Context Obstructive sleep apnea (OSA) has been increasingly implicated in the
initiation and progression of cardiovascular diseases.
Objective To systematically review the interactions of OSA with cardiovascular
pathophysiology and diseases.
Data Sources and Study Selection The MEDLINE database from January 1966 to March 2003 was searched using
the Medical Subject Headings sleep, sleep apnea, obesity, hypertension, heart failure, cardiac
arrhythmia, coronary artery disease, stroke, sympathetic activity, endothelium, inflammation, and continuous positive airway pressure (CPAP) to identify peer-reviewed studies of OSA. Priority was given
to large prospective cohort studies and to randomized controlled trials.
Data Extraction We identified 154 original investigations and reviews of sleep-related
breathing disorders. Data from these studies were examined for relevance and
extracted by one of the authors.
Data Synthesis Approximately 1 in 5 adults has at least mild OSA (apnea-hypopnea index
[ie, the number of apneic and hypopneic events per hour], 5-15), and 1 in
15 adults has at least moderate OSA (apnea-hypopnea index, 15-30). Repetitive
apneic events disrupt the normal physiologic interactions between sleep and
the cardiovascular system. Such sleep fragmentation, as well as abnormalities
evident in patients with OSA (eg, increased sympathetic activation, vascular
endothelial dysfunction, increased oxidative stress, inflammation, increased
platelet aggregability, metabolic dysregulation), may be implicated in the
initiation and progression of cardiac and vascular disease. Persuasive data
implicate OSA in the development of hypertension, and OSA also may contribute
to cardiac ischemia, congestive heart failure, cardiac arrhythmias, and perhaps
also to cerebrovascular disease and stroke.
Conclusions Obstructive sleep apnea is common, readily diagnosed, and usually treatable.
It frequently coexists undiagnosed in patients with cardiovascular disease,
activates disease mechanisms known to elicit cardiac and vascular damage,
and may be implicated in progression of cardiovascular disease and resistance
to conventional therapeutic strategies. In the absence of definitive evidence
from large-scale trials and a better understanding of potential cost-effectiveness,
the likely benefits of diagnosis and treatment of OSA are presently best appraised
on an individualized patient basis.