139 resultados para cardiovascular


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Cardiovascular diseases are the leading cause of death and morbidity in industrialized nations and are becoming an urgent health problem for all nations due to the unstoppable trend of an ageing and obese population. Due to the rapid development of micro total analysis systems (μTAS) and nanotechnology in recent years, they will play an important role in the diagnosis, management, and therapy of cardiovascular diseases. It is envisaged that the micro and nanotechnologies developed for treating other diseases shall be explored for cardiovascular applications to reduce the research effort required for commercializing the devices and drugs to meet the increasing demand of the cardiovascular patients.

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Panic disorder can serve as a clinical model for testing whether mental stress can cause heart disease. Potential neural mechanisms of cardiac risk are the sympathetic activation during panic attacks, continuing release of adrenaline as a co-transmitter in the cardiac sympathetic nerves, and impairment of noradrenaline neuronal reuptake, augmenting sympathetic neural respnses.

The phenotype of impaired neuronal reuptake of noradrenaline: an epigenetic mechanism? We suspect that this phenotype, in sensitizing people to heart symptom development, is a cause of panic disorder, and by magnifying the sympathetic neural signal in the heart, underlies increased cardiac risk. No loss of function mutations of the coding region of the norepinephrine transporter (NET) are evident, but we do detect hypermethylation of CpG islands in the NET gene promoter region. Chromatin immunoprecipitation methodology demonstrates binding of the inhibitory transcription factor, MeCP2, to promoter region DNA in panic disorder patients.

Cardiovascular illnesses co-morbid with panic disorder. Panic disorder commonly coexists with essential hypertension and the postural tachycardia syndrome. In both of these cardiovascular disorders the impaired neuronal noradrenaline reuptake phenotype is also present and, as with panic disorder, is associated with NET gene promoter region DNA hypermethylation. An epigenetic ‘co-morbidity’ perhaps underlies the clinical concordance.

Brain neurotransmitters. Using internal jugular venous sampling, in the absence of a panic attack we find normal norepinephrine turnover, but based on measurements of the overflow of the serotonin metabolite, 5HIAA, a marked increase (six to sevenfold) in brain serotonin turnover in patients with panic disorder. This appears to represent the underlying neurotransmitter substrate for the disorder. Whether this brain serotonergic activation is a prime mover, or consequential on other primary causes of panic disorder, including cardiac sensitization by faulty neuronal noradrenaline reuptake leading to cardiac symptoms and the enhanced vigilance which accompanies them, is unclear at present.

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Jamie Robinson, the Berkeley health economist, famously remarked in 2001 that ‘the three worst ways to pay doctors are salary, capitation and fee-for-service.’ Different financial incentives produce different clinical and service outcomes, sometimes perversely.1 In 2004, the UK government introduced pay for performance (P4P) for general practitioners, the Quality and Outcomes Framework (QOF). Its introduction was associated with the general trend in the National Health Service away from placing implicit trust in doctors and more active monitoring of their performance. One-quarter of GP pay can be earned from achieving scores on 147 indicators.2 These indicators were acceptable to doctors because the majority are evidence-based clinical outcome measures for 10 chronic diseases. Others relate to patient access and satisfaction, and practice organisation.

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Background: Cardiovascular disease (CVD) is the leading cause of death globally. Community pharmacist intervention studies have demonstrated clinical effectiveness for improving several leading individual CVD risk factors. Primary prevention strategies increasingly emphasise the need for consideration of overall cardiovascular risk and concurrent management of multiple risk factors. It is therefore important to demonstrate the feasibility of multiple risk factor management by community pharmacists to ensure continued currency of their role.
Methods/Design: This study will be a longitudinal pre- and post-test pilot study with a single cohort of up to 100 patients in ten pharmacies. Patients aged 50-74 years with no history of heart disease or diabetes, and taking antihypertensive or lipid-lowering medicines, will be approached for participation. Assessment of cardiovascular risk, medicines use and health behaviours will be undertaken by a research assistant at baseline and following the intervention (6 months). Validated interview scales will be used where available. Baseline data will be used by accredited medicines management pharmacists to generate a report for the treating community pharmacist. This report will highlight individual patients’ overall CVD risk and individual risk factors, as well as identifying modifiable
health behaviours for risk improvement and suggesting treatment and behavioural goals. The treating community pharmacist will use this information to finalise and implement a treatment plan in conjunction with the patient and their doctor. Community pharmacists will facilitate patient improvements in lifestyle, medicines adherence, and medicines management over the course of five counselling sessions with monthly intervals. The primary outcome will be the change to average overall cardiovascular risk, assessed using the Framingham risk equation.
Discussion: This study will assess the feasibility of implementing holistic primary CVD prevention programs into community pharmacy, one of the most accessible health services in most developed countries.

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Evidence from epidemiological studies has established that depression is a risk factor for the development of cardiovascular disease (CVD) and that the comorbidity of depression with pre-existing CVD worsens the prognosis for sufferers of CVD. Depression has also been associated with other behaviours that impact on CVD, such as medication non-compliance, and an unwillingness to adopt an exercise program, that reduce the likelihood of successful rehabilitation from CVD. Published literature on the current knowledge of the association between depression and CVD is reviewed in this paper.

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Objective: To examine population-level evidence treatment gaps for cardiovascular risk among rural patients with existing cardiovascular disease or diabetes.

Methods: Three population surveys were undertaken in the Greater Green Triangle region of southeastern Australia 2004-2006. Adults aged 25-84 yrs were randomly selected using age/sex stratified electoral role samples. A representative 1690 participants were recruited (48% participation rate). Anthropometric, clinical and self-administered questionnaire chronic disease risk data were collected in accordance with the WHO MONICA protocol. Detailed investigation of cardiovascular and diabetes history, key cardiovascular risk factors, medication use and health behaviours were included.

Results: After adjusting for age and sex, an estimated 12% (sample n=272) of the population had one or more of coronary heart disease, stroke, or diabetes. Blood pressure was at target (<130/80 mmHg) for 26% of these individuals, and 61% were treated with antihypertensive medications. Lipid targets were achieved by 17% for total cholesterol (<4 mmol/L), 18% for LDL cholesterol (<2 mmol/L), 77% for HDL cholesterol (>1.0 mmol/L) and 44% for triglycerides (<1.5 mmol/L); overall 6% achieved all four lipid targets and 60% reported use of lipid-lowering therapy, including 51% overall using statins. Ten percent were current smokers, and four in every five patients (82%) had suboptimal BMI (outside the range 18.5 - 25.0).

Conclusions: All participants with uncontrolled blood pressure and most with uncontrolled lipids should be taking medications. The magnitude of evidence treatment gaps suggests existing models of care need fundamental reform and renewed focus on prevention.