83 resultados para infarction


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Coronary heart disease (CHD) remains the greatest killer in the Western world, and although the death rate from CHD has been falling, the current increased prevalence of major risk factors including obesity and diabetes, suggests it is likely that CHD incidence will increase over the next 20 years. In conjunction with preventive strategies, major advances in the treatment of acute coronary syndromes and myocardial infarction have occurred over the past 20 years. In particular the ability to rapidly restore blood flow to the myocardium during heart attack, using interventional cardiologic or thrombolytic approaches has been a major step forward. Nevertheless, while 'reperfusion' is a major therapeutic aim, the process of ischemia followed by reperfusion is often followed by the activation of an injurious cascade. While the pathogenesis of ischemia-reperfusion is not completely understood, there is considerable evidence implicating reactive oxygen species (ROS) as an initial cause of the injury.

ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks, all potentially damaging to normal cellular function. ROS have been shown to be generated following routine clinical procedures such as coronary bypass surgery and thrombolysis, due to the unavoidable episode of ischemia-reperfusion. Furthermore, they have been associated with poor cardiac recovery post-ischemia, with recent studies supporting a role for them in infarction, necrosis, apoptosis, arrhythmogenesis and endothelial dysfunction following ischemia-reperfusion. In normal physiological condition, ROS production is usually homeostatically controlled by endogenous free radical scavengers such as superoxide dismutase, catalase, and the glutathione peroxidase and thioredoxin reductase systems. Accordingly, targeting the generation of ROS with various antioxidants has been shown to reduce injury following oxidative stress, and improve recovery from ischemia-reperfusion injury.

This review summarises the role of myocardial antioxidant enzymes in ischemia-reperfusion injury, particularly the glutathione peroxidase (GPX) and the thioredoxin reductase (TxnRed) systems. GPX and TxnRed are selenocysteine dependent enzymes, and their activity is known to be dependent upon an adequate supply of dietary selenium. Moreover, various studies suggest that the supply of selenium as a cofactor also regulates gene expression of these selenoproteins. As such, dietary selenium supplementation may provide a safe and convenient method for increasing antioxidant protection in aged individuals, particularly those at risk of ischemic heart disease, or in those undergoing clinical procedures involving transient periods of myocardial hypoxia.

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Objective To investigate whether attendance at cardiac rehabilitation (CR) independently predicts all-cause mortality over 14 years and whether there is a dose–response relationship between the proportion of CR sessions attended and long-term mortality.

Design Retrospective cohort study.

Setting CR programmes in Victoria, Australia

Patients The sample comprised 544 men and women eligible for CR following myocardial infarction, coronary artery bypass surgery or percutaneous interventions. Participants were tracked 4 months after hospital discharge to ascertain CR attendance status.

Main outcome measures All-cause mortality at 14 years ascertained through linkage to the Australian National Death Index.

Results In total, 281 (52%) men and women attended at least one CR session. There were few significant differences between non-attenders and attenders. After adjustment for age, sex, diagnosis, employment, diabetes and family history, the mortality risk for non-attenders was 58% greater than for attenders (HR=1.58, 95% CI 1.16 to 2.15). Participants who attended <25% of sessions had a mortality risk more than twice that of participants attending ≥75% of sessions (OR=2.57, 95% CI 1.04 to 6.38). This association was attenuated after adjusting for current smoking (OR=2.06, 95% CI 0.80 to 5.29).

Conclusions This study provides further evidence for the long-term benefits of CR in a contemporary, heterogeneous population. While a dose–response relationship may exist between the number of sessions attended and long-term mortality, this relationship does not occur independently of smoking differences. CR practitioners should encourage smokers to attend CR and provide support for smoking cessation.

