O bstructive sleep apnea (OSA) is characterized by intermittent hypoxemia and associated with increased prevalence of vascular dysfunction and arterial hypertension, but the underlying mechanisms are incompletely understood.1 In OSA, apneas are related to excessive throat muscle relaxation with consequent inspiratory efforts against the closed glottis, finally resulting in the patient's arousal associated with sympathetic activation and hyperventilation. The hyperventilation, in turn, contributes to the next apnea by reducing the arterial partial pressure of CO 2 toward the apnea threshold. In this scenario, arterial oxygen desaturation plays a pivotal role by narrowing the gap between the eupneic and apneic CO 2 pressure level, thereby rendering the CO 2 -controlled breathing regulation more unstable and, thus, prone to periodic breathing.
2In patients with OSA, the presence of patent foramen ovale (PFO) is associated with a marked increase in the frequency and severity of nocturnal oxygen desaturations.3 This could be related, at least in part, to right to left shunting across a PFO, as evidenced by invasive hemodynamic measurements in healthy humans, demonstrating that during the onset of simulated OSA, the right atrial pressure exceeds left atrial pressure in response to the steep decline in intrathoracic pressure. 4 Improvement of arterial oxygen saturation by PFO closure may prevent this problem.We recently reported preliminary findings showing that PFO closure in patients with newly diagnosed OSA was associated with a reduction of nocturnal apnea-hypopnea events and oxygen desaturations and decreased pulmonary artery pressure.5 Moreover, circumstantial evidence shows that intermittent hypoxia is associated with systemic endothelial dysfunction and arterial hypertension. 6,7 In line with these observations, systemic endothelial function is impaired in OSA patients without any traditional cardiovascular risk factors.8 Systemic endothelial dysfunction precedes the development of arteriosclerosis and contributes to the pathogenesis of arterial hypertension.9 Accordingly, the prevalence of arterial Abstract-Obstructive sleep apnea (OSA) is a frequent syndrome characterized by intermittent hypoxemia and increased prevalence of arterial hypertension and cardiovascular morbidity. In OSA, the presence of patent foramen ovale (PFO) is associated with increased number of apneas and more severe oxygen desaturation. We hypothesized that PFO closure improves sleep-disordered breathing and, in turn, has favorable effects on vascular function and arterial blood pressure. In 40 consecutive patients with newly diagnosed OSA, we searched for PFO. After initial cardiovascular assessment, the 14 patients with PFO underwent initial device closure and the 26 without PFO served as control group. Conventional treatment for OSA was postponed for 3 months in both groups, and polysomnographic and cardiovascular examinations were repeated at the end of the follow-up period. PFO closure significantly improved the apnea-hypopnea index ...