About this study
Congestive heart failure (CHF) affects nearly 5 million Americans and claims more than 300,000 lives annually. A primary pathophysiologic mechanism in this deadly syndrome is an abnormally enhanced sympathetic nervous system that results in profound peripheral vasoconstriction, attenuated cardiovascular reflexes, higher susceptibility to ventricular arrhythmias, and sudden cardiac death. The reduction in mortality and morbidity in CHF by pharmacologic neurohumoral antagonists such as beta-receptor inhibitor and angiotensin II-converting enzyme (ACE) inhibitor has taught us that regulation of the impaired neurohumoral axis is important for improving clinical outcome. In addition, an emerging nonpharmacologic approach, cardiac resynchronization therapy (CRT), has shown promise for improving symptoms and quality of life in patients with New York Heart Association (NYHA) functional class III or IV and intraventricular conduction delay. However, despite significant advances in CHF treatment in the past two decades, a gap remains between clinical outcome and the mechanisms of the protective effects of these modern therapies.
CHF is associated with increased concentrations of circulating norepinephrine (NE), down-regulation of adrenergic nerve terminals, and abnormal NE reuptake. The suppression of cardiac sympathetic nerve endings could be reversed by CRT, a novel anti-heart failure therapy, by rebalance cardiac sympathetic activity, and improve cardiac function in patients with heart failure.