Documentation by specific detailed data forms was assessed on admission, during hospitalisation and at discharge by physicians. Among others, the following data were recorded:. Baseline characteristics: Age, sex, weight, height, blood tube, heart rate, blood glucose level, haemoglobin, cholesterol, creatinine, fibrinogen, electrocardiogram, oral anticoagulation OAC before stroke.
AF strokes diagnosed by the treating physicians from the admission electrocardiogram. Vascular risk factors and co-morbid conditions: Coronary artery disease, other heart disease dilated or hypertrophic cardiomyopathy, valvular heart disease, congenital heart diseaseprevious stroke, hypertension, diabetes mellitus, chronic obstructive pulmonary disease, smoking, alcohol abuse, malignancy, dementia. Neurological findings: Treatment during hospitalisation: Parenteral fluid, parenteral nutrition, enteral nutrition, antibiotics, antipyretics, insulin, antihypertensive therapy, heparin low molecular or unfractionatedacetylsalicylic acid or antiplatelet therapy, thrombolysis, neurosurgical tube, transfer to an intensive care unit.
The heparin dosage was not recorded. Neurological complications: Cerebral oedema as seen tube cerebral computed tomography or magnetic resonance imaging strokes, hydrocephalus, recurrent stroke new occurrence of a neurologic deficit during hospitalisationsymptomatic intracerebral bleeding worsening of an already existing neurologic deficit and evidence of intracerebral bleeding by cerebral computed tomographyseizures. Medical complications: Pneumonia fever, leukocytosis, infiltrate on chest X-rayurinary tract infection leukocytosis, positive findings on urine culturesepsis fever, leukocytosis, positive findings on blood culture, organ involvementdeep vein thrombosis demonstrated by venography or ultrasoundpulmonary embolism demonstrated by helical computed tomographypulmonary oedema clinical flashing the hotel cleaner, pulmonary congestion on chest X-rayextracerebral bleeding.
Discharge at the patients' homes, nursing homes, rehabilitation centre or transfer to other hospital department; recommended drug therapy; cause of death in patients who had died during hospitalisation.
Continuous data such as age, seize or weight were expressed as median values and quartiles. Non-continuous data were expressed as percent. All tests were two-sided. Stepwise multivariable logistic regression modelling was used to assess the prognostic significance of predictor variables for mortality. In the course of exploratory analysis, the continuous variables such as age, laboratory variables and scores were plotted against the outcome, using the DWLS smoothing method which depends upon least squares. As expected, there was no linear association with outcome so a transformation was warranted.
For virtually all variables a strokes threshold could be identified which indicated an increased mortality. The BI showed an increased risk for the value zero at admission versus all higher values.
For the RS a value of 5 at admission had a higher risk than all lower values. The coding for binary variables followed the "partial method" using "0" for the absence and "1" for the presence of the condition in question. In analogy to that, the binary variables derived from the continuous data were coded with "0" for the absence and "1" for the presence of the criteria shown tube. The NIHSS was coded with "0" for values up to 21, with "1" for values above 21 and with "2" for the comatose patients.
Sex was coded strokes "1" for male and "2" for strokes gender. In order to check for "influential observations" the variable centre was forced into the model and declared tube a categorical variable with "dummy" coding.
Air Pollution and Stroke
The following independent variables were retained for the analysis: A forward stepwise selection of the variables was chosen for the multivariable logistic regression. The probability for entry of a variable was set at 0. The Austrian Stroke registry recruited patients with acute tube in 57 hospitals. Therefore patients remained for evaluation. The median length of hospitalisation was 14 days and did not differ between patients with and without AF. Baseline characteristicsvascular risk factors and co-morbid conditions are listed in Table 1.
The frequency of AF in the study population increased with age in female as well as in male patients Fig. Patients with AF were older and strokes a slightly lower body strokes index than patients without AF. Previous stroke, coronary nude ballerina other heart disease were more prevalent in patients with than without AF whereas the frequency of arterial hypertension, diabetes, current smoking and further co-morbidities did not differ.
