Cardiovascular consequences of Sleep Apnea
Related research into sleep apnea has long noted that patients with Obstructive Sleep Apnea (OSA) also tend to present with hypertension (high blood pressure).
The reasons for this link have been explored by a number of different studies in an attempt to determine whether one condition inexorably leads to the other, or whether they simply have related causal factors.
A recent study by Bradley and Floras from the Sleep Research Laboratory at the Toronto Rehabilitation Institute, Canada, has tracked the consequences of blood oxygen desaturation caused by frequent nocturnal apneas.
They found that OSA exposes the cardiovascular system to cycles of hypoxia, exaggerated negative intrathoracic pressure, and arousals.
These noxious stimuli can, in turn, depress myocardial contractility, activate the sympathetic nervous system, raise blood pressure, heart rate, and myocardial wall stress, depress parasympathetic activity, provoke oxidative stress and systemic inflammation, activate platelets, and impair vascular endothelial function.
Epidemiological studies have shown significant independent associations between OSA and hypertension, coronary artery disease, arrhythmias, heart failure, and stroke.
In randomised trials, treating OSA with continuous positive airway pressure lowered blood pressure, attenuated signs of early atherosclerosis, and, in patients with heart failure, improved cardiac function.
Current data therefore suggest that OSA increases the risk of developing cardiovascular diseases, and that its treatment has the potential to diminish such risk.
Clearly the cycles of oxygen desaturation which result from sleep apnea have consequences on the heart and circulatory system. Further research is required to determine the consequences of this on other major organ systems and on cognitive function which are also know to be impacted by blood oxygen desaturation.
The study appears in The Lancet, 2009