Abstract
The failing heart is adrenergically activated, which helps to maintain cardiac performance over the short term by increasing contractility and heart rate. Multiple lines of evidence indicate that it is the increase in cardiac adrenergic drive rather than an increase in circulating norepinephrine that is both initially supportive and then ultimately damaging to the failing heart. The continuously increased adrenergic drive present in the failing heart delivers adverse biological signals to the cardiac myocyte via β1-and β2-adrenergic receptors. Thus, β-adrenergic receptor blocking agents produce clinical and hemodynamic improvement in severe heart failure.
