22 resultados para CAROTID ARTERY AGENESIS
Resumo:
A síndrome ocular isquêmica (SOI) ocorre devido à hipoperfusão ocular crônica secundária à obstrução da artéria carótida. O quadro clínico inclui, entre outros, retinopatia proliferativa similar a retinopatia diabética. A SOI deve ser considerada principalmente nas retinopatias proliferativas unilaterais ou muito assimétricas e nos casos refratários ao tratamento por fotocoagulação. A indicação da endarterectomia nos pacientes com SOI isolada não é bem definida. Este trabalho relata uma paciente com SOI simulando retinopatia diabética proliferativa unilateral e tratada por endarterectomia.
Resumo:
Background Obstructive sleep apnea (OSA) is common among patients with coronary artery disease. However, OSA remains largely under recognized. The lack of clinical suspicion and difficulties to access full polysomnography (PSG) are limiting factors. The aim of this study was to evaluate, among patients referred to coronary artery bypass grafting (CABG): (i) the prevalence of OSA, (ii) the association of OSA with clinical symptoms, (iii) the performance of overnight unattended portable monitoring (PM) as an alternative method for the diagnosis of OSA. Methods Consecutive patients referred for CABG were evaluated by standard physical evaluation and validated questionnaires (Berlin questionnaire and Epworth Sleepiness Scale) and underwent full PSG and PM (Stardust II). Results We studied 70 consecutive patients (76% men), age 58 +/- 7 years (mean +/- SD), BMI [median (interquartile range)] 27.6 kg/m(2) (25.8-31.1). The prevalence of OSA (full PSG) using an apnea-hypopnea index of at least 5 events/h was 87%. Commonly used clinical traits for the screening of OSA such as the Epworth Sleepiness Scale and neck circumference had low sensitivities to detect OSA. In contrast, the Berlin questionnaire showed a good sensitivity (72%) to detect OSA. PM showed good sensitivity (92%) and specificity (67%) for the diagnosis of OSA. Conclusion OSA is strikingly common among patients referred for CABG. The Berlin questionnaire, but not symptom of excessive daytime sleepiness is a useful tool to screen OSA. PM is useful for the diagnosis of OSA and therefore is an attractive tool for widespread use among patients with coronary artery disease. Coron Artery Dis 23:31-38 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Resumo:
Background: Percutaneous coronary intervention (PCI) has increased as the initial revascularization strategy in chronic coronary artery disease. Consequently, more patients undergoing coronary artery bypass grafting (CABG) have history of coronary stent. Objective: Evaluate the impact of previous PCI on in-hospital mortality after CABG in patients with multivessel coronary artery disease. Methods: Between May/2007 and June/2009, 1099 consecutive patients underwent CABG on cardiopulmonary bypass. Patients with no PCI (n=938, 85.3%) were compared with patients with previous PCI (n=161, 14.6%). Logistic regression models and propensity score matching analysis were used to assess the risk-adjusted impact of previous PCI on in-hospital mortality. Results: Both groups were similar, except for the fact that patients with previous PCI were more likely to have unstable angina (16.1% x 9.9%, p=0.019). In-hospital mortality after CABG was higher in patients with previous PCI (9.3% x 5.1%, p=0.034) and it was comparable with EuroSCORE and 2000 Bernstein-Parsonnet risk score. Using multivariate logistic regression analysis, previous PCI emerged as an independent predictor of postoperative in-hospital mortality (odds ratio 1.94, 95% CI 1.02-3.68, p=0.044) as strong as diabetes (odds ratio 1.86, 95% CI 1.07-3.24, p=0.028). After computed propensity score matching based on preoperative risk factors, in-hospital mortality remained higher among patients with previous PCI (odds ratio 3.46, 95% CI 1.10-10.93, p=0.034). Conclusions: Previous PCI in patients with multivessel coronary artery disease is an independent risk factor for in-hospital mortality after CABG. This fact must be considered when PCI is indicated as initial alternative in patients with more severe coronary artery disease. (Arq Bras Cardiol 2012;99(1):586-595)
Resumo:
Objectives: To identify potential associations between fetal surveillance tests and acidosis at birth in pregnancies with abnormal but positive end-diastolic velocity in the umbilical artery. Methods: A prospective case-control study [group 1: pH < 7.2; group 2: pH >= 7.2] including 46 fetuses with abnormal but positive end-diastolic velocity in the umbilical artery was conducted between February 2007 and March 2009. Outcome variables were evaluated by univariate analysis and compared between the two groups. Clinically relevant and statistically significant variables were analyzed by logistic regression. Results: Abnormal nonstress test, presence of deceleration, and absent fetal breathing movements were statistically significant. Logistic regression analysis revealed that fetal heart rate (FHR) deceleration in the nonstress test is the only predictor of fetal acidosis at birth (p = 0.024; OR = 8.2; 95% CI: 1.2-52). Conclusions: In fetuses with positive end-diastolic flow velocity, acute variables of the antenatal surveillance tests are correlated with acidosis at birth and FHR deceleration in the nonstress test is the only predictor of fetal acidosis.
Resumo:
Clinical evidence has identified the pulmonary circulation as an important target of air pollution. It was previously demonstrated that in vitro exposure to fine particulate matter (aerodynamic diameter <= 2.5 mu m, PM2.5) induces endothelial dysfunction in isolated pulmonary arteries. We aimed to investigate the effects of in vivo exposure to urban concentrated PM2.5 on rat pulmonary artery reactivity and the mechanisms involved. For this, adult Wistar rats were exposed to 2 weeks of concentrated Sao Paulo city air PM2.5 at an accumulated daily dose of approximately 600 mu g/m(3). Pulmonary arteries isolated from PM2.5-exposed animals exhibited impaired endothelium-dependent relaxation to acetylcholine without significant changes in nitric oxide donor response compared to control rats. PM2.5 caused vascular oxidative stress and enhanced protein expression of Cu/Zn- and Mn-superoxide dismutase in the pulmonary artery. Protein expression of endothelial nitric oxide synthase (eNOS) was reduced, while tumor necrosis factor (TNF)-alpha was enhanced by PM2.5 inhalation in pulmonary artery. There was a significant positive correlation between eNOS expression and maximal relaxation response (E-max) to acetylcholine. A negative correlation was found between vascular TNF-alpha expression and E-max to acetylcholine. Plasma cytokine levels, blood cells count and coagulation parameters were similar between control and PM2.5-exposed rats. The present findings showed that in vivo daily exposure to concentrated urban PM2.5 could decrease endothelium-dependent relaxation and eNOS expression on pulmonary arteries associated with local high TNF-alpha level but not systemic pro-inflammatory factors. Taken together, the present results elucidate the mechanisms underlying the trigger of cardiopulmonary diseases induced by urban ambient levels of PM2.5. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
Resumo:
Fistulas between coronary artery and bronchial artery may be present from birth, with few hemodynamic consequences, and may remain closed due to similarity of the filling pressures at these 2 sites.(1) They can also be secondary to pulmonary artery occlusive disease or chronic pulmonary inflammation.(2,3) These pulmonary changes may cause a dilation of the fistula and make it functional, causing angina pectoris by coronary steal syndrome, which is the most common symptom. The presentation may also be composed of episodes of hemoptysis, heart failure, and infective endocarditis. However, most patients remain asymptomatic. The ones that need treatment may not have a good response to the medical management, requiring an intervention. This can be done using embolization coils, stents grafts, and performing surgical ligation of the fistulas.(2-4) J INVASIVE CARDIOL 2012;24(11):E303-E304