Severity of oxygen desaturation is predictive of early atherosclerosis in obstructive sleep apnoea (OSA). Leukotriene (LT)B 4 is a lipid mediator involved in atherogenesis.In 40 non-obese OSA patients, free of a cardiovascular history, and 20 healthy volunteers, the following were evaluated: 1) LTB 4 production by polymorphonuclear leukocytes (PMNs) stimulated with A23187; and 2) the relationships between LTB 4 production and both OSA severity and infraclinical atherosclerosis markers. The effect of continuous positive airway pressure (CPAP) on LTB 4 production was also studied. An overnight sleep study was followed by firstmorning blood sampling. Isolated PMNs were stimulated with A23187 in order to induce LTB 4 production, which was measured by liquid chromatography-tandem mass spectrometry. Carotid intima-media thickness (IMT) and luminal diameter were measured in subset groups of 28 OSA patients and 11 controls.LTB 4 production was increased in OSA patients compared with controls. LTB 4 levels correlated with the mean and minimal arterial oxygen saturation (Sa,O 2 ). LTB 4 production correlated with luminal diameter data in patients with a mean Sa,O 2 of f94% but not with IMT. Lastly, CPAP significantly reduced LTB 4 production by 50%.Leukotriene B 4 production is increased in obstructive sleep apnoea in relation to oxygen desaturation. Leukotriene B 4 could promote early vascular remodelling in moderate-to-severe hypoxic obstructive sleep apnoea patients.

Obstructive sleep apnoea syndrome (OSAS), due to the collapse of the upper airways, is a common but still underestimated condition. The 'dose-response' type relationship between OSAS and hypertension (HT) has now been clearly proven. There are multiple mechanisms explaining this relationship, the main one being an increase in sympathetic activity during the apnoeas. HT associated with OSAS has several characteristics: high prevalence, diastolic and nocturnal predominance, and frequent non-dipper status. Furthermore, as OSAS is found in the majority of subjects with refractory HT, it should be systematically investigated in this situation. HT associated with OSAS should be tested for by means of a clinical blood pressure (BP) measurement, to which 24-h ambulatory BP monitoring (ABPM) is often added due to the fact that BP anomalies are frequently present at night. HT during OSAS is frequently associated with metabolic anomalies (for example, obesity, dyslipidaemia and insulin resistance), therefore explaining the high prevalence of metabolic syndrome in this population. The reference treatment for OSAS-nasal continuous positive airway pressure (nCPAP)-seems to be able to lower the BP of hypertensive patients, especially if the HT is severe, untreated or refractory. Moreover, the BP response to nCPAP depends on the severity of the OSAS, in particular the scale of the nocturnal desaturations, and on patient tolerance of the treatment. Optimal treatment for HT associated with OSAS has not been evidenced. Antihypertensive drugs do not change the respiratory parameters during OSAS.

This new analysis supports the results of the earlier investigation, in that indapamide SR 1.5 mg/day appeared to be the most effective drug for producing significant reductions in SBP within 8-12 weeks, which is an essential element in optimising cardiovascular prevention among hypertensive patients. The clinical application of these results should take into consideration all the limitations discussed in this analysis.