In patients with heart failure with reduced ejection fraction (HFrEF), adverse cardiac remodeling leads to deleterious changes in cardiac structure and function, including progressive left ventricular dilatation and reduced contractile function. Adverse cardiac remodeling is central to the pathophysiology of HFrEF. The effect of pharmacologic interventions on the remodeling process mirrors their therapeutic efficacy on clinical outcomes assessed in clinical trials of patients with HFrEF in most but not all cases.1 Early studies of neurohormonal antagonists exemplify this relationship. Angiotensin-converting enzyme (ACE) inhibitors and β-adrenergic receptor blockers attenuate2 or reverse3 the remodeling process, respectively, and both agents improve survival of patients with HFrEF.4