Controle autonômico do coração e fração de ejeção na fase crônica do acidente vascular encefálico

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Variabilidade da frequencia cardíaca em fase crônica de lesão cerebrovascular

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.

Increased levels of Porphyromonas gingivalis are associated with ischemic and hemorrhagic cerebrovascular disease in humans: an in vivo study

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.

Chernobil. ¿Accidente nuclear o evento político?

[ES] El propósito de esta charla es analizar las circunstancias que dieron lugar al accidente de la Central Nuclear de Chernobil y la reacción que se suscitó como consecuencia del mismo. ¿Estaban la sociedad preparada para ello? ¿Había medidas tomadas para el caso de un accidente de esa envergadura? ¿Podría repetirse un accidente como ese? Para dar respuesta a estas cuestiones se hará un breve repaso sobre el concepto de la contaminación transfronteriza a larga distancia, las medidas de protección radiológica existentes, el accidente: ¿cómo se produjo?, ¿por qué?, para finalizar con las medidas que hubo que poner en marcha después del mismo tanto provisionales como definitivas.

Cerebrovascular accidents in adult patients with congenital heart disease

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

Cerebrovascular accidents complicating transcatheter aortic valve implantation: frequency, timing and impact on outcomes

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.

Evidence that N-acetylcysteine inhibits TNF-alpha-induced cerebrovascular endothelin-1 upregulation via inhibition of mitogen- and stress-activated protein kinase

N-acetylcysteine (NAC) is neuroprotective in animal models of acute brain injury such as caused by bacterial meningitis. However, the mechanism(s) by which NAC exerts neuroprotection is unclear. Gene expression of endothelin-1 (ET-1), which contributes to cerebral blood flow decline in acute brain injury, is partially regulated by reactive oxygen species, and thus a potential target of NAC. We therefore examined the effect of NAC on tumor necrosis factor (TNF)-alpha-induced ET-1 production in cerebrovascular endothelial cells. NAC dose dependently inhibited TNF-alpha-induced preproET-1 mRNA upregulation and ET-1 protein secretion, while upregulation of inducible nitric oxide synthase (iNOS) was unaffected. Intriguingly, NAC had no effect on the initial activation (i.e., IkappaB degradation, nuclear p65 translocation, and Ser536 phosphorylation) of NF-kappaB by TNF-alpha. However, transient inhibition of NF-kappaB DNA binding suggested that NAC may inhibit ET-1 upregulation by inhibiting (a) parallel pathway(s) necessary for full transcriptional activation of NF-kappaB-mediated ET-1 gene expression. Similar to NAC, the MEK1/2 inhibitor U0126, the p38 inhibitor SB203580, and the protein kinase inhibitor H-89 selectively inhibited ET-1 upregulation without affecting nuclear p65 translocation, suggesting that NAC inhibits ET-1 upregulation via inhibition of mitogen- and stress-activated protein kinase (MSK). Supporting this notion, cotreatment with NAC inhibited the TNF-alpha-induced rise in MSK1 and MSK2 kinase activity, while siRNA knock-down experiments showed that MSK2 is the predominant isoform involved in TNF-alpha-induced ET-1 upregulation.