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Long chain omega-3 polyunsaturated fatty acids (LC n-3 PUFA) particularly, eicosapentaenoic acid (EPA, 22: 5n-3) and docosahexaenoic acid (DHA, 22: 6n-3) have been reported to reduce the risks of cardiovascular disease (CVD) including myocardial infarction, stroke, coronary artery disease and sudden cardiac death. In addition, these fatty acids play an important role in reduction of cancer risks, Alzheimer's disease, depression and schizophrenia. Furthermore, studies also showed that EPA and DHA are important for foetal development, particularly neuronal and retinal functions. Several recent human trials have strengthened the evidence that EPA and DHA can reduce the risks of various chronic diseases although this has not been a uniform finding. In general, the high prevalence of mortality caused by chronic disease can be prevented by consumption of LC n-3 PUFA, which has been proven to have considerable health benefits. The aim of this paper was to review main scientific evidence regarding the health impact of LC n-3 PUFA, especially EPA and DHA on chronic disease including CVD, cancer, mental health, arthritis and infant development.

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Considerable variability in survival rate after an acute myocardial infarction exists and accurate risk stratification is of significant importance. The American College of Cardiology and the American Heart Association has recommended early risk stratification using several clinical risk scoring instruments to identify high risk patients. The aim of this paper is to identify secondary cardiovascular risk scoring instruments that could be utilized at the time of intervention for acute coronary syndromes and compare their psychometric properties as they were developed. A search using Medline, Cumulative Index to Nursing and Allied Health Literature and the Psychology and Behavioral Sciences Collection data-bases identified studies published between January 1990 and January 2010 used to measure risk after intervention for acute coronary syndrome. Four validated secondary risk prediction scoring instruments were identified for comparison.Secondary risk prediction scoring instruments for the acute coronary syndrome patient population are evidence based, valid and reliable. Use of the instruments by cardiac focused clinicians will aid in the determination of treatment strategies, and estimation of short and long term events and mortality.

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Background:
The use of pharmacological agents has been shown to slow down the progression of microvascular and 
macrovascular complications. Most clinical trials address one pharmacological intervention at a time. To date, only a few studies explored multi-factorial pharmacological interventions in T2DM individuals for preventing CVD related complications. Given the current therapeutic inertia in pharmacological management of CVD risk factors, it is important to establish the benefits of a more holistic approach. Therefore, the aim of this review is to assess the efficacy of multiple pharmacological interventions for cardiovascular diseases (CVD) risk factors with or without conventional care in reducing all cause mortality, CVD mortality, stroke and cardiovascular events among adults with type 2 diabetes. Current evidence fails to support the benefit of multiple pharmacological interventions on all cause mortality and death from cardiovascular causes. However, beneficial effects were seen on the reduction of the overall number of cardiovascular events and there were promising trends for secondary outcomes such as stroke, myocardial infarction, revascularisation and amputation.

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In 2003, the National Heart Foundation of Australia published a position statement on psychosocial risk factors and coronary heart disease (CHD). This consensus statement provides an updated review of the literature on psychosocial stressors, including chronic stressors (in particular, work stress), acute individual stressors and acute population stressors, to guide health professionals based on current evidence. It complements a separate updated statement on depression and CHD.

Perceived chronic job strain and shift work are associated with a small absolute increased risk of developing CHD, but there is limited evidence regarding their effect on the prognosis of CHD. Evidence regarding a relationship between CHD and job (in)security, job satisfaction, working hours, effort-reward imbalance and job loss is inconclusive.

Expert consensus is that workplace programs aimed at weight loss, exercise and other standard cardiovascular risk factors may have positive outcomes for these risk factors, but no evidence is available regarding the effect of such programs on the development of CHD.

Social isolation after myocardial infarction (MI) is associated with an adverse prognosis. Expert consensus is that although measures to reduce social isolation are likely to produce positive psychosocial effects, it is unclear whether this would also improve CHD outcomes. Acute emotional stress may trigger MI or takotsubo ("stress") cardiomyopathy, but the absolute increase in transient risk from an individual stressor is low. Psychosocial stressors have an impact on CHD, but clinical significance and prevention require further study.

Awareness of the potential for increased cardiovascular risk among populations exposed to natural disasters and other conditions of extreme stress may be useful for emergency services response planning. Wider public access to defibrillators should be available where large populations gather, such as sporting venues and airports, and as part of the response to natural and other disasters.

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In 2003, the National Heart Foundation of Australia position statement on “stress” and heart disease found that depression was an important risk factor for coronary heart disease (CHD). This 2013 statement updates the evidence on depression (mild, moderate and severe) in patients with CHD, and provides guidance for health professionals on screening and treatment for depression in patients with CHD.

