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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reflection on basic mechanisms in cardiac failure gives an insight into the modes of therapy available in management. Therapeutic options have in the past two decades expanded markedly with enhanced quality and quantity of life. With end stage disease the option of a heart transplant is providing quality of life to increasing numbers of selected patients.
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PMID:Cardiac failure. Current therapeutic concepts. 222 97

Cachexia has been known to physicians since ancient Greek times as a 'signum mali ominis' in various diseases indicating end stage disease and poor quality of life. Cardiac cachexia is recently receiving growing attention as modern treatment options prevent early death from cardiac events and more patients live with chronic compensated heart failure. Nevertheless, observation and clinical documentation of this condition go back as long as medical science itself. Pioneering studies on the reasons and mechanisms of cachexia were performed several decades ago. These studies provide fundamental insights and guidance towards a better understanding of cachexia. This review presents an overview of early thoughts and milestone studies on metabolic abnormalities and cachexia in chronic heart failure.
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PMID:Cardiac cachexia in early literature: a review of research prior to Medline. 1216 5

For the past several years, the development of new therapeutic agents for chronic heart failure (CHF) has been challenged by a number of confounding factors: (1) the large number of currently approved therapeutics that have already been shown in combination to have a beneficial effect on survival in CHF patients; (2) the number of patients required to document survival effects for any new additional agent; (3) the need to show a clear-cut effect on survival in mega-trials; (4) the chronic nature of the disease which requires long-term therapy with any new therapeutic as well as a relatively favourable long-term side effect profile; (5) a relative lack of understanding of the pivotal events that drive the onset of clinically relevant endpoints in heart failure and that might lead to their reversal; and (6) the poor druggability of many potential therapeutic targets for CHF. In this regard, recent studies in small animal models have suggested that promoting calcium cycling in the failing heart can potentially reverse severe heart failure, even at advanced stages. This offers the opportunity to design studies to reverse end stage disease, representing a new therapeutic paradigm with important implications for clinical trial design. At the same time, recent advances in catheter-based gene delivery and third-generation AAV vectors have now been shown to allow cardiac restricted, long-term, high efficiency in vivo gene delivery and expression in large animal CHF model systems with few long-term side effects. Recent collaborative studies from independent groups at the Massachusetts General Hospital, the Baker Institute and University of California San Diego have now provided direct evidence that manipulation of calcium cycling, either via the over-expression of SERCA or the blockade of the SERCA inhibitor phospholamban can reverse many important clinical endpoints that are direct surrogates of survival in the late stage failing heart. These studies have formed the foundation for the initiation of AAV-based gene therapy clinical trials in 2006-7 in the USA.
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PMID:Beyond small molecule drugs for heart failure: prospects for gene therapy. 1701 16

Heart failure (HF) is a cardiovascular disease with a permanent increase in prevalence, incidence and mortality. Current optimal therapies for HF are effective only for slowing, but not stopping, its progression. HF-related mortality is high, even at the time of the disease onset. Approximately 40% of HF-attributable deaths will be related to disease progression - however, its course is difficult to predict and therefore identifying patients experiencing the terminal stage of the disease is not correctly done. Most patients and their relatives do not identify HF as a progressive, terminal disease, and this perception also stands among health professionals - in consequence, end-stage HF patients often undergo active treatment procedures, event near the occurrence of death, although its implementation will be occasionally futile. Efforts should be undertaken by all health professionals to improve the identification and management of HF patients in the terminal stage of their disease.
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PMID:[Terminal heart failure]. 1733 40

Optimum heart failure medication and an increasing array of interventions have had an enormous effect on morbidity and mortality over the past 10 years. However, patients with end stage disease can still be highly symptomatic. Moreover, such patients are disadvantaged compared with patients with malignant disease. They are less likely to have an understanding of their illness or have access to supportive care. They are also less likely to have the opportunity to plan for care with regard to death and dying. There is increasing demand that the multi-professional clinical team gain good communication and supportive care skills, and that appropriate access to specialist palliative care services is available.
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PMID:Management of end stage cardiac failure. 1755 Oct 71

Heart failure is end-stage cardiac disease, developing in 46% of women within 6 years of having a myocardial infarction, and is the leading cause of all hospitalizations and readmissions in women over the age of 65 years. Since women present with atypical symptoms leading to inaccurate diagnosing of heart disease, education becomes a key component in increasing women's ability to self-manage heart failure symptoms and to become proactive in health-promoting behaviors. Health care providers are responsible for communicating discharge education including risk factors, causes, classification and staging, clinical presentation, diagnostic testing, and management of heart failure to assist women in managing this terminal disease and improving their quality of life.
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PMID:Heart failure: it's not just for men. 1864 17

