HF is a prevalent and debilitating disease, affecting nearly 5 million patients and perhaps an equal number with asymptomatic left ventricular dysfunction who are at high risk of atrial fibrillation developing. An estimated 550,000 new cases occur every year. HF is the most common diagnosis in hospitalized patients aged 65 and over and is a major cause of death. The median survival after onset is 1.7 years in men and 3.2 years in women. The majority of cardiac deaths in patients with HF are sudden and arrhythmogenic: the rest are due to progressive hemodynamic deterioration. A significant advance in the past decade has been the recognition of the importance of inhibiting the neurohormonal action in HF with the use of beta-blockers, angiotensin receptor, and aldosterone antagonists. In addition, a new concept in HF therapy has evolved. The view that chronic HF is an irreversible, end-stage process is being supplanted by the fact that it is possible to effect biological improvement in the intrinsic defects of function and structure in hearts afflicted with chronic HF. Reversibility of HF has been reported by (1) unloading the failing heart using an LVAD, (2) the sophisticated use of diuretic combinations and neurohormonal blocking drugs, or (3) employing continuous arteriovenous hemofiltration. Thus it is now possible to reverse a process that has long been considered irreversible. Exercise programs designed for patients with HF that have been advocated recently can be difficult to apply. Fine tuning of an exercise regimen is required because a reduction in cardiac work is mandatory when treating HF, where the concern is that the heart may not be capable of supplying the metabolic needs of the body, even in resting states. Finally, although not emphasized in the recent literature on HF, the use of diuretics and sodium restriction continue to be the mainstays of therapy without which compensation of HF is not possible.

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