The evidence linking sleep-disordered breathing to increased mortality and cardiovascular morbidity has been conflicting and inconclusive. We hypothesized that a potential adverse effect of disordered breathing would be more obvious in patients with established vascular disease. In a prospective cohort study 408 patients aged 70 yr or younger with verified coronary disease were followed for a median period of 5.1 yr. An apnea–hypopnea index (AHI) of ⩾ 10 and an oxygen desaturation index (ODI) of ⩾ 5 were used as the diagnostic criteria for sleep-disordered breathing. The primary end point was a composite of death, cerebrovascular events, and myocardial infarction. There was a 70% relative increase and a 10.7% absolute increase in the primary composite end point in patients with disordered breathing defined as an ODI of ⩾ 5 (risk ratio 1.70, 95% confidence interval [CI] 1.15–2.52, p = 0.008). Similarly, patients with an AHI of ⩾ 10 had a 62% relative increase and a 10.1% absolute increase in the composite endpoint (risk ratio 1.62, 95% CI 1.09–2.41, p = 0.017). An ODI of ⩾ 5 and an AHI of ⩾ 10 were both independently associated with cerebrovascular events (hazard ratio 2.62, 95% CI 1.26–5.46, p = 0.01, and hazard ratio 2.98, 95% CI 1.43–6.20, p = 0.004, respectively). We conclude that sleep-disordered breathing in patients with coronary artery disease is associated with a worse long-term prognosis and has an independent association with cerebrovascular events.

Background— The effect of sleep apnea on mortality and cardiovascular morbidity is mainly unknown. We aimed to study whether sleep apnea is related to stroke, death, or myocardial infarction in patients with symptomatic coronary artery disease. Methods and Results— A total of 392 men and women with coronary artery disease referred for coronary angiography were examined by use of overnight sleep apnea recordings. Sleep apnea, defined as an apnea-hypopnea index ≥5, was recorded in 54% of the patients. All patients were followed up prospectively for 10 years, and no one was lost to follow-up. Stroke occurred in 47 (12%) of 392 patients during follow-up. Sleep apnea was associated with an increased risk of stroke, with an adjusted hazard ratio of 2.89 (95% confidence interval 1.37 to 6.09, P =0.005), independent of age, body mass index, left ventricular function, diabetes mellitus, gender, intervention, hypertension, atrial fibrillation, a previous stroke or transient ischemic attack, and smoking. Patients with an apnea-hypopnea index of 5 to 15 and patients with an apnea-hypopnea index ≥15 had a 2.44 (95% confidence interval 1.08 to 5.52) and 3.56 (95% confidence interval 1.56 to 8.16) times increased risk of stroke, respectively, than patients without sleep apnea, independent of confounders ( P for trend=0.011). Death and myocardial infarction were not related to sleep apnea. Intervention in the form of coronary artery bypass grafting or percutaneous coronary intervention was related to a longer survival but did not affect the incidence of stroke. Conclusions— Sleep apnea is significantly associated with the risk of stroke among patients with coronary artery disease who are being evaluated for coronary intervention.

Nine elite canoeists were investigated concerning changes in performance, heart rate variability (HRV), and blood-chemical parameters over a 6-d training camp. The training regimen consisted of cross-country skiing and strength training, in total 13.0+/-1.6 h, corresponding to a 50% increase in training load. Time to exhaustion (RunT) decreased from 19.1+/-1.0 to 18.0+/-1.2 min (P < 0.05). VO2max and max lactate (La(max)) both decreased significantly (P < 0.05) over the training period (4.99+/-0.97 to 4.74+/-0.98 L x min(-1) and from 10.08+/-1.25 to 8.98+/-1.03 mmol x L(-1) respectively). Heart rates (HR) decreased significantly at all workloads. Plasma volume increased by 7+/-7% (P < 0.05). Resting cortisol, decreased from 677+/-244 to 492+/-222 nmol x L(-1) (P < 0.05), whereas resting levels of adrenaline and noradrenaline remained unchanged. The change between tests in RunT correlated significantly with the change in HRmax (r = 0.79; P = 0.01). There were no group changes in high or low frequency HRV, neither at rest nor following a tilt. The reduced maximal performance indicates a state of fatigue/overreaching and peripheral factors are suggested to limit performance even though HRmax and La(max) both were reduced. The reduced submaximal heart rates are probably a result of increased plasma volume. HRV in this group didn't seem to be affected by short-term overtraining.