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Published on: February 14, 2021
Central sleep apnea is associated with blunted baroreflex sensitivity in patients with myocardial infarction
Alan Strassburg1, Benina Majunke, Jana K Nötges
1Medizinische Klinik III, Universitätsklinikum Schleswig-Holstein Campus Lübeck, Lübeck, Germany.
Insights
Patients after acute myocardial infarction (AMI) show a higher incidence of central sleep apnea (CSA). Impaired baroreflex sensitivity (BRS) in AMI patients with CSA suggests a link between autonomic dysfunction and prognosis.
Area of Science:
- Cardiology
- Sleep Medicine
- Autonomic Neuroscience
Background:
- Central sleep apnea (CSA) and blunted baroreflex sensitivity (BRS) predict mortality in heart failure.
- BRS is well-studied post-acute myocardial infarction (AMI), but CSA incidence is unknown.
- Hypothesized interrelation between CSA and BRS due to sleep apnea's role in autonomic modulation.
Purpose of the Study:
- Investigate the association between central sleep apnea (CSA) and baroreflex sensitivity (BRS).
- Examine CSA and BRS in patients during the subacute phase of acute myocardial infarction (AMI).
Main Methods:
- Polysomnography with simultaneous ECG and blood pressure monitoring.
- 17 male patients post-AMI and 8 healthy male controls.
- Sleep stage-specific BRS calculated using time-domain sequential technique.
Main Results:
- AMI patients had higher incidence and duration of central apneas across all sleep stages.
- No significant sleep stage differences in BRS between groups.
- AMI patients with CSA exhibited blunted BRS, inversely correlated with central apnea incidence.
Conclusions:
- Suggests a direct relationship between impaired BRS and CSA occurrence post-AMI.
- Reflex cardiac autonomic control (BRS) may link CSA to prognosis after AMI.
Objectives:
The purpose of this study was to investigate the association of central sleep apnea (CSA) and baroreflex sensitivity (BRS) after acute myocardial infarction.
Background:
Both, CSA and blunted BRS have been shown to be independent predictors for cardiovascular mortality in patients with heart failure. But in contrast to BRS, which has been extensively studied in the setting of AMI, the incidence of CSA in patients recovering from AMI is thus far unknown. As previous reports suggested a potential role of sleep apnoea in augmenting reflex autonomic modulation, we hypothesized that there is a strong interrelation between CSA and BRS.
Methods:
Seventeen male patients in the subacute phase of a first uncomplicated ST-segment elevation AMI and eight healthy male controls without evidence of coronary artery disease underwent polysomnography with simultaneous beat-to-beat ECG- and blood-pressure recordings. Sleep stage specific spontaneous BRS was calculated from blood pressure and RR-interval fluctuations by using the time domain sequential technique.
Results:
AMI patients revealed to have a higher incidence and longer duration of central apnoeas in all sleep stages, light sleep, deep sleep and dream sleep. There were no significant sleep stage specific differences regarding BRS between groups, however, AMI patients with central sleep apnea exhibited blunted BRS which was inversely correlated to incidences of central apnea in all sleep stages.
Conclusions:
Our findings suggest a direct relationship between impaired BRS and repetitive occurrence of CSA by inverse correlation in all sleep stages in the subacute phase of AMI. Thus, reflex cardiac autonomic nervous control, being represented by the BRS, may be the link between CSA and prognosis.
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