Background
The Treatment of sleep apnoea Early After Myocardial infarction with Adaptive Servo-Ventilation (TEAM-ASV I) trial showed that adding adaptive servo-ventilation (ASV) to treat sleep-disordered breathing (SDB) early after acute myocardial infarction (AMI) improved myocardial salvage and decreased infarct size. It is purported that ASV may mitigate the inflammatory response, cardiac congestion, or fibrosis, but evidence supporting this assertion is sparse.
Methods
This ancillary analysis of the multicentre, randomised, open-label TEAM-ASV I trial assessed patients with analysable blood samples at baseline and 12-week follow-up. Patients were randomised to early ASV treatment in addition to standard care for AMI and standard care alone (control). Changes in the levels of circulating biomarkers of inflammation (high-sensitivity C-reactive protein [hs-CRP], fibrinogen, interleukin [IL]-6, and interleukin-33 receptor [IL-33R]), fluid overload (N-terminal pro-B-type natriuretic peptide [NT-proBNP] and antigen carbohydrate [CA]-125), and fibrosis (procollagen III type aminoterminal propeptide [PIIINP] and matrix metalloproteinase [MMP]-9) were compared between the ASV and control groups.
Results
Forty SDB patients were analysed. The reduction in IL-33R was greater in the control group than in the ASV group (−1.94 [-3.88, 1.56] versus −4.30 [-6.46, −2.02] ng·ml−1). However, changes in other biomarkers of inflammation (hs-CRP, fibrinogen, and IL-6), fluid overload (NT-proBNP and CA-125), and fibrosis (PIIINP and MMP-9) were similar in both groups.
Conclusions
This ancillary analysis of TEAM-ASV I does not support that treatment of SDB in the early phase after AMI with ASV has a clinically relevant short-term effect on biomarkers of inflammation, fluid overload, or fibrosis. Further studies are warranted to explain how early treatment with ASV results in increased myocardial salvage after AMI beyond the effects of SDB treatment on hemodynamics and oxygen demand‒supply mismatch.