10.12: Heart Failure Drugs: β-Blockers
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and vasoconstriction. Additionally, they inhibit renin release from the macula densa and hepatic glucose production. β-blockers play a crucial role in heart failure therapy and should be initiated at low doses, gradually increasing over time. They shift the concentration-response curve of catecholamines to the right, reversing the adverse gene program caused by chronic sympathetic stimulation. These medications improve left ventricular ejection fraction, reduce the risk of sudden cardiac death, decrease energy consumption, enhance contractile function, and improve myocardial perfusion.
Several β-blockers have been tested in clinical trials, including metoprolol, bisoprolol, carvedilol, and nebivolol. Carvedilol is a non-selective β-blocker and an α1-receptor antagonist, while nebivolol is selective for β1-receptors and has additional vasodilatory actions. Proper dosing is essential for successful therapy, taking into account pharmacokinetic differences. β-blockers are recommended for clinically stable patients with symptomatic heart failure or left ventricular dysfunction after myocardial infarction. Their adverse effects may include heart rate lowering, AV block, bronchoconstriction, and peripheral vasoconstriction, which should be monitored and managed. In summary, β-blockers have been shown to improve survival in patients with chronic heart failure by reducing sympathetic nervous system activity. They are an integral part of heart failure treatment, but their dosage should be carefully titrated to achieve optimal benefits while monitoring potential adverse effects.
