Izolde Bouloukaki1, Ludger Grote2, Walter T McNicholas3, Jan Hedner2, Johan Verbraecken4, Gianfranco Parati5, Carolina Lombardi5, Ozen K Basoglu6, Athanasia Pataka7, Oreste Marrone8, Paschalis Steiropoulos9, Marisa R Bonsignore10, Sophia E Schiza1. 1. Sleep Disorders Center, Department of Respiratory Medicine, University of Crete, Heraklion, Greece. 2. Department of Sleep Medicine, Sahlgrenska University Hospital, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden. 3. Department of Respiratory and Sleep Medicine, St. Vincent's University Hospital, School of Medicine, University College, Dublin, Ireland. 4. Antwerp University Hospital, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium. 5. Department of Medicine and Surgery, University of Milano-Bicocca, Milan, Italy. 6. Department of Chest Diseases, Ege University Faculty of Medicine, Izmir, Turkey. 7. Department of Respiratory Medicine, Respiratory Failure Unit, G. Papanikolaou Hospital, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece. 8. National Research Council (CNR), Istituto per la Ricerca e l'Innovazione Biomedica, Palermo, Italy. 9. Sleep Unit, Department of Pneumonology, Democritus University of Thrace, Alexandroupolis, Greece. 10. Dipartimento di Promozione della Salute, Materno-Infantile, Medicina Interna e Specialistica di Eccellenza (PROMISE), University of Palermo, Palermo, Italy; *Contributed equally.
Abstract
STUDY OBJECTIVES: The association of mild obstructive sleep apnea (OSA) with important clinical outcomes remains unclear. We aimed to investigate the association between mild OSA and systemic arterial hypertension (SAH) in the European Sleep Apnea Database cohort. METHODS: In a multicenter sample of 4,732 participants, we analyzed the risk of mild OSA (subclassified into 2 groups: mildAHI 5-<11/h (apnea-hypopnea index [AHI], 5 to <11 events/h) and mildAHI 11-<15/h (AHI, ≥11 to <15 events/h) compared with nonapneic snorers for prevalent SAH after adjustment for relevant confounding factors including sex, age, smoking, obesity, daytime sleepiness, dyslipidemia, chronic obstructive pulmonary disease, type 2 diabetes, and sleep test methodology (polygraphy or polysomnography). RESULTS: SAH prevalence was higher in the mildAHI 11-<15/h OSA group compared with the mildAHI 5-<11/h group and nonapneic snorers (52% vs 45% vs 30%; P < .001). Corresponding adjusted odds ratios for SAH were 1.789 (mildAHI 11-<15/h; 95% confidence interval [CI], 1.49-2.15) and 1.558 (mildAHI 5-<11/h; 95%, CI, 1.34-1.82), respectively (P < .001). In sensitivity analysis, mildAHI 11-<15/h OSA remained a significant predictor for SAH both in the polygraphy (odds ratio, 1.779; 95% CI, 1.403-2.256; P < .001) and polysomnography groups (odds ratio, 1.424; 95% CI, 1.047-1.939; P = .025). CONCLUSIONS: Our data suggest a dose-response relationship between mild OSA and SAH risk, starting from 5 events/h in polygraphy recordings and continuing with a further risk increase in the 11- to <150-events/h range. These findings potentially introduce a challenge to traditional thresholds of OSA severity and may help to stratify participants with OSA according to cardiovascular risk.
STUDY OBJECTIVES: The association of mild obstructive sleep apnea (OSA) with important clinical outcomes remains unclear. We aimed to investigate the association between mild OSA and systemic arterial hypertension (SAH) in the European Sleep Apnea Database cohort. METHODS: In a multicenter sample of 4,732 participants, we analyzed the risk of mild OSA (subclassified into 2 groups: mildAHI 5-<11/h (apnea-hypopnea index [AHI], 5 to <11 events/h) and mildAHI 11-<15/h (AHI, ≥11 to <15 events/h) compared with nonapneic snorers for prevalent SAH after adjustment for relevant confounding factors including sex, age, smoking, obesity, daytime sleepiness, dyslipidemia, chronic obstructive pulmonary disease, type 2 diabetes, and sleep test methodology (polygraphy or polysomnography). RESULTS:SAH prevalence was higher in the mildAHI 11-<15/h OSA group compared with the mildAHI 5-<11/h group and nonapneic snorers (52% vs 45% vs 30%; P < .001). Corresponding adjusted odds ratios for SAH were 1.789 (mildAHI 11-<15/h; 95% confidence interval [CI], 1.49-2.15) and 1.558 (mildAHI 5-<11/h; 95%, CI, 1.34-1.82), respectively (P < .001). In sensitivity analysis, mildAHI 11-<15/h OSA remained a significant predictor for SAH both in the polygraphy (odds ratio, 1.779; 95% CI, 1.403-2.256; P < .001) and polysomnography groups (odds ratio, 1.424; 95% CI, 1.047-1.939; P = .025). CONCLUSIONS: Our data suggest a dose-response relationship between mild OSA and SAH risk, starting from 5 events/h in polygraphy recordings and continuing with a further risk increase in the 11- to <150-events/h range. These findings potentially introduce a challenge to traditional thresholds of OSA severity and may help to stratify participants with OSA according to cardiovascular risk.
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