1,721,382 research outputs found
Reverse remodeling in heart failure - fact or fiction?
No full textMaladaptive remodeling is associated with impaired prognosis in heart failure, and prevention of remodeling is an established therapeutic target. However, it is much less clear whether remodeling may be reversed once it has developed. In the last decade, anti-neuroendocrine therapy with ACE inhibitors, and even more potently, beta-blockers, was shown to improve surrogate markers for reverse remodeling, such as ejection fraction (EF), ventricular volumes, and mass. For beta-blockers, reverse molecular remodeling was also shown in biopsy specimens on the cellular and subcellular level. Both moderate endurance training and continuous positive airway pressure (CPAP) therapy in heart failure patients with steep apnea induce reverse remodeling. Cardiac resynchronization therapy improves exercise capacity and quality of life in patients with ventricular dyssynchrony and is clearly associated with geometrical and functional reverse remodeling over time. Whether this translates into improved survival remains to be demonstrated. Surgical approaches for reverse remodeling, such as mitral valve replacement, aneurysmectomy, and volume reduction (Batista procedure) have been developed, but may also be associated with high perioperative mortality. Mechanical unloading of the failing ventricles by left ventricular assist systems (LVAD) induces well-characterized reverse remodeling on the cellular and subcellular level. However, persistent functional improvement in a significant subset of patients that would allow weaning form the device is still under debate. Novel, complementary approaches, such as gene transfer or stem cell therapy are under pre-clinical and clinical investigation. Taken together, reverse remodeling can be induced by pharmacological and non-pharmacotogical therapy and may serve as a surrogate parameter for therapeutic success in the individual patient. Since maladaptive remodeling is associated with poor prognosis, identification of novel strategies to reverse this process remains a promising target. (C) 2004 Published by Elsevier Ltd on behalf of The European Society of Cardiology
Can brain natriuretic peptide be used to diagnose and manage patients with diastolic heart failure?
No full textDiastolic Heart Failure: Diagnosis, Therapy and Impact of Exercise Training
No full textHeart failure is a major health problem m the community Nearly half the patients suffering from signs and symptoms of heart failure have preserved systolic function and evidence of diastolic dysfunction. Comparable to systolic heart failure, patients with diastolic heart failure are characterised by high morbidity and mortality. Despite the urgent need of therapeutic strategies no evidence-based therapy is established in this condition. Exercise training, as a therapeutic approach, can prevent the age dependent occurrence of diastolic dysfunction. Moreover, there is little published evidence that exercise training may improve clinical outcome in patients with diastolic heart failure. but randomised trials using sufficient endpoints are lacking. Whether exercise training improves exercise capacity quality of life and diastolic function are objectives of the prospective, randomised. controlled Ex-DHF-P study. The preliminary results are promising, but need to be confirmed in a larger trial which also has to investigate the effects of exercise training on prognosis in patients with diastolic heart failure
Mild hypothermia leads to an increased sensitivity of the myofilaments for calcium in human myocardium
No full textMild hypothermia leads to an increased sensitivity of the myofilaments for calcium in human myocardium
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Phosphorylation of the cardiac ryanodine receptor by Ca2+/calmodulin-dependent protein kinase II - The dominating twin of protein kinase A?
No full textExercise training in heart failure
No full textIn patients with chronic but stable heart failure (HF) exercise training is a recommended and widely accepted adjunct to an evidence-based management involving pharmacological and non-pharmacological therapies. Various pathophysiological mechanisms, such as central hemodynamics, vasculature, ventilation, skeletal muscle function as well as neurohormonal activation and inflammation are responsible for exercise intolerance described in HF patients. There is sufficient and growing evidence that exercise training in HF with reduced (HFrEF) and with preserved ejection fraction (HFpEF) is effective in improving exercise capacity, HF symptoms and quality of life. The positive effects of exercise training in HF are mediated by an improvement of central hemodynamics, endothelial function, inflammatory markers, neurohumoral activation, as well as skeletal muscle structure and function. In contrast to convincing data from a large meta-analysis, the large HF-ACTION study (Heart Failure-A Controlled Trial Investigating Outcomes of exercise TraiNing) only demonstrated a modest improvement of all cause mortality and hospitalizations in HFrEF. Outcome data in HFpEF are lacking. Whether interval training incorporating variable and higher intensities or the addition of resistance exercise to a standard aerobic prescription is superior in improving clinical status of HF patients is currently being examined. Despite increasing validation of the potential of exercise training in chronic HF, challenges remain in the routine therapeutic application, including interdisciplinary management, financing of long-term exercise programs and the need to improve short-term and long-term adherence to exercise training
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