Our data indicate that the treatment of OSA in CAD patients is associated with a decrease in the occurrence of new cardiovascular events, and an increase in the time to such events.
Treatment of OSAS with auto-nCPAP initiated at home is effective and reliable and reduces the time from diagnosis to therapy and the cost of treatment.
We investigated the effects of posture and nasal ventilation with continuous airway pressure (CPAP) on nasal resistance in snorers with or without obstructive sleep apnea (OSA). Posterior rhinomanometry was performed in 70 snorers referred for polysomnography and in 11 nonsnoring volunteers, (1) in the seated posture; (2) and (3) after 10 minutes in the supine position, before and after inhalation of oxymetazoline; and (4) 10 minutes after return to the seated position. The effect of CPAP on posterior rhinomanometry was also examined in the nonsnorers and in 12 of the snorers. Changing from the seated to the supine position resulted in an increase in resistance in snorers and nonsnorers (resistance supine 182 +/- 10.9% and 128 +/- 6.7% respectively of seated value, p < 0.05). After oxymetazoline instillation, resistance in the supine position decreased but remained higher in snorers than baseline value in the seated position. Effects of posture and oxymetazoline were similar in snorers with or without sleep apnea. During nasal ventilation with CPAP, resistance was 30 +/- 3.8 and 45 +/- 4.4% of value before CPAP in snorers and nonsnorers, respectively (p < 0.05). These effects of posture and CPAP were also observed when resistance was measured with anterior rhinomanometry. In conclusion, nasal resistance measured with posterior rhinomanometry in the supine position is not predictive for OSA. Nasal ventilation with CPAP resulted in an acute and marked decrease in nasal resistance.
In normal subjects, the level and variability of blood pressure decrease during non-rapid eye movement (non-REM) sleep. In contrast, sleep apnea is associated with large swings in nocturnal pressure. In this study, we evaluated a computer-derived index of all-night blood pressure variability in normotensive snorers with or without sleep apnea. We also examined this index in snorers receiving medical treatment for coexistent ischemic heart disease. Beat-to-beat blood pressure was recorded with a photoplethysmographic device (Finapres) throughout polysomnography. Subjects were categorized into four groups: those without cardiovascular disease without or with sleep apnea (> or = 15 apnea plus hypopnea per hour of sleep), and those with ischemic heart disease without or with sleep apnea. A frequency distribution histogram of all increases and decreases of blood pressure according to their amplitudes was drawn and the SD of the distribution used as an estimation of variability. Mean systolic and diastolic pressures during the total sleep time were not different among the four groups. In contrast, the SD of the distribution of systolic and diastolic pressure variations that were higher in the apneic than in the nonapneic groups (P < .05) correlated with apnea plus hypopnea (P < .0001) and transient electroencephalographic arousal number per hour of sleep (P < .0001). In both apneic and nonapneic subjects, blood pressure variability as assessed by SD decreased during stages 3 and 4 of non-REM sleep compared with stages 1 and 2 and REM sleep (P < .001). Blood pressure variability was similarly increased in apneic subjects with or without ischemic heart disease. We speculate that in apneic individuals with coexistent ischemic heart disease, pressure variability that is increased despite treatment with beta-blockers or calcium antagonists may be a risk factor for acute coronary events.
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