First, we would like to thank Dr. Custodio and colleagues for their thoughtful comments regarding our recent publication “The impact of sleep disordered breathing on cardiac troponin in acutely decompensated heart failure” [1].

My co-authors and I acknowledge several issues that were raised regarding our work with which we agree. These include the relatively small sample size, as well as the potential effect of multiple confounding variables that may affect sleep disordered breathing, cardiac troponin levels, or both. Several of these variables were recognized by Custodio et al. in their letter including age, gender, history of coronary artery disease, creatinine clearance, presence of tachyarrhythmia, in-hospital supplemental oxygen use, and sedative/opiate use, though certainly others exist [2].

In order to minimize the effect of so many confounding variables, our study was specifically designed to measure overnight high-sensitivity troponin change and not absolute troponin levels, results that were then compared with sleep apnea testing characteristics [1]. Under this paradigm, subjects were compared with themselves, obviating the need to control for potential confounders. That being said, certainly it may make sense to group subjects according to physiological categories, such as HFpEF vs HFrEF, or type of heart failure exacerbation though our small sample size precluded such analysis.

Also worth mentioning is the difficulty inherent in studying this patient population, and the appropriateness of studying patients who require supplemental oxygen. Most of our patients required such therapy [1].

We would also reiterate our concern that despite medical management of heart failure, the apnea hypopnea index increased in most of our subjects on serial tests [1]. Better understanding of this pathophysiology is needed, and additional biomarkers (both cardiac and renal) should be studied. Ultimately larger studies with positive airway pressure treatment in these patients may help determine if sleep apnea is indeed the cause of subclinical myocardial injury, or merely guilty by association.