897 resultados para cerebrovascular insult


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Arterial stiffness assessed by carotid-femoral pulse wave velocity (cfPWV) measurement is now well accepted as an independent predictor of vascular mortality and morbidity. However, the value of cfPWV has been considered to be limited for risk classification in patients with several vascular risk factors. Magnetic resonance (MR) allows measurement of PWV between two points, though to date mainly used to study the aorta. To assess the common carotid artery pulse wave velocity by magnetic resonance, determine their association with classical vascular risk factors and ischemic brain injury burden in patients with suspected ischemic cerebrovascular disease

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Acute lung injury following intestinal I/R depends on neutrophil-endothelial cell interactions and on cytokines drained from the gut through the lymph. Among the mediators generated during I/R, increased serum levels of IL-6 and NO are also found and might be involved in acute lung injury. Once intestinal ischemia itself may be a factor of tissue injury, in this study, we investigated the presence of IL-6 in lymph after intestinal ischemia and its effects on human umbilical vein endothelial cells (HUVECs) detachment. The involvement of NO on the increase of lung and intestinal microvascular permeability and the lymph effects on HUVEC detachment were also studied. Upon anesthesia, male Wistar rats were subjected to occlusion of the superior mesenteric artery during 45 min, followed by 2-h intestinal reperfusion. Rats were treated with the nonselective NO synthase (NOS) inhibitor L-NAME (N(omega)-nitro-L-arginine methyl ester) or with the selective inhibitor of iNOS aminoguanidine 1 h before superior mesenteric artery occlusion. Whereas treatment with L-NAME during ischemia increased both IL-6 levels in lymph and lung microvascular permeability, aminoguanidine restored the augmented intestinal plasma extravasation due to ischemia and did not induce IL-6 in lymph. On the other hand, IL-6 and lymph of intestinal I/R detached the HUVECs, whereas lymph of ischemic rats upon L-NAME treatment when incubated with anti-IL-6 prevented HUVEC detachment. It is shown that the intestinal ischemia itself is sufficient to increase intestinal microvascular permeability with involvement of iNOS activation. Intestinal ischemia and absence of constitutive NOS activity leading to additional intestinal stress both cause release of IL-6 and increase of lung microvascular permeability. Because anti-IL-6 prevented the endothelial cell injury caused by lymph at the ischemia period, the lymph-borne IL-6 might be involved with endothelial cell activation. At the reperfusion period, this cytokine does not seem to be modulated by NO.

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Chronic chagasic cardiac patients are exposed to oxidative stress that apparently contributes to disease progression. Benznidazole (BZN) is the main drug used for the treatment of chagasic patients and its action involves the generation of reactive species. 41 patients with Chagas` heart disease were selected and biomarkers of oxidative stress were measured before and after 2 months of BZN treatment (5 mg/kg/day) and the subsequent antioxidant supplementation with vitamin E (800 UI/day) and C (500 mg/day) during 6 months. Patients were classified according to the modified Los Andes clinical hemodynamic classification in groups IA, IB, II and III, and the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione reductase (GR), as well as the contents of reduced glutathione (GSH), thiobarbituric acid reactive species (TBARS), protein carbonyl (PC), vitamin E and C and nitric oxide (NO), myeloperoxidase (MPO) and adenosine deaminase (ADA) activities were measured in their blood. Excepting in group III, after BZN treatment SOD, CAT, GPx and GST activities as well as PC levels were enhanced while vitamin E levels were decreased in these groups. After antioxidant supplementation the activities of SOD, GPx and GR were decreased whereas PC, TBARS, NO, and GSH levels were decreased. In conclusion, BZN treatment promoted an oxidative insult in such patients while the antioxidant supplementation was able to attenuate this effect by increasing vitamin E levels, decreasing PC and TBARS levels, inhibiting SOD, GPx and GR activities as well as inflammatory markers, mainly in stages with less cardiac involvement. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

