β-Blockers improve cardiac function in heart failure by which of the following mechanisms?

β-Blockers improve cardiac function in heart failure primarily by decreasing cardiac remodeling. In heart failure, the heart undergoes structural changes, referred to as remodeling, which can lead to further decline in cardiac function. β-Blockers help mitigate these pathological changes by reducing the effects of excessive sympathetic nervous system stimulation. When norepinephrine levels are high, as often occurs in heart failure, this can lead to increased heart rate and myocardial contractility initially, but over time it contributes to detrimental remodeling and worsening heart function.

By blocking the β-adrenergic receptors, these medications decrease the influence of excess sympathetic activity, which not only slows heart rate but also reduces myocardial oxygen demand and helps improve the efficiency of the heart. Additionally, β-Blockers have been shown to positively affect myocyte survival and reduce fibrosis, both of which are critical in preventing adverse remodeling of the heart muscle.

In contrast, increasing heart rate, increasing renin release, and activating norepinephrine are mechanisms that would not contribute positively to heart failure treatment; in fact, they are generally counterproductive to improving heart function in this context. Thus, the mechanism through which β-Blockers exert their beneficial effects is linked to their ability to decrease cardiac remodeling, which is crucial to