Sleep · 2026
Effects of treatment with minute-ventilation triggered adaptive servo-ventilation early after acute myocardial infarction on nocturnal hypoxemic burden: results from TEAM-ASV I.
СтатьяРандомизированное исследованиеМногоцентровое исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Pec Jan, Baumert Mathias, Fox Henrik, Stadler Stefan, Driendl Sarah, Oldenburg Olaf, Zeman Florian, Tanacli Radu, Kelle Sebastian, Buchner Stefan, Arzt Michael
Аннотация
STUDY OBJECTIVES: In patients with acute myocardial infarction (AMI), early use of minute-ventilation triggered adaptive servo-ventilation (ASVmv) for sleep-disordered breathing has been proposed as a therapeutic intervention to reduce infarct expansion. This study aims to assess the efficacy of ASVmv in modulating nocturnal hypoxemic burden and evaluate its association with infarct size.
METHODS: This ancillary analysis of the multicenter, randomized, open-label TEAM-ASV I trial included patients with first-time AMI and sleep-disordered breathing, defined by an apnea-hypopnea index ≥ 15 events h-1 assessed with polygraphy. Infarct size was quantified via cardiac magnetic resonance imaging. Nocturnal hypoxemic burden was quantified by the time in bed spent with oxygen saturation below 90% (T90) and further decomposed into desaturation-related components (T90desaturation) and non-specific drifts (T90non-specific).
RESULTS: Thirty-five patients with infarct size 15.5 ± 6.9% of left ventricular mass were randomized to early ASVmv treatment in addition to standard care of AMI (n = 16) and standard care alone (control, n = 19). Compared with baseline, all components of hypoxemic burden, T90 (9.25% [1.34-16.32] vs. 0.03% [0.00-1.72; p = .003]), T90desaturation (0.72% [0.49-7.97] vs. 0.00% [0.00-0.06]; p < .001), and T90non-specific (4.75% [0.38-10.30] vs. 0.00% [0.00-1.73]; p < .001) were significantly reduced during the ASVmv treatment initiation night. After 12 weeks, ASVmv treatment showed lower median T90desaturation compared to the control group (ASVmv: 0.10% [0.00-0.40] vs. control: 0.40% [0.22-1.80]; p = .020) but not T90non-specific. T90 (rs = 0.437, p = .023) and its component, T90non-specific, were both associated with infarct size (rs = 0.424; p = .028).
CONCLUSIONS: ASVmv treatment suppresses the sleep apnea-related nocturnal hypoxemic burden following AMI. Higher T90, particularly non-specific drifts in SpO₂, were associated with larger infarct size. These findings are exploratory and should be regarded as hypothesis generating.
CLINICAL TRIAL REGISTRATION: NCT02093377.
METHODS: This ancillary analysis of the multicenter, randomized, open-label TEAM-ASV I trial included patients with first-time AMI and sleep-disordered breathing, defined by an apnea-hypopnea index ≥ 15 events h-1 assessed with polygraphy. Infarct size was quantified via cardiac magnetic resonance imaging. Nocturnal hypoxemic burden was quantified by the time in bed spent with oxygen saturation below 90% (T90) and further decomposed into desaturation-related components (T90desaturation) and non-specific drifts (T90non-specific).
RESULTS: Thirty-five patients with infarct size 15.5 ± 6.9% of left ventricular mass were randomized to early ASVmv treatment in addition to standard care of AMI (n = 16) and standard care alone (control, n = 19). Compared with baseline, all components of hypoxemic burden, T90 (9.25% [1.34-16.32] vs. 0.03% [0.00-1.72; p = .003]), T90desaturation (0.72% [0.49-7.97] vs. 0.00% [0.00-0.06]; p < .001), and T90non-specific (4.75% [0.38-10.30] vs. 0.00% [0.00-1.73]; p < .001) were significantly reduced during the ASVmv treatment initiation night. After 12 weeks, ASVmv treatment showed lower median T90desaturation compared to the control group (ASVmv: 0.10% [0.00-0.40] vs. control: 0.40% [0.22-1.80]; p = .020) but not T90non-specific. T90 (rs = 0.437, p = .023) and its component, T90non-specific, were both associated with infarct size (rs = 0.424; p = .028).
CONCLUSIONS: ASVmv treatment suppresses the sleep apnea-related nocturnal hypoxemic burden following AMI. Higher T90, particularly non-specific drifts in SpO₂, were associated with larger infarct size. These findings are exploratory and should be regarded as hypothesis generating.
CLINICAL TRIAL REGISTRATION: NCT02093377.