STUDY OBJECTIVES: The association of mild obstructive sleep apnoea (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 Apnoea Database (ESADA) cohort. METHODS: In a multicentre sample of 4732 patients we analyzed the risk of mild OSA (sub-classified into two groups: mildAHI 5-<11/h (apnoea-hypopnoea frequency/hour [AHI] 5 to <11/h) and mildAHI 11-<15/hOSA (AHI >=11 to <15/h ) compared to non-apnoeic snorers for prevalent SAH after adjustment for relevant confounding factors including gender, age, smoking, obesity, daytime sleepiness, dyslipidaemia, chronic obstructive pulmonary disease, type 2 diabetes and sleep test methodology [polygraphy (PG) or polysomnography (PSG)]. RESULTS: SAH prevalence was higher in the mildAHI 11-<15/h OSA group compared with the mildAHI 5-<11/h group and non-apnoeic snorers (52 vs 45 vs 30%, p<0.001). Corresponding adjusted Odds Ratios (OR) 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<0.001. In sensitivity analysis, mildAHI 11-<15/h OSA remained a significant predictor for SAH both in PG (OR = 1.779, 95% CI 1.403-2.256; p<0.001) and PSG group (OR = 1.424, 95% CI 1.047-1.939; p=0.025). CONCLUSION: Our data suggest a dose response relationship between mild OSA and SAH risk, starting from 5 events/hour in PG-recordings and continuing with a further risk increase in the 11 to <15 range. These findings potentially introduce a challenge to traditional thresholds of OSA severity and may help to stratify OSA patients according to cardiovascular risk.
Mild Obstructive Sleep Apnea Increases Hypertension Risk Challenging Traditional Severity Classification
Oreste Marrone;
2020
Abstract
STUDY OBJECTIVES: The association of mild obstructive sleep apnoea (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 Apnoea Database (ESADA) cohort. METHODS: In a multicentre sample of 4732 patients we analyzed the risk of mild OSA (sub-classified into two groups: mildAHI 5-<11/h (apnoea-hypopnoea frequency/hour [AHI] 5 to <11/h) and mildAHI 11-<15/hOSA (AHI >=11 to <15/h ) compared to non-apnoeic snorers for prevalent SAH after adjustment for relevant confounding factors including gender, age, smoking, obesity, daytime sleepiness, dyslipidaemia, chronic obstructive pulmonary disease, type 2 diabetes and sleep test methodology [polygraphy (PG) or polysomnography (PSG)]. RESULTS: SAH prevalence was higher in the mildAHI 11-<15/h OSA group compared with the mildAHI 5-<11/h group and non-apnoeic snorers (52 vs 45 vs 30%, p<0.001). Corresponding adjusted Odds Ratios (OR) 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<0.001. In sensitivity analysis, mildAHI 11-<15/h OSA remained a significant predictor for SAH both in PG (OR = 1.779, 95% CI 1.403-2.256; p<0.001) and PSG group (OR = 1.424, 95% CI 1.047-1.939; p=0.025). CONCLUSION: Our data suggest a dose response relationship between mild OSA and SAH risk, starting from 5 events/hour in PG-recordings and continuing with a further risk increase in the 11 to <15 range. These findings potentially introduce a challenge to traditional thresholds of OSA severity and may help to stratify OSA patients according to cardiovascular risk.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