The prevalence of depression is high in patients with CHD and it has a significant impact on the patient’s quality of life and adherence to therapy, and an independent effect on prognosis. Rates of major depressive disorder of around 15% have been reported in patients after myocardial infarction or coronary artery bypass grafting.

To provide the best possible care, it is important to recognise depression in patients with CHD. Routine screening for depression in all patients with CHD is indicated at first presentation, and again at the next follow-up appointment. A follow-up screen should occur 2–3 months after a CHD event. Screening should then be considered on a yearly basis, as for any other major risk factor for CHD.

A simple tool for initial screening, such as the Patient Health Questionnaire-2 (PHQ-2) or the short-form Cardiac Depression Scale (CDS), can be incorporated into usual clinical practice with minimum interference, and may increase uptake of screening.

Patients with positive screening results may need further evaluation. Appropriate treatment should be commenced, and the patient monitored. If screening is followed by comprehensive care, depression outcomes are likely to be improved.

Patients with CHD and depression respond to cognitive behaviour therapy, collaborative care, exercise and some drug therapies in a similar way to the general population. However, tricyclic antidepressant drugs may worsen CHD outcomes and should be avoided.

Coordination of care between health care providers is essential for optimal outcomes for patients. The benefits of treating depression include improved quality of life, improved adherence to other therapies and, potentially, improved CHD outcomes.

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The World Health Organization has recently focused attention on guidelines for night noise in urban areas, based on significant medical evidence of the adverse impacts of exposure to excessive traffic noise on health, especially caused by sleep disturbance. This includes serious illnesses, such as hypertension, arteriosclerosis and myocardial infarction. 2Loud? is a research project with the aim of developing and testing a mobile phone application to allow a community to monitor traffic noise in their environment, with focus on the night period and indoor measurement. Individuals, using mobile phones, provide data on characteristics of their dwellings and systematically record the level of noise inside their homes overnight. The records from multiple individuals are sent to a server, integrated into indicators and shared through mapping. The 2Loud? application is not designed to replace existing scientific measurements, but to add information which is currently not available. Noise measurements to assist the planning and management of traffic noise are normally carried out by designated technicians, using sophisticated equipment, and following specific guidelines for outdoors locations. This process provides very accurate records, however, for being a time consuming and expensive system, it results in a limited number of locations being surveyed and long time between updates. Moreover, scientific noise measurements do not survey inside dwellings. In this paper we present and discuss the participatory process proposed, and currently under implementation and test, to characterize the levels of exposure to traffic noise of residents living in the vicinity of highways in the City of Boroondara (Victoria, Australia) using the 2Loud? application.

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Background The metabolic syndrome (MetS) is a complex of multiple risk factors that contribute to the onset of cardiovascular disorder, including lowered levels of high-density lipoprotein (HDL) and abdominal obesity. Smoking, mood disorders, and oxidative stress are associated with the MetS. Paraoxonase (PON)1 is an antioxidant bound to HDL, that is under genetic control by functional polymorphisms in the PON1 Q192R coding sequence. Aims and methods This study aimed to delineate the associations of the MetS with plasma PON1 activity, PON1 Q192R genotypes, smoking, and mood disorders (major depression and bipolar disorder), while adjusting for HDL cholesterol, body mass index, age, gender, and sociodemographic data. We measured plasma PON1 activity and serum HDL cholesterol and determined PON1 Q192R genotypes through functional analysis in 335 subjects, consisting of 97 with and 238 without MetS. The severity of nicotine dependence was measured using the Fagerström Nicotine Dependence Scale. Results PON1 Q192R functional genotypes and PON1 Q192R genotypes by smoking interactions were associated with the MetS. The QQ and QR genotypes were protective against MetS while smoking increased metabolic risk in QQ carriers only. There were no significant associations between PON1 Q192R genotypes and smoking by genotype interactions and obesity or overweight, while body mass index significantly increased MetS risk. Smoking and especially severe nicotine dependence are significantly associated with the MetS although these effects were no longer significant after considering the effects of the smoking by PON1 Q192R genotype interaction. The MetS was not associated with mood disorders, major depression or bipolar disorder. Discussion PON1 Q192R genotypes and genotypes by smoking interactions are risk factors for the MetS that together with lowered HDL and increased body mass and age contribute to the MetS.

