A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Arterial bicarbonate is associated with hypoxic burden and uncontrolled hypertension in obstructive sleep apnea - The ESADA cohort
Tekijät: Zou Ding, Grote Ludger, Basoglu Ozen K., Verbraecken Johan, Schiza Sophia, Sliwinski Pawel, Steiropoulos Paschalis, Lombardi Carolina, Hein Holger, Pépin Jean-Louis, Parati Gianfranco, McNicholas Walter T., Hedner Jan; ESADA collaborators
Kustantaja: Elsevier
Julkaisuvuosi: 2023
Journal: Sleep Medicine
Tietokannassa oleva lehden nimi: Sleep Medicine
Vuosikerta: 102
Aloitussivu: 39
Lopetussivu: 45
ISSN: 1389-9457
eISSN: 1878-5506
DOI: https://doi.org/10.1016/j.sleep.2022.11.041
Verkko-osoite: https://doi.org/10.1016/j.sleep.2022.11.041
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/381255153
Objective Blood bicarbonate concentration plays an important role for obstructive sleep apnea (OSA) patients to maintain acid-base balance. We investigated the association between arterial standard bicarbonate ([HCO3-]) and nocturnal hypoxia as well as comorbid hypertension in OSA. Methods A cross-sectional analysis of 3329 patients in the European Sleep Apnea Database (ESADA) was performed. Arterial blood gas analysis and lung function test were performed in conjunction with polysomnographic sleep studies. The 4% oxygen desaturation index (ODI), mean and minimum oxygen saturation (SpO2), and percentage of time with SpO2 below 90% (T90%) were used to reflect nocturnal hypoxic burden. Arterial hypertension was defined as a physician diagnosis of hypertension with ongoing antihypertensive medication. Hypertensive patients with SBP/DBP below or above 140/90 mmHg were classified as controlled-, uncontrolled hypertension, respectively. Results The [HCO3-] level was normal in most patients (average 24.0 ± 2.5 mmol/L). ODI, T90% increased whereas mean and minimum SpO2 decreased across [HCO3-] tertiles (ANOVA, p = 0.030, <0.001, <0.001, and <0.001, respectively). [HCO3-] was independently associated with ODI, mean SpO2, minimum SpO2, and T90% after adjusting for confounders (β value [95%CI]: 1.21 [0.88–1.54], −0.16 [-0.20 to −0.11], −0.51 [-0.64 to −0.37], 1.76 [1.48–2.04], respectively, all p < 0.001). 1 mmol/L elevation of [HCO3-] was associated with a 4% increased odds of uncontrolled hypertension (OR: 1.04 [1.01–1.08], p = 0.013). Conclusion We first demonstrated an independent association between [HCO3-] and nocturnal hypoxic burden as well as uncontrolled hypertension in OSA patients. Bicarbonate levels as an adjunctive measure provide insight into the pathophysiology of hypertension in OSA.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
