Cao N, et al. - Researchers determined how the imbalance between β1-adrenergic receptor autoantibodies (β1-AAs) and β2-adrenergic receptor autoantibodies (β2-AAs) influences cardiac structure in heart failure (HF) and its underlying mechanisms. Participants were patients with left systolic HF who suffered from coronary heart disease (65.9%) or dilated cardiomyopathy (34.1%). These subjects were grouped into New York Heart Association Classes I–II (n=51) and Classes III–IV (n=37) and compared with healthy volunteers as controls (n=41). They found that, both in vitro and in vivo, β1-AAs-imposed impacts were antagonized by β2-AAs. The suggested mechanism underlying HF progression involved the imbalance of β1-AAs and β2-AAs in HF patients. Clinically, the increasing ratio of β1-AAs/β2-AAs should be considered while evaluating deterioration of cardiac function in patients with HF.