BACKGROUND: Obstructive sleep apnoea (OSA) causes recurrent rises in blood pressure during sleep, and recent community surveys have suggested a link between mild OSA and diurnal hypertension. The fact that OSA and hypertension share some risk factors, as well as problems accurately quantifying OSA severity, have diluted the power of such studies. This study tries to circumvent some of these problems by measuring the overnight change in blood pressure and relating it to relevant measures of the severity of upper airway obstruction on the same night. METHODS: Men born between 1930 and 1960 and their wives living in a market town north of Oxford were identified from a GP practice register. Enough couples were recruited to provide approximately 10 (20 individuals) per year of birth. Subjects were visited at home where a questionnaire was administered, anthropometric measurements made, blood pressures taken (including by the subject), and sensors applied for a subsequent overnight sleep study. The sleep study measured indices of hypoxia, snoring, autonomic arousal, degree of respiratory effort; the last two of these derived from measurements of pulse transit time (indirect beat to beat blood pressure). After waking the following morning, the subjects took their own blood pressures again. RESULTS: Data were available from 224 couples (448 subjects). On average, systolic BP fell 8 mm Hg from evening to morning. Only hypoxic dips (>4% SaO(2) dips/h) and the measure of degree of respiratory effort were significant independent predictors of this overnight change in systolic BP, together accounting for 7-10% of the variation (p<0.0001). Dividing the subjects into quartiles according to the respiratory effort overnight showed a progressive reduction in the fall of systolic BP overnight: 13.6, 10.8, 7.3, and 5.6 mm Hg, lowest to highest quartiles. CONCLUSIONS: This study suggests that increased respiratory effort during sleep (seen in OSA and related syndromes of increased upper airway resistance during sleep) offsets the normal fall in BP that occurs overnight, even within this community population. This may be one of the mechanisms by which hypertension is carried over into the waking hours in patients with OSA.
BACKGROUND: Obstructive sleep apnoea (OSA) causes recurrent rises in blood pressure during sleep, and recent community surveys have suggested a link between mild OSA and diurnal hypertension. The fact that OSA and hypertension share some risk factors, as well as problems accurately quantifying OSA severity, have diluted the power of such studies. This study tries to circumvent some of these problems by measuring the overnight change in blood pressure and relating it to relevant measures of the severity of upper airway obstruction on the same night. METHODS:Men born between 1930 and 1960 and their wives living in a market town north of Oxford were identified from a GP practice register. Enough couples were recruited to provide approximately 10 (20 individuals) per year of birth. Subjects were visited at home where a questionnaire was administered, anthropometric measurements made, blood pressures taken (including by the subject), and sensors applied for a subsequent overnight sleep study. The sleep study measured indices of hypoxia, snoring, autonomic arousal, degree of respiratory effort; the last two of these derived from measurements of pulse transit time (indirect beat to beat blood pressure). After waking the following morning, the subjects took their own blood pressures again. RESULTS: Data were available from 224 couples (448 subjects). On average, systolic BP fell 8 mm Hg from evening to morning. Only hypoxic dips (>4% SaO(2) dips/h) and the measure of degree of respiratory effort were significant independent predictors of this overnight change in systolic BP, together accounting for 7-10% of the variation (p<0.0001). Dividing the subjects into quartiles according to the respiratory effort overnight showed a progressive reduction in the fall of systolic BP overnight: 13.6, 10.8, 7.3, and 5.6 mm Hg, lowest to highest quartiles. CONCLUSIONS: This study suggests that increased respiratory effort during sleep (seen in OSA and related syndromes of increased upper airway resistance during sleep) offsets the normal fall in BP that occurs overnight, even within this community population. This may be one of the mechanisms by which hypertension is carried over into the waking hours in patients with OSA.