2022
DOI: 10.1007/s11325-022-02606-1
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Potential Use of SGLT-2 Inhibitors in Obstructive Sleep Apnea: A new treatment on the horizon

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Cited by 11 publications
(7 citation statements)
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“…According to multiple studies using animal models receiving empagliflozin after myocardial infarction, SGLT2i may also work by inhibiting sympathetic nervous system activation [43]. Through this mechanism, SGLT2i may theoretically lessen circadian sympathetic overactivity and associated symptoms in OSA patients, including nocturnal hypertension, the non-dipping phenomena [44]. Dapagliflozin only significantly improves moderate-to-severe sleep disordered breathing (SDB), not mild SDB, according to Furukawa et al [32].…”
Section: Discussionmentioning
confidence: 99%
“…According to multiple studies using animal models receiving empagliflozin after myocardial infarction, SGLT2i may also work by inhibiting sympathetic nervous system activation [43]. Through this mechanism, SGLT2i may theoretically lessen circadian sympathetic overactivity and associated symptoms in OSA patients, including nocturnal hypertension, the non-dipping phenomena [44]. Dapagliflozin only significantly improves moderate-to-severe sleep disordered breathing (SDB), not mild SDB, according to Furukawa et al [32].…”
Section: Discussionmentioning
confidence: 99%
“…SGLT2i have been found to reduce apnea-hypopnea index in patients with T2DM with OSAS in small studies, though their beneficial effects on OSA or sleep-disordered breathing have not been substantiated by other studies or meta-analyses[ 47 - 49 ]. Apart from weight reduction, other postulated beneficial mechanisms could include rostral nasal fluid shift due to diuresis and reduction of circadian sympathetic nerve activity, nocturnal hypertension, and oxidative stress by which SGLT2i might reduce the incidence or the CV effects of OSA[ 50 , 51 ]. Further studies are required to elucidate the benefits of SGLT2i in this regard.…”
Section: Effects Of Sglt2i On Different CV Risk Factorsmentioning
confidence: 99%
“…In this way, SGLT2 inhibitors may decrease rostral-to-caudal fluid shifts in the recumbent sleep position, cardiac preload, and intrathoracic fluid retention; (iii) due to the modest increase in urinary frequency, manifested usually as nocturia, SGLT2 inhibitors could promote interrupted sleep cycles and suppress the duration of REM sleep (a higher risk period for OSA events); (iv) SGLT2 inhibitors can suppress circadian sympathetic nervous system activation and its related conditions (such as non-dipping pattern of hypertension, cardiac autonomic neuropathy, and stroke); (v) forced glucosuria after their administration can reduce the availability of glucose as an energy fuel. In this way other substrates are utilized, and less endogenous CO 2 production is expected, with less CO 2 to be removed by the respiratory tract; and (vi) modulation of arousal threshold, muscle compensation, and loop gain [78,[93][94][95][96][97][98].…”
Section: Pathophysiological Conceptsmentioning
confidence: 99%