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Coronary blood flow becomes uncoupled from myocardial work during obstructive sleep apnea in the presence of

Garun S Hamilton1, Peter Solin, Adrian Walker

  • 1Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.

Sleep
|June 14, 2008
PubMed

Insights

Coronary blood flow (CBF) normally matches heart workload during obstructive sleep apnea (OSA). However, endothelial dysfunction disrupts this link, impacting oxygen supply to the heart muscle.

Area of Science:

  • Cardiovascular Physiology
  • Sleep Medicine
  • Respiratory Physiology

Background:

  • Obstructive sleep apnea (OSA) is linked to poor outcomes in patients with coronary artery disease.
  • The relationship between coronary blood flow (CBF) and myocardial metabolic demands during OSA is not fully understood.
  • Coronary artery endothelial dysfunction may alter the CBF response to OSA.

Purpose of the Study:

  • To assess the coronary blood flow (CBF) response during obstructive sleep apnea (OSA).
  • To determine if the CBF response is adequate for myocardial metabolic requirements.
  • To evaluate the CBF response before and after inducing coronary artery endothelial dysfunction.

Main Methods:

  • Newborn lambs were instrumented for hemodynamic monitoring and EEG recordings.
  • Obstructive sleep apnea (OSA) was modeled using a tracheostomy during sleep.
  • Coronary artery endothelial dysfunction was induced with lipopolysaccharide (LPS) infusions.
  • Coronary blood flow (CBF) was measured and compared to myocardial work (RPP), O2 saturation, and cortical arousal.

Main Results:

  • During OSA, CBF increased appropriately with myocardial work before LPS infusion.
  • Post-apnea CBF correlated with rate-pressure product, O2 saturation, and cortical arousal pre-LPS.
  • Following LPS-induced endothelial dysfunction, only O2 desaturation predicted CBF changes.

Conclusions:

  • In healthy lambs, CBF adequately matches myocardial work demands during OSA.
  • Coronary artery endothelial dysfunction, induced by LPS, uncouples the normal CBF-myocardial work relationship.
  • This suggests impaired coronary vasoreactivity in OSA patients with endothelial dysfunction.
Abstract

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