The heart failure illness trajectory is both complex and unpredictable, which makes providing palliative care services to patients with heart failure a challenge. As a result, although services are needed, few tend to be offered beyond basic medical management. The traditional model of palliative care is typically based on palliative care being considered a system of care delivery most appropriate for patients with a predictable illness/death trajectory, such as terminal cancer. This type of model, which is based on the ability to predict the course of a terminal disease, does not fit the heart failure trajectory. In this article, we propose a new model of palliative care that conceptualizes palliative care as a philosophy of care that encompasses the unpredictable nature of heart failure.
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PMID:Review article: a model of palliative care for heart failure. 1982 Feb 4

Heart failure is a terminal disease with a very poor prognosis. Although the gold standard of treatment remains heart transplant, only a minority of patients can benefit from transplants. Another promising alternative is mechanical circulatory assistance using ventricular assist devices. The authors envision a completely implantable cardiac assist system affording tether-free mobility in an unrestricted space powered wirelessly by the innovative Free-Range Resonant Electrical Energy Device (FREE-D) system. Patients will have no power drivelines traversing the skin, and this system will allow power to be delivered over room distances and will eliminate trouble-prone wirings, bulky consoles, and replaceable batteries.
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PMID:Toward total implantability using free-range resonant electrical energy delivery system: achieving untethered ventricular assist device operation over large distances. 2206 13

Cardiovascular implantable electronic devices (CIED) are implanted increasingly frequently. CIEDs are indicated for the treatment of bradycardia, tachycardia and heart failure and therefore improve quality of life and life expectancy. CIED can treat ventricular arrhythmias that would be fatal without immediate care. However, CIEDs raise several patient education, medico-legal, and ethical questions that will be addressed in this article. Information is a patient's right, and necessary for informed consent. When implanting a CIED, the patient must be educated about the need for the device, the function of the device, any restrictions that apply postimplant, and postimplant follow-up methods and schedules. This transfer of information to the patient makes the patient responsible. The occupational physician can determine whether a patient wearing a CIED is able to work. Under current French law, patients are not prohibited from working while wearing a CIED. However, access to certain job categories remains limited, such as jobs involving mechanical stress to the chest, exposure to electromagnetic fields, or jobs requiring permanent vigilance. Pacemakers and defibrillators are medical treatments and are subject to the same ethical and clinical considerations as any other treatment. However, stopping a pacemaker or a defibrillator raises different ethical issues. Implantable Cardioverter Defibrillator shocks can be considered to be equivalent to resuscitation efforts and can be interpreted as being unreasonable in an end-of-life patient. Pacing is painless and it is unlikely to unnecessarily prolong the life of a patient with a terminal disease. Patients with a CIED should live as normally as possible, but must also be informed about the constraints related to the device and must inform each caregiver about the presence of the device. The forensic and ethical implications must be assessed in relation to current legislation.
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PMID:Cardiovascular implantable electronic devices: patient education, information and ethical issues. 2324 37

Huntington's disease (HD) is neurodegenerative disorder for which the mutation results in an extra-long tract of glutamines that causes the huntingtin protein to aggregate. It is characterized by neurological symptoms and brain pathology that is associated with nuclear and cytoplasmic aggregates and with transcriptional deregulation. Despite the fact that HD has been recognized principally as a neurological disease, there are multiple epidemiological studies showing that HD patients exhibit a high rate of cardiovascular events leading to heart failure. To unravel the mechanistic basis of cardiac dysfunction in HD, we employed a wide range of molecular techniques using the well-established genetic R6/2 mouse model that develop a considerable degree of the cardiac atrophy at end stage disease. We found that chronic treatment with isoproterenol, a potent beta-adrenoreceptor agonist, did not change the overall gross morphology of the HD murine hearts. However, there was a partial response to the beta-adrenergenic stimulation by the further re-expression of foetal genes. In addition we have profiled the expression level of Hdacs in the R6/2 murine hearts and found that the isoproterenol stimulation of Hdac expression was partially blocked. For the first time we established the Hdac transcriptional profile under hypertrophic conditions and found 10 out of 18 Hdacs to be markedly deregulated. Therefore, we conclude that R6/2 murine hearts are not able to respond to the chronic isoproterenol treatment to the same degree as wild type hearts and some of the hypertrophic signals are likely attenuated in the symptomatic HD animals.
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PMID:The Huntington's disease-related cardiomyopathy prevents a hypertrophic response in the R6/2 mouse model. 2526 75


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