Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.
Metabolic syndrome (MetS) is a leading public health and clinical challenge worldwide. MetS represents a group of interrelated risk factors that predict cardiovascular diseases (CVD) and diabetes mellitus (DM). Its prevalence ranges between 10 and 84%, depending on the geographic region, urban or rural environment, individual demographic characteristics of the population studied (sex, age, racial and ethnic origin), as well as the criteria used to define MetS. Persons with MetS have higher mortality rate when compared with people without MetS, primarily caused by progressive atherosclerosis, accelerated by pro-inflammatory and pro-coagulation components of MetS. Considering the high prevalence of metabolic disorders (glucose metabolism disorder, hypertension, dyslipidaemia, obesity etc.), preventive healthcare should focus on changing lifestyle in order to reduce obesity and increase physical activity. This narrative review considers the available evidence from clinical and experimental studies dealing with MetS, and current treatment options for patients with insulin resistance and MetS.
In our group of patients, patients suffering from MS had significantly more IJV morphological changes and haemodynamic abnormalities when compared with healthy individuals not suffering from MS. These findings can be well demonstrated by non-invasive and cost-effective Doppler ultrasound.
We report the relations between comorbidities and chronic venous disease. In this cross-sectional study, information was gathered from 1679 Serbian patients. The majority (65.0%) of patients were women. Mild forms of chronic venous disease (clinical, etiologic, anatomic and pathophysiologic [CEAP] classification; C0s-C1) were more frequent in women (11.6%), while severe forms (CEAP C4-C6) were more commonly encountered in men (42.1%). The most frequent comorbidity was emphysema/chronic obstructive pulmonary disease in both groups (74.3% in males and 70.6% in females). For females, diabetes mellitus (P < .005), arterial hypertension (P < .000), and skeletal/joint diseases (P < .042) were more commonly found in the C4 to C6 category. Both males and females, with severe form of chronic venous disease, may benefit from additional screening for comorbidities. Further studies are needed to clarify the nature of association among comorbidities and chronic venous disease.
Objective: Procedural characteristics, including stent design, may influence the outcome of carotid artery stenting (CAS). A thorough comparison of the effect of stent design on outcome of CAS is thus warranted to allow for optimal evidence-based clinical decision making. This study sought to evaluate the effect of stent design on clinical and radiological outcomes of CAS.Methods: A systematic search was conducted in MEDLINE, Embase, and Cochrane databases in May 2018. Included were articles reporting on the occurrence of clinical short-and long-term major adverse events (MAE, any stroke or death) or radiological adverse events (new ischemic lesions on postprocedural magnetic resonance diffusion-weighted imaging (MR-DWI), restenosis or stent fracture) in different stent designs used to treat carotid artery stenosis.Random effects models were used to calculate combined overall effect sizes. Meta-regression was performed to identify the effect of specific stents on MAE rates. Results: From 2,654 unique identified articles, two randomized controlled trials and 66 cohort studies were eligible for analysis (including 46,728 procedures). Short-term clinical MAE rates were similar for patients treated with open cell versus closed cell or hybrid stents. Use of Acculink stent was associated with a higher risk of MAE compared to Wallstent (RR: 1.51, p=0.03), as was true for use of Precise stent versus Xact stent (RR: 1.55, p<0.001). Long-term clinical MAE rates were similar for open versus closed cell stents. Use of open cell stents predisposed to a 25% higher chance (RR: 1.25; p=0.03) of developing postprocedural new ischemic lesions on MR-DWI. No differences were observed in incidence of restenosis, stent fracture, or intraprocedural hemodynamic depression with respect to different stent design. [Type here] Conclusions: Stent design does not affect short-or long-term clinical MAE rates in patients undergoing CAS. Furthermore, the division in open and closed cell stent design might conceal true differences in single stent efficacy. Nevertheless, open cell stenting resulted in a significantly higher number of MR-DWI-detected subclinical postprocedural new ischemic lesions compared with closed cell stenting. An individualized patient data meta-analysis,including future studies with prospective homogenous study design, is required to adequately correct for known risk factors and provide definite conclusions with respect to carotid stent design for specific subgroups.
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