The exact influence of sleep-related breathing disorder (SRBD) on blood pressure control remains unknown. We investigated the influence of different degrees of SRBD on daytime blood pressure and its association to documented hypertension by examining 1,190 consecutive patients referred for diagnosis of SRBD. The protocol includes clinical interview, physical examination, office blood pressure measurement, cholesterol, and blood gas analysis. Unattended home monitoring of nocturnal breathing was performed for assessment of SRBD activity (respiratory disturbance index [RDI]). RDI was independently and linearly associated with systolic blood pressure (unstandardized coefficient [B] = 0.07 +/- 0.03, p = 0.03), diastolic blood pressure (B = 0.07 +/- 0.02, p = 0 < 0.001), and heart rate (B = 0.10 +/- 0.02, p < 0.001) at rest. The relative risk for hypertension (blood pressure >/= 160/95 mm Hg) increased with SRBD severity (odds ratio [OR], 4.15 for RDI >/= 40 versus < 5 [95% CI, 2.7 to 6.5]). This relative risk was also elevated in younger ( 50 yr) (OR, 7.15 versus 2.70 for RDI >/= 40 versus < 5). These cross-sectional clinical data suggest a relationship between SRBD severity and systolic blood pressure, diastolic blood pressure, and heart rate after control for confounders such as body mass index (BMI), age, alcohol/nicotine consumption, cholesterol level, and daytime PO(2) and PCO(2). SRBD is an independent risk factor for systemic hypertension with an increased likelihood in subjects

Obstructive sleep apnea is the most common sleep-related breathing disorder, with a surprisingly high prevalence. The treatment of choice is nasal continuous positive airway pressure (CPAP) ventilation during sleep, which has to be applied throughout the patient's whole life. Because of various underlying pathomechanisms in patients with certain craniofacial disorders--narrow posterior airway space and maxillary-mandibular deficiency--surgical therapy by craniofacial osteotomies seems possible. A series of 38 consecutive patients were treated by 10-mm maxillomandibular advancement by retromolar sagittal split osteotomy and Le Fort I osteotomy, respectively. Obstructive sleep apnea syndrome was improved considerably in all patients; there was no significant difference compared to the results under nasal CPAP. In 37 of 38 patients, the postoperative apnea-hypopnea index was reduced clearly to under 10 per hour, oxygen saturation rose, and sleep quality improved. This was achieved by maxillomandibular advancement of 10 mm without secondary refinements in all but 2 patients. In one patient, the apnea-hypopnea index could only be reduced to 20 per hour, probably because of insufficient maxillary advancement. These results indicate that successful surgical treatment is possible in a high percentage of selected patients with certain craniofacial characteristics. In addition to cardiorespiratory polysomnography, there should be routine cephalometric evaluation of all patients. Maxillomandibular advancement should be offered as an alternative therapy to all patients with maxillary and/or mandibular deficiency or dolichofacial type in combination with narrow posterior airway space.

This study demonstrates that maxillomandibular advancement is successful in a high percentage of patients carefully selected by cephalometric and polysomnographic investigation. Postoperative success has proved to be stable over a period of 2 yrs. Further preoperative evaluation seems necessary in patients with predominantly mixed or central apnoeas.

Complex sleep apnoea (CompSA) may be observed following continuous positive airway pressure (CPAP) treatment.In a prospective study, 675 obstructive sleep apnoea patients (mean age 55.9 yrs; 13.9% female) participated. Full-night polysomnography was performed at diagnosis, during the first night with stable CPAP and after 3 months of CPAP.12.2% (82 out of 675 patients) had initial CompSA. 28 of those were lost to follow-up. Only 14 out of the remaining 54 patients continued to satisfy criteria for CompSA at follow-up. 16 out of 382 patients not initially diagnosed with CompSA exhibited novel CompSA after 3 months. 30 (6.9%) out of 436 patients had follow-up CompSA. Individuals with CompSA were 5 yrs older and 40% had coronary artery disease. At diagnosis, they had similar sleep quality but more central and mixed apnoeas. On the first CPAP night and at follow-up, sleep quality was impaired (more wakefulness after sleep onset) for patients with CompSA. Sleepiness was improved with CPAP, and was similar for patients with or without CompSA at diagnosis and follow-up.CompSA is not stable over time and is mainly observed in predisposed patients on nights with impaired sleep quality. It remains unclear to what extent sleep impairment is cause or effect of CompSA.

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