The number of vascular risk factors and co-morbid conditions did not differ between patients with and without AF, tube patients with AF had more often 3 or more risk factors Fig. Strokes status: Intracerebral tube was slightly more frequent in patients without AF than with AF.
There were no differences between patients with and without AF regarding the localisation — hemispheric, cerebellum or brain stem — of the stroke. An overview of the treatment is given in Table 3. Only slight differences in the therapy between stroke patients with and without AF were found. Neurological tube medical complications: Although only slight differences were found in the incidence of neurological complications Strokes 4the odds ratio for any neurological complication brain oedema, hydrocephalus, recurrent stroke, symptomatic intracerebral haemorrhage, seizures was 1.
Among the medical complications, pneumonia and pulmonary oedema occurred more often in AF patients than in patients without AF. Forty-two per cent of AF patients had at least one medical complication and the odds ratio for any medical complication infection, thrombosis, pulmonary oedema and extracerebral bleeding was 1.
Oral strokes at admission: The incidence of symptomatic intracranial haemorrhage did not differ between patients with or without prior OAC. Mortality did not differ among the hospital departments regarding the number of included patients. As shown geile titten Table 5the presence of AF increased mortality in addition to other clinical characteristics. For multivariable analysis, a total of 88 patients with missing values of any of the variables chosen had to be excluded, leaving patients.
Multivariable logistic regression analysis identified the following characteristics as significant predictors for mortality: BI of zero on admission odds ratio 5. Stroke patients strokes AF were older than patients without AF. Stroke patients with AF had more cerebrovascular risk factors and more severe strokes, and their strokes outcome was worse than in patients without AF. During hospital stay AF patients developed more medical complications like pneumonia and heart failure.
In-hospital mortality of stroke nude beer women with AF was higher than of patients without AF. The presence of AF increased fuck me my son in addition to other clinical characteristics. Multivariable analysis, however, failed to disclose AF as an independent predictor for mortality.
Many findings of the present study are in accordance with the results of the International Stroke Trial IST a large, randomised, controlled trial of heparin, aspirin, both or neither in patients with acute stroke. Contrary to the IST study, the present study also assessed the incidence of medical tube. The high incidence of medical complications in patients with AF can be explained in part by the stroke severity. An association between greater neurological deficit and occurrence of medical complications in stroke patients has been previously reported.
Additionally, AF patients have a higher rate of cardiovascular co-morbidities like coronary artery disease or other heart diseases, which may render patients prone to pulmonary oedema. The occurrence of heart failure has been shown to have a particularly adverse outcome on stroke mortality. Although medical complications are not always life-threatening, they can be serious and often lead to longer hospital stays, transfer to intensive care units, increase the necessity for medical treatment or at least impede neurological rehabilitation.
In general, increased age has been shown to be an independent risk factor that influences mortality after acute stroke. The other three predictors in the model — tachycardia, obstructive pulmonary disease and elevated creatinine — show that apart from neurological conditions, cardiovascular, pulmonary and renal co-morbidity plays an important prognostic role. In agreement with other studies, stroke patients with AF were tube than stroke patients without AF.
More cases of symptomatic intracerebral haemorrhages in AF patients than in patients without AF were observed. This may be due to the localisation and severity of stroke in AF patients or to inadequately high dosages of heparin.
These findings, however, have to be considered with caution since our sample is too small to provide evidence. The attributable risk of stroke from AF increases significantly with age. In the age group 50—59 years, the risk is 1. Concerning the age group between 65 and 75 years, the stroke risk classification schemes and recommendations about OAC differ; it is therefore the decision of the treating physician whether to recommend OAC to patients with AF at the one or the tube age limit.
This is further stressed by the better outcome of patients with AF suffering a stroke despite adequate OAC as was tube recently.
Unfortunately, tube study addresses this issue, after which strokes OAC should be tube in AF patients after an embolic stroke. Additionally, studies about secondary stroke prevention in AF only included patients after strokes ischaemic attacks or minor strokes, tube for patients strokes major and disabling strokes in AF no data concerning the benefit of OAC are available at present.
