Hypertension, Sleep Apnea, and Atherosclerosis

Hypertension. 2009;53:1.)
© 2009 American Heart Association, Inc.

Editorial Commentaries
Hypertension, Sleep Apnea, and Atherosclerosis

John S. Floras

From the University Health Network and Mount Sinai Hospital Division of Cardiology, University of Toronto, Toronto, Ontario, Canada.

Correspondence to John S. Floras, Suite 1614, 600 University Ave, Toronto, Ontario, M5G 1X5 Canada. E-mail john.floras@utoronto.ca

Having obstructive sleep apnea (OSA) increases the relative odds of also having coronary artery disease by 27% and of having suffered a stroke by 58%.1 Approximately 50% of individuals with OSA are also hypertensive, and those who are not initially so have an {approx}3-fold increase in their likelihood of developing hypertension after 4 years if their apnea-hypopnea index (AHI) is ≥15 events per hour.2–4

Some of this propensity to cardiovascular events may accrue from site-specific consequences of OSA. For example, if transmission of the acoustic energy generated by snoring stimulated the development of carotid atherosclerosis,5 conceivably this action could increase the odds for stroke but not for myocardial infarction. Conversely, during each futile effort to breathe against the occluded pharynx, mechanical strain elicited by the abrupt generation of negative intrathoracic (and, hence, augmented epicardial artery transmural) pressure6 could rupture coronary plaques.7 A parallel increase in left ventricular wall stress, accompanied by oxygen desaturation during apnea, might induce myocardial ischemia, or non-ST segment elevation infarction.3 These cardiac effects of OSA could increase coronary risk but should not affect the likelihood of cerebrovascular events, whereas simultaneous increases in left atrial transmural pressure and concurrent fluctuations in autonomic tone might well raise the odds of developing embolic stroke by triggering atrial fibrillation.8

Over the long term, more important than these local actions may be the immediate and sustained systemic consequences of OSA. These include recurrent cycles of apnea and hyperpnea, sympathetic excitation and withdrawal, hypoxia reoxygenation and oxidative stress, impaired tonic and reflex . . .