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BackgroundMajor depressive disorder (MDD) is an independent risk factor for coronary heart disease (CHD), and influences the occurrence and prognosis of cardiovascular events. Although there is evidence that antidepressants may be cardioprotective after acute myocardial infarction (AMI) comorbid with MDD, the operative pathophysiological mechanisms remain unclear. Our aim was therefore to explore the molecular mechanisms of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 in a rat model of depression during myocardial ischemia/reperfusion (I/R).MethodsRats were divided randomly into 3 groups (n = 8): D group (depression), DI/R group (depression with myocardial I/R) and escitalopram + DI/R group. The rats in all three groups underwent the same chronic mild stress and separation for 21 days, at the same time, in the escitalopram + DI/R group, rats were administered escitalopram by gavage (10 mg/kg/day). Ligation of the rat¿s left anterior descending branch was done in the myocardial I/R model. Following which behavioral tests were done. The size of the myocardial infarction was detected using 1.5% TTC dye. The Tunel method was used to detect apoptotic myocardial cells, and both the Rt-PCR method and immunohistochemical techniques were used to detect the expression of Bcl¿2 and Bax.ResultsCompared with the D and DI/R groups, rats in Escitalopram + DI/R group showed significantly increased movements and sucrose consumption (P < .01). Compared with the DI/R group, the myocardial infarct size in the escitalopram + DI/R group was significantly decreased (P < .01). Compared with the D group, there were significantly increased apoptotic myocardial cells in the DI/R and escitalopram + DI/R groups (P < .01); however compared with the DI/R group, apoptotic myocardial cell numbers in the escitalopram + DI/R group were significantly decreased (P < .01). Compared with the DI/R group, there was a down-regulated Bax:Bcl-2 ratio in the escitalopram + DI/R group (P < .01).ConclusionsThese results suggest that in patients with AMI comorbid with MDD, there is an increase in pro-apoptotic pathways that is reversed by escitalopram. This suggests that clinically escitalopram may have a direct cardioprotective after acute myocardial infarction.

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 Cardiovascular diseases are the most prevalent medical conditions affecting the modern world, reducing the quality of life for those affected and causing an ever increasing burden on clinical resources. Cardiac biomarkers are crucial in the diagnosis and management of patient outcomes. In that respect, such proteins are desirable to be measured at the point of care, overcoming the shortcomings of current instrumentation. We present a CO2 laser engraving technique for the rapid prototyping of a polymeric autonomous capillary system with embedded on-chip planar lenses and biosensing elements, the first step towards a fully miniaturised and integrated cardiac biosensing platform. The system has been applied to the detection of cardiac Troponin I, the gold standard biomarker for the diagnosis of acute myocardial infarction. The devised lab-on-a-chip device was demonstrated to have 24 pg/ml limit of detection, which is well within the minimum threshold for clinically applicable concentrations. Assays were completed within approximately 7–9 min. Initial results suggest that, given the portability, low power consumption and high sensitivity of the device, this technology could be developed further into point of care instrumentation useful in the diagnosis of various forms of cardiovascular diseases. 2014 Elsevier B.V. All rights reserved.

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It has long been established in traditional forms of medicine and in anecdotal knowledge that the health of the body and the mind are inextricably linked. Strong and continually developing evidence now suggests a link between disorders which involve Hypothalamic-Pituitary-Adrenal axis (HPA) dysregulation and the risk of developing psychiatric disease. For instance, adverse or excessive responses to stressful experiences are built into the diagnostic criteria for several psychiatric disorders, including depression and anxiety disorders. Interestingly, peripheral disorders such as metabolic disorders and cardiovascular diseases are also associated with HPA changes. Furthermore, many other systemic disorders associated with a higher incidence of psychiatric disease involve a significant inflammatory component. In fact, inflammatory and endocrine pathways seem to interact in both the periphery and the central nervous system (CNS) to potentiate states of psychiatric dysfunction. This review synthesizes clinical and animal data looking at interactions between peripheral and central factors, developing an understanding at the molecular and cellular level of how processes in the entire body can impact on mental state and psychiatric health.