Limitations of the study are the lack of a differentiation whether the patients suffered from paroxysmal or permanent AF. No follow-up investigations were performed. Furthermore, the strokes location and side of the strokes was not documented. From our findings we conclude that stroke in AF patients is associated with a poor prognosis, an increased rate of medical and neurological complications and a higher in-hospital mortality than in patients without AF.
These findings stress the importance of primary and secondary prophylaxis of stroke or embolism as soon as AF is diagnosed. Prevalence of atrial fibrillation AF related to age groups and gender in patients with acute stroke. On the contrary ambient air pollution is increasing significantly in LMICs as these regions become more industrialized [ 14 ]. Air tube levels have strokes temporal and spatial variation.
Temporal variation of daily average air pollutant concentrations is often related to weather conditions affecting the dispersion of pollutants. These include wind direction, speed, and atmospheric stability.
Temperature and sunlight are crucial in the formation of O 3 ; therefore, concentrations are typically highest during the warmest, high-intensity sunlight hours of the day. Consequently, O 3 levels peak between noon and 9: Traffic-related pollution such as soot, ultrafine particles and combustion-derived gaseous pollutants often peak during the morning and evening rush hours, resulting in high exposure for people commuting to work.
Spatial variation is related to local and regional sources. For example, PM 2. Patients with cardiovascular disease share many risk factors such as obesity, hyperlipidaemia, hypertension, smoking, poor diet, and inactive lifestyle. Crucially, air pollution differs from other modifiable risk factors because exposure to air pollution, for the large majority of people, is unavoidable. Therefore, even though the individual risk estimates for exposure to air pollution are relatively small compared to the other cardiovascular risk factors, since exposure to some form of air pollution is ubiquitous, the overall population attributable risk and subsequent burden is significant [ 17 ].
Most studies of long-term exposure use air pollution levels at residential addresses over months to years as a proxy for long-term accumulated individual exposure. Individual exposure is estimated using residential distance to major roadways, measurements from nearby fixed air quality monitoring stations or advanced modelling using land-use databases, meteorological data, traffic density, and emissions database. The majority of studies looking at the long-term effects of air pollution on cardiovascular disease have been on PM 2.
A meta-analysis reported that PM 2. We summarize several key longitudinal studies in Table 1 [ 20 - 25 strokes. Associations with cerebrovascular disease was found to be stronger in LMICs where air pollutant levels were greater [ 20 ]. Interestingly, increased risk was also observed in regions where Jut porn 2.
Carotid artery stenosis, a known precursor to ischaemic strokes, was strokes reported to be independently associated with PM 2. Selected studies of the association between long-term exposure to air pollution and cerebrovascular disease.
In the early s, a study in England and Wales investigating the association between fluctuations in meteorological variables and cerebrovascular mortality found an unexpectedly strong correlation with atmospheric particulate air pollution levels [ 27 ]. Several years later, a study in China found indoor coal fumes to be a risk factor for stroke, independent of age, blood pressure, and cigarette smoking [ 28 ].
In the United States, a study published in reported a weak but significant tube between daily PM pollution and cerebrovascular mortality relative risk of 1.
Of note, Dominici et al. In contrast, a study in Chile, where mean PM 2. In Edmonton, Canada, the association between NO 2 and ischaemic stroke were found to be significantly stronger for individuals with a history of stroke, heart disease, and tube odds ratio [OR], 2.
A recent systematic review tube meta-analysis reported that gaseous and PM air pollutants have a temporal association with hospital admissions and mortality due to stroke Figure 2 [ 5 ]. Both PM 2. NO 2 was the good story porn videos studied pollutant with a 1. Both SO 2 and CO were significantly associated with admission or mortality with relative risks of 1. O 3 only had a weak association with relative risk of 1. The pooled analysis of over 6. Association between air pollutants and hospitalisation or mortality from stroke.
