÃO: Este novo valor de cut-offpara a homocisteína discrimina claramente a ausência ou presença de AVCI (sensibilidade >63 por cento, especificidade >68 por cento) independente do gênero ou idade e deve ser aplicado para uma melhor avaliação precoce de pacientes jovens com risco de AVCI.

Inflammatory markers and conventional atherosclerotic risk factors in acute ischemic stroke: comparative study between vascular disease subtypes.

BACKGROUND: Large vessel atherosclerosis and small vessel disease are two major causes of ischemic stroke. In patients with large vessel disease, the lesions can be located in the extracranial carotid or intracranial arteries. OBJECTIVE: To search for the differences of risk factors and inflammatory markers among patients with each subtype of vascular disease. MATERIAL AND METHOD: Patients with acute ischemic stroke who had large vessel atherosclerosis or small vessel disease were studied. Patients with large vessel atherosclerosis were subdivided into extracranial carotid and intracranial stenosis groups. Blood samples were collected for c-reactive protein, erythrocyte sedimentation rate, hemoglobin A1C fibrinogen, fasting plasma glucose, cholesterol, triglyceride, and low-density and high-density lipoproteins. Risk factors and results of the blood tests between the groups of patients were compared. RESULTS: There were 116 patients in the study. Sixty-three patients had large vessel disease, whereas 53 patients had small vessel disease. More prevalence of diabetes and higher c-reactive protein were significantly found in patients with large vessel disease. C-reactive protein on admission was also higher in patients with extracranial carotid stenosis than those with intracranial stenosis. Serum cholesterol and low-density lipoprotein was significantly higher in patients with intracranial stenosis than those with small vessel extracranial disease. CONCLUSION: Diabetes and higher c-reactive protein on admission were associated with large vessel disease. c-reactive protein was also higher in patients with extracranial carotid stenosis but their cholesterol and low-density lipoprotein were significantly lower than those with intracranial disease.

The role of lipid profile as a risk factor indicator for ischemic stroke at Cipto Mangunkusumo Hospital, Jakarta.

AIM: to determine the role of low HDL-cholesterol, and high total cholesterol, LDL-Cholesterol and triglyceride as risk factors for ischemic stroke at Dr. Cipto Mangunkusumo Hospital. METHOD: a study was conducted on 76 patients with an age range of 40-70 years. Subjects consisted of 38 post ischemic stroke patients and 38 control subjects with a diagnosis other than stroke. The study sample consisted of serum for lipid profile assessment. Total cholesterol and triglyceride were assessed using enzymatic method, while HDL-cholesterol and LDL-cholesterol using direct homogenous enzymatic method. Statistical analysis was performed using chi-square and multivariate analysis using logistic regression. RESULTS: low HDL-cholesterol was found in ischemic stroke patients and demonstrated a significant difference compared to control subjects (p<0.05). The results of total cholesterol, triglyceride, LDL-cholesterol did not demonstrate a significant difference. The odds ratio (3.09; CI 95%: 1.04; 8.73) demonstrates that low HDL-cholesterol is a risk factor for ischemic stroke. CONCLUSION: a low HDL-cholesterol level is a risk factor for ischemic stroke, with an odds ratio of 3.09, while total cholesterol, triglyceride and high LDL-cholesterol levels were not risk factors for ischemic stroke.

Association of plasma homocysteine and ischaemic stroke in a nigerian population

Epidemiologic evidence suggests that raised plasma homocysteine is an independent risk factor for ischaemic stroke. However, other studies found no association between plasma homocysteine and stroke. Our objective was to determine the relationship between plasma homocysteine concentrations and ischaemic stroke in the Nigerian population where there is no existing published data. Case-control study. University of Maiduyguri Teaching Hospital, Maidyguri, Nigeria. Fifty patients with ischaemic stroke and 50 control subjects, aged and sex-matched, were studied in relation to plasma homocysteine and other vascular risk factors. Comparison of mean plasma homocysteine between stroke cases and control subjects and Odds Ratios for stroke in patients with hyperhomocysteinemia. Mean plasma homocysteine was significantly higher in stroke cases than in control subjects [mean +/- SD: 20.8 +/- 10.2 micro mol/Lvs. 13.1 +/- 4.5 micro mol/L; P<0.001]. Other factors associated with ischaemic stroke were obesity, hypertension and elevated serum cholesterol. Using logistic regression analysis, there was an adjusted Odds Ratio of 1.9 [95% CI, 1.16-3.08] for ischaemic stroke for every 5 micro mol/L increase in plasma homocysteine concentrations. Raised plasma homocysteine was significantly associated with ischaemic stroke and treating hyperhomocysteinemia may be an effective way of decreasing the incidence of stroke

The role of persistent anticardiolipin antibody as risk factor of ischemic stroke.