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Background and Purpose - the purpose of this research was to evaluate whether an association exists between the presence of atherosclerotic plaque in the thoracic aorta and left ventricular hypertrophy (LVH) in patients with a cerebrovascular event.Methods - We included 116 consecutive patients ( 79 men; mean age, 62 +/- 12.4 years) with previous history of stroke or transient ischemic attack in a cross-sectional study. Transthoracic echocardiogram was performed to diagnose LVH and transesophageal echocardiogram for the detection of atheromas of the thoracic aorta. Continuous variables were analyzed by Student t or Mann-Whitney tests and categorized variables by Goodman test. From the significant association of LVH and age with atheromatous disease of the aorta, an adjustment to the multivariate logistic model was made using high blood pressure history or age as covariates. All of the statistical tests were carried out at a level of 5% significance.Results - Almost half of the patients (43.1%) presented atherosclerotic lesions in the aorta. LVH was present in 90.0% of patients with plaque and in only 30.3% of patients without plaque. Using high blood pressure as a covariate, the risk of patients with LVH presenting atherosclerotic plaque in the aorta was 18.23-fold greater than the risk for patients without LVH (95% CI, 5.68 to 58.54; P < 0.0001). Adding age into the model, the risk increased to 26.36 ( 95% CI, 7.14 to 97.30; P < 0.0001).Conclusions - LVH detected by conventional echocardiogram is associated with high risk of atherosclerotic plaque in the aorta and would be used as a criterion for indication of transesophageal echocardiography in patients with previous stroke or transient ischemic attack LVH.

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Background: It is well known that the presence of atheroma of the thoracic aorta is a risk factor for cerebrovascular events. We sought to evaluate whether the presence and the morphology of atherosclerotic plaque in the carotid artery detected by duplex ultrasonography is associated with disease in the proximal aorta visualized by transesophageal echocardiogram in patients with a cerebrovascular event. Methods: We carried out a cross-sectional prospective study including 147 consecutive patients with prior stroke or transient ischemic attack (TIA). Neurological evaluations were performed by an expert neurologist using clinical and tomographic diagnostic criteria including the definition of etiology and whether the patient suffered from stroke or TIA. Transthoracic and transesophageal echocardiograms and carotid artery duplex ultrasonography were performed by the same examiner. Patients with and without plaque in the carotid artery were compared using Student's t test or the χ2 test. Regression analysis was used to determine whether the presence of plaque in the carotid artery was predictive of the presence of plaque in the proximal aorta and to analyze the relationship between the echogenicity of carotid and aortic plaques. The significance level was set at p < 0.05. Results: All 147 patients (95 men) were included in the analysis. Patients' ages ranged from 23 to 85 years (65 ± 12.4 years). Most of the patients (58.5%) were Caucasian, while 41.5% were African-Brazilian. Arterial hypertension, diabetes and tobacco use were more frequent among patients with atherosclerotic plaque in the aorta. A normal carotid intima-media thickness halved the risk of atherosclerotic plaque in the aorta [odds ratio (OR) 0.46, 95% confidence interval (CI) 0.23-0.91; p = 0.026]. The presence of carotid plaque increased the risk of aortic plaque by 70-fold (OR 73.2, 95% CI 25.6-2,018.6; p < 0.001) in univariate analysis. The absence of atherosclerotic plaque in the carotid artery reduced the risk of plaque in the aorta to almost 0 (OR 0.014, 95% CI 0.004-0.041; p < 0.001). Considering the 86 patients with both aortic and carotid plaques, the presence of hypoechoic plaque in the carotid artery was a predictor of hypoechoic plaque in the aorta (OR 10.1, 95% CI 3.3-31.2; p < 0.001). Conclusions: The carotid artery atherosclerotic profile defined by ultrasonography is a strong predictor of the atherosclerotic profile of the proximal aorta. This should be taken into consideration before referring patients with acute cerebrovascular events for transesophageal echocardiogram. © 2013 S. Karger AG, Basel.

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The stroke, cause of morbidity and mortality, has been associated with imbalance in the neural control of the heart, which contributes to the decrease in heart rate variability (HRV) and a prognostic factor for cardiacevents and arrhythmias. The aim of this study was to in investigate the autonomic modulation of heart rate of men suffering from lesions stroke in chronicphase. Eight menaged 58.62 ± 2.88 years, 27.41 ± 5.33 kg/m2of bodymass índex, with paresis for at least six months were studied. Heart rate (HR) and RR intervals (iR-R) were recorded at rest in supine position for 10 minutes. Geometric índices of the Poincaré plot were calculated: SD1, associatedwith vagal activity; SD2, associated with global activity but sympathetic predominance, and the relationship of both (SD1/SD2). Geometric index values in the sample: SD1 = 20,54 ± 9,90ms; SD2 = 36,80 ± 30,61ms; SD1/SD2 = 0,49 ± 0,04. The reference values from literature for healthy subjects are: SD1 = 19.6 ± 9.4ms e 22.8 ± 16.1 ms; SD2 = 43.2 ± 17.7 ms e 56.3 ± 12.3 ms; SD1/SD2 = 0.49 ± 0.21ms. Men in chronic phase of stroke haven't autonomic dysfunction analyzed by nonlinear method – Poincaré geometricíndices.