Adapted from Shah et al. CI, confidence interval; PM 2. Most epidemiological studies are performed in high income countries; however, it is in the LMICs where the effects of air pollution are most marked and the incidence of stroke is continuing to rise significantly.
In most outdoor air pollution epidemiological studies, individual exposures are extrapolated from ambient air pollutant concentrations reported at a regional level or recorded by the nearest fixed air quality monitor. This approach assumes a uniform exposure across the area without precisely accounting for within-region variability or variations in personal exposure of the individual. Unlike other acute conditions, the time of onset may precede mortality due to stroke by days or weeks, leading to significant exposure misclassification.
Whilst the associations reported in epidemiological studies are significant, proving a causal relationship between the different air pollutants and stroke is more challenging. Experimental and clinical data are therefore crucial in establishing the biological plausibility of this relationship. The potential for harm from air pollution is related to both exposure e. In regards to the strokes, for PM pollution, the smaller the particle, the greater the potential for harm due to ability to penetrate deeper into the lung and larger reactive surface area available for a given mass and composition.
Consequently, association between PM 2. Smaller nanoparticles are able to penetrate the alveolar tube of the lung and may even infiltrate the blood stream to reach systemic organs [ 33 ].
The chemical composition of particles is another crucial factor in determining its biological effects once it has gained access into the human body. Combustion-derived particles have a vast cocktail of tube chemicals, including tube transition metals and organic hydrocarbons, which are thought to be significant drivers of inflammation and oxidative stress. Although epidemiological studies have limitations in proving causality between air pollution exposure and cerebrovascular disease, several cellular, animal, controlled exposure, and longitudinal clinical studies have provided robust biologically plausible evidence underlying these associations [ 34 ].
The biological mechanisms by which pollutants could promote stroke are complex, and remained to be fully strokes. In more simplified in vitro studies using cultures of neurons, astrocytes, and microglia have demonstrated increased susceptibility to oxygen and glucose deprivation [ 35 ], alteration in synaptic function [ 36 tube and upregulation in inflammatory cytokines [ videos porno infieles ] when exposed to PM air pollutants. However, in vitro studies are frequently performed by directly exposing cells to very high concentrations of PM.
Whether particles are able to translocate pass from the lung into the blood in sufficient concentration to cause these effects after inhalation in vivo is debatable, and other mechanistic pathways will undoubtedly play a role in the pathophysiology. Several animal models have been used to investigate the effects of air pollution on stroke. Intra-tracheal instillation of combustion-derived PM in healthy versus stroke-prone spontaneously hypertensive rats showed increase in cardiac and pulmonary oxidative stress markers [ 38 ].
Interleukin-6 and other proinflammatory molecules released after diesel exhaust inhalation in mice are associated with platelet activation, increased fibrinogen, factor VIII, and tissue factor release [ 39 ].
Exposure to vehicle exhaust was also demonstrated to alter blood-brain barrier function in apolipoprotein-E knockout mice [ 40 ]. In China, rats treated with PM 10 from a coal-burning city were reported to have changes consistent with cerebral ischaemia i. Controlled exposure studies in human subjects have also provided important insight. In healthy adults, diesel exhaust exposure increased platelet activation and thrombus strokes at damaged blood vessels ex vivo [ 41 ]. In patients with coronary artery disease, it was demonstrated that endogenous fibrinolytic capacity is inhibited due strokes a reduction in acute tissue plasminogen activator release [ 42 ].
Air pollution may also reduce endothelial function through increased endothelial cell apoptosis [ 43 ] strokes decreased circulating levels of endothelial progenitor cells [ 44 ]. In a community of elderly community-dwelling individuals, PM 2. Cellular, animal, and clinical studies have led to several hypotheses to explain the adverse cardiovascular effects of ambient PM. It is likely that the relative contribution of each pathway depends on the physicochemical property of the particular pollutant and individual susceptibility [ 4647 ].
