Abstract
The incidence of congestive heart failure (CHF) continues to increase worldwide. Approximately 550,000 patients with CHF are newly diagnosed per year in the USA, which adds to the existing 5 million patients currently afflicted with this disease. Furthermore, there are approximately 3.1 million hospital admissions/year for heart failure, costing over US$23 billion (source: www.americanheartassociation.com). There is no cure for CHF and current therapies try to achieve relief of symptoms, improving a patient’s quality of life, and possibly lessening the progression of disease. Various classes of pharmaceuticals, such as diuretics, beta blockers, and angiotensin-converting enzyme inhibitors, have been the accepted therapy for CHF [Halawa, 1999]. These mainstream pharmaceuticals focus on lowering systolic and diastolic blood pressure, control of ventricular rate for atrial fibrillation, and decrease volume overload [Baliga and Young, 2008]. Acute achievement of these parameters can occur; however, chronic control is usually not maintained due to the progression of disease.
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