• Dimitar Sajkov and R Doug McEvoy.
• Flinders Medical Center, Bedford Park, SA, Australia.
• Prog Cardiovasc Dis. 2009 Mar 1;51(5):363-70.

AbstractObstructive sleep apnea (OSA) is associated with repetitive nocturnal arterial oxygen desaturation and hypercapnia, large intrathoracic negative pressure swings, and acute increases in pulmonary artery pressure. Rodents when exposed to brief, intermittent hypoxia for several hours per day to mimic OSA developed pulmonary vascular remodeling and sustained pulmonary hypertension and right ventricular hypertrophy within a few weeks. Until recently, however, it was unclear whether episodic nocturnal hypoxemia associated with OSA was sufficient to cause similar changes in humans. This controversy appears to have been resolved by several recent studies that have shown (a) pulmonary hypertension in 20% to 40% of patients with OSA in the absence of other known cardiopulmonary disorders and (b) reductions in pulmonary artery pressure in patients with OSA after nocturnal continuous positive airway pressure (CPAP) treatment. The pulmonary hypertension associated with OSA appears to be mild and may be due to a combination of precapillary and postcapillary factors including pulmonary arteriolar remodeling and hyperreactivity to hypoxia and left ventricular diastolic dysfunction and left atrial enlargement. Although measurable changes in the structure and function of the right ventricle have been reported in association with OSA, the clinical significance of these changes is uncertain. Right ventricular failure in OSA appears to be uncommon and is more likely if there is coexisting left-sided heart disease or chronic hypoxic respiratory disease.

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