Response to Comment on Neeland et al. The Impact of Empagliflozin on Obstructive Sleep Apnea and Cardiovascular and Renal Outcomes: An Exploratory Analysis of the EMPA-REG OUTCOME Trial. Diabetes Care 2020;43:3007–3015
Abstract
We acknowledge the thought-provoking hypothesis that Brikman and Dori (1) suggest to explain the lower incidence of new-onset obstructive sleep apnea (OSA) observed among participants treated with empagli fl ozin compared with placebo we recently reported. They suggest that sodium – glucose cotransporter 2 inhibition (SGLT2i) de-creases endogenous carbon dioxide (CO 2 ) through a shift in metabolic substrate away from carbohydrates and toward utilization of lipids and proteins, leading to a lower concentration of CO 2 in the pulmonary circulation and lower likelihood of apneic events during sleep. While the mechanisms explaining our ob-servations remain unknown and open to discussion, we disagree with the physio-logical description proposed and believe this hypothesis is unlikely to be correct. First, alkalization of the blood through lower CO 2 production should decrease, not increase, ventilatory drive as the apneic threshold is approached. This might lead to actual induction of central sleep apnea and reduced upper airway muscle In several inves-tigated the use of acetazolamide, a anhydrase inhibitor that increases urinary bicarbonate excretion leading to acidi fi cation of the to treat central sleep apnea by causing compensato-ry hyperventilation (the opposite of and
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Evidence Hub reads this as a secondary / pooled analysis. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence.
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