Does obstructive sleep apnea (OSA) increase overall risk of sudden cardiac death (SCD) independent of traditional risks?
All individuals referred for sleep studies to a single institution between July 1, 1987 and July 31, 2003 were studied. The vast majority of subjects were suspected to have sleep disordered breathing. The study sample was limited to residents 18 years or older who underwent their first-ever overnight sleep study (polysomnogram). Excluded were individuals with a prior diagnosis of OSA, or a history of resuscitated SCD. Numerical data such as cholesterol levels or blood pressures were not collected. Due to the retrospective methodology, the presence and effects of treatment for these conditions, and the development or resolution of these conditions during follow-up, were not measured. Sleep data collected included: the apnea-hypopnea index (AHI), the awake oxygen saturation, mean nocturnal oxygen saturation, lowest nocturnal oxygen saturation, arousal index, and sleep efficiency. An AHI ≥5 established the diagnosis of OSA. SCD was established when the cause of death was sudden cardiac death, (fatal) cardiac dysrhythmia, (fatal) cardiac arrhythmia, cardiac arrest, cardiorespiratory arrest, or coronary heart disease or myocardial infarction when the time interval from symptoms to death was specified ≤1 hour.
The study sample consisted of 10,701 adults; 68% were men with an average age 53 ± 14 years. OSA was diagnosed by polysomnography in 78% of study subjects with a mean AHI of 31 ± 32 events per hour. During an average follow-up of 5.3 years, 142 subjects had fatal or resuscitated SCD, or an average annual risk of SCD of 0.27% for the study population. This is higher than the estimated annual risk of SCD in the general population, of 0.1-0.2%. Univariate analyses found SCD was best predicted by these thresholds for the following continuous variables: age 60 years (hazard ratio [HR], 5.53; 95% confidence interval [CI], 3.84-7.94; p < 0.0001), AHI 20 (HR, 1.60; 95% CI, 1.14-2.24; p = 0.007), mean nocturnal oxygen saturation 93% (HR, 2.93; 95% CI, 1.98-4.33; p < 0.0001), and lowest oxygen saturation 78% (HR, 2.60; 95% CI, 1.85-3.65; p < 0.0001). Multivariate analysis determined lowest nocturnal oxygen saturation of 78% had an HR for SCD of 1.81 (95% CI, 1.28-2.56; p = 0.0008).
The authors concluded that among 10,701 adults referred for sleep studies, the presence of OSA predicted incident SCD, and the magnitude of risk was predicted by multiple parameters that characterize OSA severity, including the AHI and nocturnal oxygen desaturation. Further analysis showed that the lowest nocturnal oxygen saturation threshold of 78% predicts an 81% increase in the risk of SCD.
While the precise link between OSA and SCD remains largely unknown, multiple plausible pathophysiological mechanisms are discussed, including OSA’s effect on cardiac autonomic dysfunction, heart rate variability, QTc interval dispersion, chronic sympathetic overdrive, neurohumoral activation, and myocardial remodeling. These results support the need for further research on the mechanisms of SCD in individuals with OSA. Last, clinical trials of OSA therapy in populations at risk for SCD are needed.
Peter M. Farrehi, MD, F.A.C.C. (Disclosure)
General Cardiology, Heart Failure/Transplant, SleepApnea