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The deleterious consequences of sympathetic activation in chronic heart failure (CHF) have been recognized for nearly 2 decades. 1 The degree of excess neurohormonal activation in this condition correlates with disease severity, is associated with progressive deterioration of cardiac function, accelerates abnormal myocardial remodeling after an infarction, and increases mortality rates. [2][3][4] In recent years, an interest in beta-adrenergic blocking agents as a therapeutic option in heart failure From the

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