AIM: To determine the role of persistent ACA and hyperviscosity as risk factor of ischemic stroke. Methods: A study was conducted on 76 subjects whose age 40 to 70 years. Subjects consisted of 38 patients of post ischemic stroke and 38 controls with diagnosis other than stroke. Fresh blood samples were taken and mixed with EDTA for viscosity examination and serum for ACA IgM and IgG examination. The laboratory examination for persistent ACA IgM and IgG used ELISA method, while viscosity analysis was using viscometer. Statistic analysis used chi-square and multivariate analysis with logistic regression. RESULTS: In this study we found persistent ACA IgG in 25% of case group , and 2.63% in control group. Multivariate analysis showed persistent ACA IgG as risk factor for ischemic stroke with p < 0.05 and OR 14.11 (CI 95%:1.64;121.11). We found persistent ACA IgM in 2.78% of case group and 5.26% in control group. High blood viscosity was found in 15.79% case group and 10.53% in a control group. Statistical analysis showed no significant difference of viscosity (p = 0.740) and persistent ACA IgM (p = 1.000) between case and control group. CONCLUSION: study showed that persistent ACA IgG in stroke ischemic was higher than in control subjects. Blood viscosity examination and persistent ACA IgM did not show significant difference. While persistent ACA IgG with OR 14.11 (CI: 1.64; 121.11) was the risk factor for ischemic stroke. Blood viscosity and persistent ACA IgM were not risk factors for ischemic stroke.

The effects of hematocrit and age on transcranial Doppler measurements in patients with recent ischemic stroke.

BACKGROUND: The effects of age and hematocrit on transcranial Doppler (TCD) velocities have not been evaluated in a large patient group with recent ischemic stroke. AIM: This study assessed the effects of age and hematocrit on TCD measurements in patients with recent ischemic stroke compared to patients with non-vascular diseases. SETTINGS AND DESIGN: University Hospital, retrospective study. MATERIALS AND METHODS: TCD records and data files of 862 consecutive patients (mean age, 57+/-16 years) with various neurological diagnoses were reviewed retrospectively. The peak systolic, end diastolic and mean flow velocities (FV), systolic/diastolic ratios and pulsatility indices (PI) in the middle cerebral arteries were averaged and the effect of age and hematocrit values on these TCD values was studied. Independent samples t test, Pearson's coefficients of correlation, and linear regression test were used for statistical analysis. RESULTS: Among 862 patients, 413 were women (mean age, 53+/-17 years) and 449 were men (mean age, 60+/-13 years). Peak systolic and mean FV were higher and hematocrit concentration was lower in women compared to men (P< 0.001). The relation of TCD velocities with age and hematocrit was more remarkable in the group of patients with non-vascular neurological disorders. PI values demonstrated a significant correlation to age (r=+0.47) (P< 0.001), but did not change significantly with hematocrit level. CONCLUSIONS: It should be remembered that blood FV measured by TCD may be significantly affected by age and hematocrit level. However, there seems to be no significant association between TCD velocities and hematocrit in patients with a recent ischemic stroke.

Effects of sevoflurane and desflurane in CA1 after incomplete cerebral ischemia in rats

We compared the postischemic cerebral protective effects of sevoflurane and desflurane in rats with incomplete cerebral ischemia. This study was performed in Ataturk University Medical Faculty in Erzurum, Turkey in 2003. All rats were anesthetized with 5% isoflurane, intubated and mechanically ventilated, then given 2% isoflurane in 70% nitrous oxide and 30% O2. The femoral artery was cannulated. Five minutes before ischemia, and at the end of ischemia, arterial blood was taken for plasma glucose, hematocrit and blood gas analysis. Hypotension was induced by hemorrhage, and then both common carotid arteries were clamped for 10 minutes. In the control group, the arteries were then unclamped and the rats were extubated. In the other 2 groups, isoflurane was discontinued after carotid artery unclamping, and either 2% sevoflurane or 6% desflurane in 70% nitrous oxide and 30% O2 was given for 30 minutes, after which the rats were extubated. Five days later, they were sacrificed, and histological scores in CA1 were graded on a scale 0-3. Histopathological outcome in sevoflurane and desflurane group was not different, but there were differences between sevoflurane and control [p<0.05], and desflurane and control [p<0.01]. These data indicate that sevoflurane and desflurane have cerebral protective effects when given after ischemia

Neuronal and endothelial nitric oxide synthase gene knockout mice

Targeted disruption of the neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS) genes has led to knockout mice that lack these isoforms. These animal models have been useful to study the roles of nitric oxide (NO) in physiologic processes. nNOS knockout mice have enlarged stomachs and defects in the inhibitory junction potential involved in gastrointestinal motility. eNOS knockout mice are hypertensive and lack endothelium-derived relaxing factor activity. When these animals are subjected to models of focal ischemia, the nNOS mutant mice develop smaller infarcts, consistent with a role for nNOS in neurotoxicity following cerebral ischemia. In contrast, eNOS mutant mice develop larger infarcts, and show a more pronounced hemodynamic effect of vascular occlusion. The knockout mice also show that nNOS and eNOS isoforms differentially modulate the release of neurotransmitters in various regions of the brain. eNOS knockout mice respond to vessel injury with greater neointimal proliferation, confirming that reduced NO levels seen in endothelial dysfunction change the vessel response to injury. Furthermore, eNOS mutant mice still show a protective effect of female gender, indicating that the mechanism of this protection cannot be limited to upregulation of eNOS expression. The eNOS mutant mice also prove that eNOS modulates the cardiac contractile response to ß-adrenergic agonists and baseline diastolic relaxation. Atrial natriuretic peptide, upregulated in the hearts of eNOS mutant mice, normalizes cGMP levels and restores normal diastolic relaxation.

Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats

Brain ischemia followed by reperfusion causes neuronal death related to oxidative damage. Furthermore, it has been reported that subjects suffering from ischemic cerebrovascular disorders exhibit changes in circulating platelet aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide-initiated plasma chemiluminescence and thiol content as measures of peripheral oxidative damage in naive and preconditioned rats submitted to forebrain ischemia produced by the 4-vessel occlusion method. Rats were submitted to 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted to a 10-min ischemic episode 1 day after a 2-min ischemic event (2 + 10 min), followed by 60 min or 1 or 2 days of reperfusion. It has been demonstrated that such preconditioning protects against neuronal death in rats and gerbils submitted to a lethal (10 min) ischemic episode. The results show that both 2 and 10 min of ischemia cause an increase of plasma chemiluminescence when compared to control and sham rats. In the 2-min ischemic group, the effect was not present after reperfusion. In the 10-min ischemic group, the increase was present up to 1 day after recirculation and values returned to control levels after 2 days. However, rats preconditioned to ischemia (2 + 10 min) and reperfusion showed no differences in plasma chemiluminescence when compared to controls. We also analyzed plasma thiol content since it has been described that sulfhydryl (SH) groups significantly contribute to the antioxidant capacity of plasma. There was a significant decrease of plasma thiol content after 2, 10 and 2 + 10 min of ischemia followed by reperfusion when compared to controls. We conclude that ischemia may cause, along with brain oxidative damage and cell death, a peripheral oxidative damage that is reduced by the preconditioning phenomenon

Blood glucose and ischemic brain damage.

The effect of hyperglycemia on ischemic brain damage was studied in a rat model of incomplete ischemia. Incomplete ischemia was produced by permanent occlusion of one (either left or right) common carotid artery (CCA). Hyperglycemia was induced by intraperitoneal injection of 50% glucose, and same volume of physiological saline was injected in the controls 40 min before CCA ligation. Serum glucose level, at the time of vessel ligation, was 33.3 mMol/L. After CCA ligation, the rats were allowed to wake up and survive for upto 1 month. Perfusion-fixed brains were embedded in paraffin, subserially sectioned, and stained with haematoxylin-eosin/cresyl violet. Brain from sham-operated animals showed no damage neurons. Only mild neuronal damage was observed in saline pre-treated rats in CA1 area. Histological examination 24 h after CCA occlusion revealed ischemic neuronal cell damage to be more extensive in hyperglycemic rats. Neuronal damage was found in the major brain structures vulnerable to several insults. Some of those damaged neurons recovered well, but presence of some damaged neurons at 1 month of recovery suggesting delayed recovery. The results indicate that increased blood glucose level (hyperglycemia) during brain ischemia exaggerates structural alterations and leads to delay in recovery.

Fibrogênio como fator de risco independente de doença vascular cerebral / Fibrinogen as independent risk factor for ischemic stroke

No protocolo de avaliaçäo clínico-laboratorial de pacientes com acidente vascular cerebral (AVC) aterotrombótico dosamos e analisamos níveis de fibrinogênio plasmático (técnica de Clauss automatizada), para determinar seu possível papel como fator de risco trombogênico em 29 pacientes (20 homens e 9 mulheres) com idades entre 25 a 79 anos (mediana=55); todos tinham tido AVC aterotrombótico. Eles foram classificados em 2 grupos segundo alteraçöes de fluxo nas carótidas: g1 - sem alteraçäo de fluxo (n=19) e g2 - com alteraçöes de fluxo (n=10). Resultados- A média das dosagens de fibrinogênio no g1 foi de 269 e no g2 de 353 mg/dl. Quarenta e sete por cento dos pacientes do g1 e 80 por cento do g2, apresentaram medidas >300 mg/dl. As diferenças obtidas entre os grupos neste estudo foram significante. Conclusäo- Considerando o nível de risco epidemiológico de 300 mg/dl, nossos resultados sugerem que o fibrinogênio é um fator de risco independente para AVC aterotrombótico, especialmente naqueles com alteraçäo de fluxo carotídeo.

Clinical profile of stroke in relation to glycaemic status of patients.

Present study was undertaken in fifty consecutive patients of acute stroke to assess the role of glycemic status on clinical profile of stroke. Majority of patients (76%) were in age group of 41-70 years. The patients were classified into four groups: euglycemics (33), known diabetics (8), newly diagnosed diabetics (6) and stress hyperglycemics (3). Diabetics as well as stress hyperglycemics had higher prevalence of larger sized severe haemorrhagic stroke with poor outcome and there was positive correlation between them.