John E Madias1. 1. Icahn School of Medicine at Mount Sinai, New York, NY, and the Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, United States. Electronic address: madiasj@nychhc.org.
Author's replyDear Dr Madias, thank you for your comments on my review [1]. As you question, desensitization ofβ1-AR [2] alone may not explain apical akinesis, because β1-AR is not essential for myocardial contraction in physiological conditions. Therefore, combination of desensitization of β1-AR and upregulation of the β2-AR may be necessary to explain akinesis in super physiological condition. Causal relationship is another challenging issue. As you pointed out, desensitization of β1- or β2-AR may be aftermath rather than cause of myocardial dysfunction. Results from our previous study using serial endomyocardial biopsy specimens showing that GRK-2 and β-arrestin2 on the cell membrane were markedly reduced in the recovery phase from acute phase may support our hypothesis [2]. Thank you again for your interest and valuable comments.