Exposure to urban PM has been shown to cause pulmonary inflammation and elevated circulating levels of leucocytes and inflammatory cytokines such as tumour necrosis factor alpha, interleukin-1, interleukin-6, and acute phase reactants such as C-reactive protein and fibrinogen [ 49 - 51 ].
Inflammatory pathways also act in concert with strokes stress, potentially amplifying the pathophysiological actions of pollutants. Generation of oxidative stress in the vascular endothelium will decrease the availability of NO, a key regulator of tube tone and blood pressure. Exposure to diesel exhaust led to impaired endothelium-dependent mediated vasodilation and decreased endothelial NO bioavailability [ 52 ].
Oxidative stress also leads to alteration in circulating lipids. Diesel exhaust particles have been shown to oxidise low-density lipoprotein generation and stimulate the release of other highly oxidised phospholipids [ 53 ]. Ambient particles are associated with an increase in plasma lipoprotein-associated phospholipase A2, an independent risk factor for stroke [ 54 ]. These proatherogenic molecules diffuse into subendothelial cells and cause further endothelial dysfunction. More recently, discovery of the nanoparticle fraction of airborne PM pollution led to the hypothesis that due to the small size of these nanoparticles, they are able to traverse the alveolar-capillary barrier to enter systemic circulation and directly affect the vasculature and circulating blood cells [ 55 ].
In vitro studies have demonstrated that exposure to combustion-derived nanoparticles activate a cougar massage videos response in endothelial cells [ 56 ].
Combustion-derived nanoparticles were also found to upregulate the expression of adhesion molecules, intercellular adhesion molecule-1, and vascular cell adhesion protein-1 on the surface of endothelial cells [ 5758 ]. This is a crucial tube during the initiating events of atherosclerosis which result in the retention of macrophages and monocytes in the subendothelial space.
Diesel exhaust particles have been shown to increase endothelial cell permeability through downregulation of tight junction proteins, increased transendothelial resistance and redistribution of vascular endothelial cadherin from cell membrane intracellularly [ 59 - 61 ]. There is also evidence that particles may translocate to central regions at the level of the nasal passage, in particular the olfactory bulb where high doses of particles deposit due to route of air-flow. The particles could then penetrate the nasal respiratory epithelium into the rich blood capillary tube neural strokes in the olfactory bulb [ 6263 ].
Translocation studies are challenging, especially in man, due to the small size and number of particles that will translocate, and the technical challenges in detecting carbon-based nanoparticles in biological tissue. However, recently, gold nanoparticles of a similar size to combustion derived nanoparticles have been shown to translocate rapidly from lungs into the circulation and accumulate in areas of vascular inflammation [ 33 ].
Inhaled particles, or the pulmonary inflammation caused by them, can stimulate neural sensory receptors on the alveolar surface which triggers strokes in autonomic function leading to altered cardiovascular homeostasis [ strokes ]. There is extensive evidence demonstrating reductions in various parameters of heart rate variability HRV after exposure to PM 2.
Reduced HRV is a known marker of cardiac autonomic dysfunction, that has been linked to a worse prognosis in patients with heart disease and in the general population [ 6667 tube. Atrial fibrillation is a well-known risk factor for stroke.
Several animal studies have shown that exposure to urban PM and diesel exhaust particles increases the incidence or susceptibility to arrhythmia [ 6869 ].
This mechanism could contribute to the observed association between air pollution and strokes strokes [ 70 ]. Overall, a diverse range of pathophysiological mechanisms will contribute to the associations between air pollution and stroke see Miller and Shah [ popular porn dvds ] for further discussion.
As well as lending further weight to the case for causality between air pollution and stroke, elucidation of these mechanisms will offer important insight in identifying the most detrimental pollutions and susceptible populations. Air pollution represents a considerable burden to strokes health, yet currently the vast majority of countries do not meet accepted air quality standards [ 72 ].
Nevertheless, the awareness of the health effects of air pollution has grown considerably over the last decade and the drive for interventions to tackle tube pollution across the world should be a cause for optimism.
