The incidence of a cardiovascular disease (CVD) was explored in a consecutive sleep clinic cohort of 182 middle-aged men (mean age, 46.8 +/- 9.3; range, 30-69 years in 1991) with or without obstructive sleep apnea (OSA). All subjects were free of hypertension or other CVD, pulmonary disease, diabetes mellitus, psychiatric disorder, alcohol dependency, as well as malignancy at baseline. Data were collected via the Swedish Hospital Discharge Register covering a 7-year period before December 31, 1998, as well as questionnaires. Effectiveness of OSA treatment initiated during the period as well as age, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP) at baseline, and smoking habits were controlled. The incidence of at least one CVD was observed in 22 of 60 (36.7%) cases with OSA (overnight oxygen desaturations of 30 or more) compared with in 8 of 122 (6.6%) subjects without OSA (p < 0.001). In a multiple logistic regression model, significant predictors of CVD incidence were OSA at baseline (odds ratio [OR] 4.9; 95% confidence interval [CI], 1.8-13.6) and age (OR 23.4; 95% CI, 2.7-197.5) after adjustment for BMI, SBP, and DBP at baseline. In the OSA group, CVD incidence was observed in 21 of 37 (56.8%) incompletely treated cases compared with in 1 of 15 (6.7%) efficiently treated subjects (p < 0.001). In a multiple regression analysis, efficient treatment was associated with a significant risk reduction for CVD incidence (OR 0.1; 95% CI, 0.0-0.7) after adjustment for age and SBP at baseline in the OSA subjects. We conclude that the risk of developing CVD is increased in middle-aged OSA subjects independently of age, BMI, SBP, DBP, and smoking. Furthermore, efficient treatment of OSA reduces the excess CVD risk and may be considered also in relatively mild OSA without regard to daytime sleepiness.

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An increased incidence of cardiovascular disease has previously been reported in middle-aged males during a follow-up period of 7 yrs. The aim of the present study was to address the incidence of coronary artery disease (CAD) in a larger sample without any heart disease at baseline.The population comprised 308 snorers (245 males and 63 females) with a mean¡SD age of 49.0¡9.9 yrs in 1991. Data were collected via the Swedish Hospital Discharge Register, National Cause of Death Registry, clinical charts and questionnaires.Over 7 yrs, CAD was observed in 17 (16.2%) of 105 patients with obstructive sleep apnoea (OSA; overnight (6 h) oxygen desaturations o30 events) compared with 11 (5.4%) of 203 snorers without OSA. OSA diagnosis at baseline was associated with an increased risk of development of CAD in a multivariate model. In the OSA group, CAD was confirmed in 16 (24.6%) of 65 incompletely treated patients compared with one (3.9%) of 26 efficiently treated subjects. Efficient treatment of OSA reduced this risk.It is concluded that middle-aged sleep apnoeics are at high risk of developing coronary artery disease if they are not treated efficiently, which should be considered in cardiovascular disease prevention models.

R Re ed du uc ct ti io on n i in n s sy ym mp pa at th he et ti ic c a ac ct ti iv vi it ty y a af ft te er r l lo on ng g--t te er rm m C CP PA AP P t tr re ea at tm me en nt t i in n s sl le ee ep p a ap pn no oe ea a: : c ca ar rd di io ov va as sc cu ul la ar r i im mp pl li ic ca at ti io on ns s It is concluded that obstructive sleep apnoea is associated with high sympathetic activity both during sleep and waking periods. Urinary metanephrine excretion seemed to reflect blood pressure, but neither daytime nor night-time catecholamine excretion was directly related to disease severity in patients with severe obstructive sleep apnoea. In spite of a marked reduction of catecholamine excretion at followup, BP and cardiac structure remained unchanged. Although increased sympathetic activity may act as a contributory trigger for cardiovascular disease in sleep apnoea, a reduction of activity after nasal CPAP is not associated with changes in blood pressure or cardiac structure.

Objective To evaluate endothelium-dependent vascular function in obstructive sleep apnoea patients.Design and methods Forearm blood flow and vascular resistance were studied in eight normotensives and eight obstructive sleep apnoea patients and also in eight normotensive and eight hypertensive controls after graded brachial artery infusion of acetylcholine (10-60ug/min) and sodium nitroprusside (1-6ug/min), respectively. Patients and controls were matched for age, sex and body weightResults Forearm blood flow after acetylcholine infusion was reduced in patients compared with that in controls (peak flows were 6.0 ±0.7 and 9.8±1.5ml/min for "lOOg, respectively), but there was no difference between hypertensive and normotensive subjects. However, the hypertensive obstructive sleep apnoea group exhibited a reduced flow response to sodium nitroprusside compared with that of their corresponding hypertensive controls. Minimal forearm vascular resistance after acetylcholine infusion and after sodium nitroprusside infusion was higher in obstructive sleep apnoea patients than it was in controls.Conclusions Endothelium-dependent vascular relaxation in patients with obstructive sleep apnoea was reduced independently of hypertension. An additional defect in endothelium-independent vascular relaxation was found in obstructive sleep apnoea patients with hypertension. These findings suggest a vascular pathogenetic link between obstructive sleep apnoea and systemic hypertension.