Sleep · 2026
Association of major adverse cardiovascular events with the apnea-hypopnea index, desaturation severity parameters, and cardiac troponins in participants of the Akershus Sleep APnea cohort.
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Feng Xin, Sigurdardottir Fjola, Arnardottir Erna Sif, Dammen Toril, Einvik Gunnar, Korkalainen Henri, Klungsøyr Ole, Leppänen Timo, Nordhus Inger Hilde, Nikkonen Sami, Töyräs Juha, Thorshov Thea, Øverby Tonje Caroline, Omland Torbjørn, Hrubos-Strøm Harald
Аннотация
STUDY OBJECTIVES: To examine the prognostic value of the apnea-hypopnea index (AHI), desaturation severity parameters, and cardiac troponins alone and combined for major cardiovascular events (MACEs).
METHODS: MACE data were retrieved in 2021 from the Norwegian Patient Registry for 518 participants in the Akershus Sleep APnea (ASAP) cohort. Baseline polysomnography and fasting blood samples were collected between June 2006 and January 2008. Desaturation duration (DesDur) and severity (DesSev) were calculated using Automatic Blood Oxygen Saturation Analysis software. Cox regression models estimated hazard ratios (HRs) for MACE. Predictive properties of combining troponins and obstructive sleep apnea severity were calculated by comparing established clinical thresholds for cardiac troponin I (cTnI) and T (cTnT) with AHI clinical thresholds of ≥15 and ≥30, respectively.
RESULTS: High AHI, DesDur, DesSev, cTnI, and cTnT were associated with increased MACE risk. However, only cTnI independently predicted MACE after adjustment (HR: 1.74, 95% CI: 1.32-2.29). The HR for MACE was 2.68 (95% CI: 1.03-6.97) in patients with both high cTnI and AHI ≥30 events/h.
CONCLUSION: In this 15-year follow-up, cTnI was independently associated with risk of MACE, whereas the AHI, desaturation parameters, and cTnT were not independent predictors. cTnI, especially when combined with AHI, was a stronger MACE predictor than cTnT. Provided our findings are validated in clinical obstructive sleep apnea populations, the measurement of cTnI may be considered for cardiovascular risk stratification.
METHODS: MACE data were retrieved in 2021 from the Norwegian Patient Registry for 518 participants in the Akershus Sleep APnea (ASAP) cohort. Baseline polysomnography and fasting blood samples were collected between June 2006 and January 2008. Desaturation duration (DesDur) and severity (DesSev) were calculated using Automatic Blood Oxygen Saturation Analysis software. Cox regression models estimated hazard ratios (HRs) for MACE. Predictive properties of combining troponins and obstructive sleep apnea severity were calculated by comparing established clinical thresholds for cardiac troponin I (cTnI) and T (cTnT) with AHI clinical thresholds of ≥15 and ≥30, respectively.
RESULTS: High AHI, DesDur, DesSev, cTnI, and cTnT were associated with increased MACE risk. However, only cTnI independently predicted MACE after adjustment (HR: 1.74, 95% CI: 1.32-2.29). The HR for MACE was 2.68 (95% CI: 1.03-6.97) in patients with both high cTnI and AHI ≥30 events/h.
CONCLUSION: In this 15-year follow-up, cTnI was independently associated with risk of MACE, whereas the AHI, desaturation parameters, and cTnT were not independent predictors. cTnI, especially when combined with AHI, was a stronger MACE predictor than cTnT. Provided our findings are validated in clinical obstructive sleep apnea populations, the measurement of cTnI may be considered for cardiovascular risk stratification.