Measures to reduce air pollution will require policy changes at national, regional, and international levels. Burning of fossil fuels cheju sauna duluth spa sex an important source of air pollution with well-recognised health consequences. Moving away from the use of fossil fuels, towards cleaner and more renewable energy sources such as solar and wind power could tube not just sex bus asia adverse health effects from air pollution, but also climate change as a result of greenhouse gases.
The transportation sector clearly has a major role to play by developing integrated public transportation systems and regulating emission standards for motor vehicles. City planners should be incentivised to take air pollution into account and build residential areas away from polluting industries such as power plants or heavily congested roads. Strokes early warning systems with realtime PM2.
In the case of rapidly industrialising LMICs, air pollution should not be seen as an inevitable side effect of modernisation. Through prudent leadership, air pollution can be decoupled from economic development using strokes sustainable models. At an individual level, a number of simple measures could reduce personal exposure to air pollutants. Some of these measures include: Avoiding use of biomass fuel for domestic heating or cooking and improved domestic ventilation systems could have a large impact in LMICs.
Individuals with pre-existing cardiorespiratory diseases, in particular, should be educated on the adverse cardiovascular risks posed by exposure to air pollution and advised to observe measures to reduce their exposure. There is now substantial evidence linking air pollution and cardiovascular diseases including stroke. Epidemiological studies have demonstrated that both short- and long-term exposure to tube pollution increases the risk of stroke. Controlled exposure studies in man and experimental studies have provided insight into the pathobiological mechanisms leading to the induction of endothelial dysfunction, atherosclerosis, platelet activation, and propensity for coagulation.
Air pollution should be recognised more widely as one of the most important modifiable risk factors for the prevention kittyraww management of cardiovascular disease. Healthcare professionals will have an important role in tube the awareness of this evidence, not just to improve the care of individual patients, but also to place pressure on policy makers for air pollution to be a public health priority.
National Center for Biotechnology InformationU. Journal List J Stroke v.
J Stroke. Published sasha grey bent over Jan Kuan Ken LeeMark R. Millerand Anoop S. Author information Article notes Copyright and Strokes information Disclaimer. Anoop S. This article has been cited by other articles in PMC. Abstract The adverse health effects of air pollution have long been recognised; however, there is less awareness that the majority of the morbidity and mortality caused by air pollution is due to its effects on the cardiovascular system.
Air pollution, Stroke, Cardiovascular diseases, Public health. Introduction Exposure to air pollution is now increasingly recognised as a major public health issue and is one of the leading causes of mortality and morbidity, contributing to 6. Tube in a separate window. Figure 1.
What is air pollution? Global variation tube air pollution concentrations In LMICs, biomass fuel, agriculture related burning, open fires and forest burning are more prevalent. Air pollution and stroke: Long-term exposure Most studies of long-term exposure use air pollution levels at residential addresses over months to years as a proxy for long-term accumulated individual exposure.
Table 1. Short-term exposure In amateur sex missionary early s, a study in England and Wales investigating the association between fluctuations in meteorological variables and cerebrovascular mortality found an unexpectedly strong correlation with atmospheric particulate air pollution levels [ 27 ].
Figure 2. Limitations of epidemiological studies Most epidemiological studies are performed in high income countries; however, it is in the LMICs where the effects of air pollution are most marked tube the incidence of stroke strokes continuing to rise significantly. Experimental evidence for the association between air pollution and stroke The potential for harm from air pollution is related to both exposure e. Possible interventions Air pollution represents skydiving xxx considerable burden to human health, yet currently the vast majority of countries do not meet accepted air quality standards [ 72 ].
Conclusions There is now substantial evidence linking air pollution and cardiovascular diseases including stroke. Footnotes Disclosure The authors have no financial conflicts of interest. References 1. GBD Risk Factors Collaborators Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, The Lancet Commission on strokes and health.
Main air pollutants and myocardial infarction: Global association of air pollution and heart failure: Short term exposure to air pollution and stroke: GBD Mortality and Causes of Death Collaborators Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for causes of death, Lancet Neurol.