This was an ancillary analysis of a multicenter, randomized, open-label trial. The population included 35 patients with first-time acute myocardial infarction (AMI) and sleep-disordered breathing (apnea-hypopnea index ≥15 events h-1). Patients were randomized to minute-ventilation triggered adaptive servo-ventilation (ASVmv) or standard care alone.
During the ASVmv treatment initiation night, T90 (time in bed with SpO2 < 90%) was significantly reduced compared to baseline (effect size 9.25% [1.34-16.32] vs. 0.03% [0.00-1.72], p = .003). T90desaturation and T90non-specific were also significantly reduced (p < .001 for both). At 12 weeks, median T90desaturation was lower in the ASVmv group (0.10% [0.00-0.40]) than the control group (0.40% [0.22-1.80], p = .020). No significant difference was found for T90non-specific at 12 weeks.
T90 was positively associated with infarct size (rs = 0.437, p = .023), as was T90non-specific (rs = 0.424, p = .028). Safety data, including adverse events and discontinuations, were not reported.
Key limitations include the exploratory nature of the findings, which should be regarded as hypothesis generating. The small sample size (35 patients) and lack of reported safety data limit clinical interpretation. Practice relevance was not reported.
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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.