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Objective: This study investigated the role of periodontal disease in the development of stroke or cerebral infarction in patients by evaluating the clinical periodontal conditions and the subgingival levels of periodontopathogens. Material and Methods: Twenty patients with ischemic (I-CVA) or hemorrhagic (H-CVA) cerebrovascular episodes (test group) and 60 systemically healthy patients (control group) were evaluated for: probing depth, clinical attachment level, bleeding on probing and plaque index. Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were both identified and quantified in subgingival plaque samples by conventional and real-time PCR, respectively. Results: The test group showed a significant increase in each of the following parameters: pocket depth, clinical attachment loss, bleeding on probing, plaque index and number of missing teeth when compared to control values (p<0.05, unpaired t-test). Likewise, the test group had increased numbers of sites that were contaminated with P. gingivalis (60%x10%; p<0.001; chi-squared test) and displayed greater prevalence of periodontal disease, with an odds ratio of 48.06 (95% CI: 5.96-387.72; p<0.001). Notably, a positive correlation between probing depth and the levels of P. gingivalis in ischemic stroke was found (r=0.60; p=0.03; Spearman's rank correlation coefficient test). A. actinomycetemcomitans DNA was not detected in any of the groups by conventional or real-time PCR. Conclusions: Stroke patients had deeper pockets, more severe attachment loss, increased bleeding on probing, increased plaque indexes, and in their pockets harbored increased levels of P. gingivalis. These findings suggest that periodontal disease is a risk factor for the development of cerebral hemorrhage or infarction. Early treatment of periodontitis may counteract the development of cerebrovascular episodes.

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Background. Intestinal ischemia and reperfusion (I/R) is a documented cause of acute lung injury (ALI) and systemic inflammation. We previously reported that obstruction of thoracic lymphatic flow during intestinal I/R blunts pulmonary neutrophil recruitment and microvascular injury and decreases the systemic levels of tumor necrosis factor. Here, we consider the existence of a gut-lung axis promoting the induction of systemic inflammation, whereby drained intestinal lymph stimulates lung expression of adhesion molecules and matrix components and generation of inflammatory mediators. Material and Methods. Upon administration of anesthesia, male Wistar rats were subjected to occlusion of the superior mesenteric artery for 45 min, followed by 2 h of intestinal reperfusion (I/R); groups of rats were subjected to I/R with or without thoracic lymphatic duct ligation immediately before the procedure. The non-manipulated rats were used to investigate basal parameters. Results. Obstruction of thoracic lymphatic flow before intestinal I/R decreased the ability of cultured lung tissue explants to release IL-1 beta, IL-10, and VEGF. In contrast, lymphatic obstruction normalized the elevated lung expression of PECAM-1 caused by intestinal I/R. On the other hand, lung E-selectin expression was significantly reduced, whereas fibronectin expression and collagen synthesis were not affected. Lymph levels of LTB4 and TXB2 were found to be significantly increased. Conclusions. These data suggest that lymph factors drained from the intestine during ischemic trauma stimulate the lung to generate inflammatory mediators and alter the expression of adhesion molecules. Disturbances in lung homeostasis mediated by lymph might contribute to the spread of inflammatory processes, thereby accounting for the systemic inflammation induced by intestinal I/R. (C) 2012 Elsevier Inc. All rights reserved.

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To investigate the prevalence and characteristics of cerebrovascular accidents (CVA) in a large population of adults with congenital heart disease (CHD).

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Cerebrovascular accidents (CVA) are considered among the most serious adverse events after transcatheter aortic valve implantation (TAVI). The objective of the present study was to evaluate the frequency and timing of CVA after TAVI and to investigate the impact on clinical outcomes within 30 days of the procedure.

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