Cardiac autonomic control in sleep apneas and risk of nocturnal myocardial ischemia

Sleep apnea is a condition that afflicts millions of people, contributing to numerous related problems ranging from automobile accidents due to excessive sleepiness to cardiac infarctions and stroke. The present study investigated whether autonomic control of the heart of persons with low and high levels of sleep apnea differed between sleep stages and across the nocturnal sleep period. During normal non-REM sleep the heart tends to slow down gradually under increasing parasympathetic dominance and sympathetic withdrawal. About every 90 minutes this process is normally interrupted by REM sleep, which is under sympathetic dominance and parasympathetic withdrawal and accelerates the heart to a rate almost as fast as that of wakefulness. Individuals with sleep apnea could have this process disrupted by successive arousals and oxygen desaturation, increasing cardiac rate across the sleep period.; Electrocardiography and impedance cardiography of 24 patients referred to polysomnographic studies were recorded through the sleep period. Heart period, high frequency- heart rate variability, and pre-ejection period measured by electro- and impedance cardiography were computed respectively as measures of heart rate, and estimates of parasympathetic and sympathetic control. The continuous recordings were scored and staged in 1-min epochs, and means per epoch were further analyzed in four quarters of the sleep period per participant.; Two groups were compared, one consisting of participants with low rates of apneas-hypopneas per hour and the other with high rates of apneas-hypopneas per hour. Results indicated that cardiac rates of the two groups decreased incrementally through the sleep period. Cardiovascular measures during sleep did not differ significantly between the two groups. However, significant differences were found when cardiovascular measures of each group were compared to their wake baselines. In both groups, cardiac deceleration was associated with an increase in parasympathetic dominance, but with little change in sympathetic withdrawal. Parasympathetic activation during light non-REM sleep was significantly higher than during REM sleep. These results indicate that higher levels of apnea-hypopnea are associated with higher levels of parasympathetic control, especially during lighter, non-REM sleep. A possible explanation for this observation is a compensatory response to oxygen desaturation caused by disturbed breathing.