Heart failure monitor最新文献

Mechanical circulatory support devices (MCSDs) have been developed with the aim of bridging patients with advanced heart failure to cardiac transplantation, to recovery, and to serve as permanent support devices. The current generation of devices provides a differentiated spectrum of support, ranging from short-term to intermediate- and long-term duration, partial left ventricular (LV), complete LV, right ventricular, and biventricular options which can be tailored individually. The device positions range from paracorporeal to intracorporeal pumps with transcutaneous drivelines, to completely implantable systems. Major limitations are infection, coagulopathies, and device dysfunction. In this review, we discuss the history and experience with currently available MCSD options capable of supporting the circulation for 30 days.

Heart failure (HF) is an important cause of morbidity and mortality. Obesity is an increasingly prevalent condition that has been associated with increased cardiovascular risk, including increased risk of developing HF. Based on the associations of obesity with cardiac structural and hemodynamic alterations, as well as case reports of reversal of cardiomyopathy with weight loss, obesity has been presumed to have a deleterious effect in patients with HF. However, several recent studies have shown that in patients with established HF, obesity is not associated with increased mortality, but rather is associated with improved survival. Potential mechanisms for cardioprotection in obesity include a diminished activation of the neurohumoral system, an enhanced protection against endotoxin/inflammatory cytokines, and an increased nutritional and metabolic reserve. Further investigations into the relationship between obesity and the progression of HF are necessary. Ultimately, clinical trials are needed to provide definitive guidance to the management of obese and overweight HF patients.

Heart failure is the term used for a cardiovascular syndrome whose definition lacks uniform criteria. It is associated with a very high mortality rate. Approximately 50% of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT). In severe heart failure, death may also occur due to bradyarrhythmias. Other arrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation, and sustained or non-sustained VT. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations (such as fibrosis) may be prominent. Re-entrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. The treatment of the underlying disease process and optimal management of heart failure is of major importance. Revascularization, beta-blocker therapy, and angiotensin converting enzyme inhibitors are all essential to appropriate therapy. Treatment of arrhythmias is performed either because patients are symptomatic or to reduce the risk of sudden cardiac death. The implantable cardioverter-defibrillator (ICD) is the best available therapy to prevent sudden cardiac death from VT. Devices with back-up pacing also offer protection against bradyarrhythmias. There is evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy (e.g. amiodarone) because of atrial fibrillation or non-sustained VT that may activate the device.

It is well known that both atrial and ventricular arrhythmias play a key role in morbidity and overall mortality among patients with heart failure. In addition to pharmacological treatment, up-to-date and evidence-based use of invasive electrophysiology, including implantable cardioverter defibrillator implantation, is recommended in the global management of patients with heart failure. This article will review current clinical indications for invasive electrophysiology, either acknowledged or under evaluation, focusing on the scientific background and some technical and practical aspects. The discussion is organized in an arrhythmia-based manner so that ventricular-, atrial-, and heart transplant-related arrhythmias will be discussed separately.

Chronic heart failure (CHF) is associated with an increase in the production and secretion of various regulatory hormones that are initially beneficial, but become deleterious when elevated for prolonged periods. The neurohumoral excitation that occurs in the CHF state is mediated, in part, by abnormal inhibitory cardiovascular reflexes, such as the arterial baroreflex and the cardiopulmonary reflex. In addition, two sympatho-excitatory reflexes have been shown to be enhanced in CHF: the arterial chemoreflex and the cardiac sympathetic afferent reflex. While these reflexes may play a role in the sympatho-excitation of the CHF state, there is an important central modulation of sympathetic outflow by a variety of hormones that are elevated in CHF and have been shown to have neural effects. These include angiotensin II (Ang II), nitric oxide (NO), and endothelin-1. In fact, experimental animal data suggest that a central reciprocal relationship exists between Ang II and NO in their ability to modulate sympathetic outflow. These substances may also participate in the beneficial effects of exercise training in the CHF state. Exercise training lowers sympathetic nerve activity and plasma Ang II, and enhances arterial baroreflex function. This review emphasizes the neurohormonal and reflex regulation of sympathetic outflow in heart failure. While abnormal reflex regulation may predict a poor outcome, new treatment options may emerge from a better understanding of reflex regulation in CHF.