Background

During sleep, the tone of upper airway dilator muscles normally decreases, favouring collapse of the nasopharyngeal region of the upper airway. Upper airway narrowing is responsible for snoring, whereas complete closure causes apneic events associated with persistence of respiratory movements, characteristic of the ?obstructive? pattern. Airflow obstruction during sleep can be partial (hypopnea) or complete (apnea), and is resolved by an arousal, i.e. a short interruption of sleep, which re-establishes muscle tone and airway patency. As the subject goes back to sleep, however, upper airway obstruction can reappear, and in the most severe cases the cycle is repeated up to hundreds of times during a single night.

In normal adults episodes of upper airway obstruction may occur during sleep, but they are fewer than 5 per hour of sleep, i.e. the Apnea Hypopnea Index (AHI) is < 5/h. In the general adult population, 9% of men and 4% of women show an AHI >5/h, and 4 and 2%, respectively, also refer clinical symptoms of the obstructive sleep apnea syndrome (OSAS). Sleep apnea is particularly frequent in overweight or obese subjects, suggesting that its prevalence may increase in the near future due to sedentary lifestyle in Western countries.

?The main clinical features of OSAS include a history of loud snoring (indicating vibration of soft tissues during upper airway obstruction), a variable degree of impairment of daytime function (excessive daytime sleepiness secondary to sleep fragmentation) and several alterations secondary to nocturnal oscillations in oxygen content of arterial blood. These changes jointly cause profound alteration of autonomic nervous system activity, by increasing sympathetic and decreasing vagal activity. During sleep, hypertensive peaks occur after each apnea. In addition, about 50% of patients with OSAS are hypertensive during wakefulness, and often show a poor response to antihypertensive treatment. OSAS is included as a potential cause of increased blood pressure in the most recent guidelines on management of hypertension. Besides its causal relationship with systemic hypertension, OSAS has been strongly implicated as a risk factor for coronary artery disease and stroke. Uncontrolled studies indicate that cardiovascular mortality is increased in patients with untreated OSAS. In summary, the major adverse health consequences of OSAS in the long-term appear to involve the cardiovascular system, but firm evidence is still lacking and pathogenetic mechanism(s) are to some extent unclear.

The ?gold standard? treatment for OSAS is nasal continuous positive airway pressure (CPAP). CPAP application during sleep, after titration of the appropriate pressure level, stabilizes upper airway walls and patency, normalizes sleep structure, respiration and arterial oxygenation, and prevents sympathetic overactivity and blood pressure swings during sleep. The long-term effects of CPAP treatment on cardiovascular risk are still uncertain. Uncontrolled studies have reported that cardiovascular morbidity and mortality in treated patients are similar to those recorded in the general population. However, the variable degree of patient compliance to treatment constitutes a major problem in assessing the effects of CPAP. Other treatment options exist (upper airway surgery and oral appliances) aimed at increasing the dimensions of the nasopharyngeal tract of the upper airways.

Obesity is a major and well-known risk factor for cardiovascular disease. Consequently, the association between OSAS with obesity complicates studies on the independent impact of OSAS on the cardiovascular system. The effects of OSAS treatment on cardiovascular risk are currently unproven although a moderate blood pressure reduction has been documented in treated patients. Other additional factors may play an important role in this interaction. For instance, metabolic alterations (insulin resistance, leptin resistance), increased concentrations of pro-inflammatory mediators (interleukin 6 and C reactive protein) and oxidative stress have been found in OSAS patients, but the relative roles of OSAS and obesity in causing these changes are unclear. Ongoing studies on the role of genetic factors are complicated by the complexity of OSAS phenotype. Studies in large patient samples are therefore necessary to clarify the role of OSAS and obesity in the pathogenesis of cardiovascular and metabolic alterations as possible causes of accelerated atherogenesis, as well as the effects of CPAP treatment.

To study the role of OSAS as a cardiovascular risk factor, we believe that it is particularly timely and necessary to establish an European network on OSAS, in order to promote collaboration between Sleep Laboratories and attain a critical mass of data for assessment of the incidence of cardiovascular events during follow-up in treated and untreated OSAS patients. This network will include groups involved in clinical and basic research to provide new insights into pathogenetic mechanisms and improve our approach to patient management. Currently, the working group on sleep disordered breathing of the European Respiratory Society (ERS) promotes cooperation among laboratories, but contacts are restricted to ERS Annual Meetings and for this reason appear inadequate to generate a continuous cooperation between researchers. The present COST Action aims at establishing a permanent network among outstanding groups actively contributing to studies on OSAS in different European countries, in order to pursue advancement in clinical and basic research on OSAS and cardiovascular risk.