J. H. Peter

Surgical maxillofacial treatment of obstructive sleep apnea.

&NA; Obstructive sleep apnea is the most common sleeprelated 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 patients 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. (Plast. Reconstr. Surg. 99: 619, 1997.)

Sleep-related breathing disorder is an independent risk factor for uncontrolled hypertension

Objective To test the hypothesis that sleep-related breathing disorder (SRBD) is associated with poor blood pressure control in hypertensive patients independent from confounding factors such as age, body mass index, alcohol, smoking and daytime blood gases. Design and methods This cross-sectional study of a sleep laboratory cohort was carried out at the University Hospital Sleep Disorders Centre, Marburg. The study comprised 599 patients referred for a sleep study, all of them with a documented history of systemic hypertension and/or previously initiated antihypertensive therapy. Data were obtained from a clinical interview, two unattended sleep studies and assessment of clinic blood pressure, cholesterol level, alcohol and nicotine consumption and daytime blood gases. The main outcome measure was a post hoc analysis of predictors for poor blood pressure control. Results Respiratory disturbance index (RDI) was significantly higher in patients with uncontrolled hypertension (blood pressure ⩾ 160 and/or 95 mmHg, n = 463) than in those with controlled hypertension (n = 136) (34.0 ± 26.8 versus 27.0 ± 23.5, P <0.01). The relative proportion of patients with uncontrolled hypertension increased significantly as SRBD activity increased (χ2, P <0.05). Body mass index was the only independent predictor (P = 0.006) of uncontrolled hypertension in the whole study sample. However, in the subset of patients aged ⩽ 50 years, RDI (P = 0.006) and age (P = 0.016) were the only independent predictors. The probability of uncontrolled hypertension increased by approximately 2% (B = 0.019, P = 0.006) for each RDI unit. Conclusion SRBD should be considered, in addition to traditional confounders, as a risk factor for poor blood pressure control in younger hypertensive patients (⩽ 50 years of age).

Electrophysiologic evaluation of sinus node function and atrioventricular conduction in patients with prolonged ventricular asystole during obstructive sleep apnea

In 15 patients with ventricular asystole of 8.5 +/- 3.5 seconds (range 5.0 to 16.8) occurring exclusively during obstructive sleep apnea, electrophysiologic study of sinus node function and atrioventricular conduction before and after administration of intravenous atropine (0.02 mg/kg) was performed. Electrophysiologic parameters of sinus node function were normal in 12 of 15 patients (80%) and atrioventricular (AV) nodal function was normal in 7 patients (47%). Almost all abnormal findings of sinus node function and AV nodal function were reversible by administration of atropine. The HisPurkinje system function was normal in 6 patients (40%). Prolonged HV intervals (57 to 73 ms) were found in 9 patients (60%). Intra- or infra-His block was not observed in any patient. In summary, electrophysiologic parameters of sinus node function and AV conduction were normal or only slightly abnormal in all 15 study patients, which suggests that prolonged ventricular asystole during obstructive sleep apnea is not due to fixed or anatomic disease of the sinus node or the AV conduction system.

Outcome of patients with sleep apnea–associated severe bradyarrhythmias after continuous positive airway pressure therapy

Twenty-nine patients in whom severe bradyarrhythmias occurred exclusively during obstructive sleep apnea and in whom advanced sinus node disease or atrioventricular conduction system dysfunction had been excluded by invasive electrophysiologic evaluation were prospectively followed on nasal continuous positive airway pressure. During 54 +/- 10 months follow-up, no syncope and no sudden deaths were observed, suggesting that patients with sleep apnea-associated bradyarrhythmias and a normal electrophysiologic study appear to have a favorable prognosis with continuous positive airway pressure.

Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease

SummaryTo study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over; 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phases of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia: and increased electrical instability.

Sleep apnea and pulmonary hypertension

SummaryThe pulmonary artery pressure values of 65 patients with sleep apnea syndrome were measured at rest and during ergometer exercise up to 100 W. Pulmonary hypertension at rest was found in 13, and during exercise in 31 more patients. Only 8 patients with pathological pressure findings suffered from pulmonary hypertension in combination with a pulmonary or cardiac disease. In the other 36 patients, no indication of a primary cause of pulmonary hypertension apart from sleep apnea syndrome could be found. Out of the 65 patients, 11 with a finding of more than 20 apnea episodes per hours sleep underwent polysomnographic recordings in the sleep laboratory. The hemodynamic parameters were continuously measured. All 11 patients had a finding of severe sleep apnea with more than 300 apnea episodes during the night of recording. In 6 patients, the appearance of apnea episodes was accompanied by only moderate changes in pulmonary artery pressure. In 5 patients, there were critical increases in pulmonary artery pressure, which went along with increases in cardiac output and in pulmonary capillary wedge pressure. Increases in pulmonary vascular resistance were established in 3 out of these 5 patients, and a slight decrease in 2. The mechanism of hypoxic vasoconstriction of the pulmonary arteries may account for the pressure increases in 3 of our patients, but fails to explain the findings in the other 2 patients. Nocturnal changes in pulmonary artery pressure in patients with sleep apnea may therefore have different causes. Pulmonary hypertension constitutes a severe complication in patients with sleep apnea. As 55% of all sleep apnea patients were found to suffer from pulmonary hypertension without any indication of a primary pulmonary or cardiac disease, the possibility that pulmonary hypertension results should not be underestimated in patients with suspected sleep apnea syndrome. Measurements of the pulmonary artery pressure must therefore be included in the examination regimen of such patients.

Sleep related disorders and internal diseases

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Relations among hypoxemia, sleep stage, and bradyarrhythmia during obstructive sleep apnea

BACKGROUND Obesity, apneic hypoxemia, and rapid eye movement (REM) sleep are supposed to be the major causes for bradyarrhythmia in patients with obstructive sleep apnea. The aims of this study were to compare clinical findings and diagnoses in patients with obstructive sleep apnea with and without nocturnal bradyarrhythmia and to analyze the relations among hypoxemia, sleep stage, and bradyarrhythmia. METHODS During a 17-month period 239 patients were found to have sleep apnea in an ambulatory study. Patients with nocturnal bradyarrhythmia were hospitalized for 3 days and polysomnographies were performed over 2 successive nights. A Holter electrocardiogram was recorded for 48 hours. RESULTS Nocturnal episodes of bradyarrhythmia were identified in 17 (7%) of 239 patients. Body mass index (39 +/- 7 vs 31 +/- 5 kg/m(2)) and respiratory disturbance index (90 +/- 36 per hour vs 24 +/- 24 per hour) were significantly different (P <.01) between patients with (n = 17) and without bradyarrhythmia (n = 222). Bradyarrhythmia occurred significantly more often during REM than non-REM sleep (P <.01). There was a significant difference in end-apneic oxygen saturation in apnea/hypopnea episodes with and without bradyarrhythmia (71% +/- 9% vs 75% +/- 10%; P <.01). A linear relation between end-apneic oxygen saturation and number of sinus arrests and heart blocks could not be found. CONCLUSIONS Patients with apnea-associated bradyarrhythmia are more overweight than patients without bradyarrhythmia. The higher respiratory disturbance index measurements found in these patients may be caused by this difference. Bradyarrhythmia occurs predominantly during REM sleep and occurred independently from decrease in oxygen saturation; a threshold value as an upper limit could not be found.

Influence of metoprolol and cilazapril on blood pressure and on sleep apnea activity

Summary: Up to 50% of hypertensive men are subject to sleep apnea (SA). With a prevalence in men of up to 10%, SA is a common illness and hypertension (HT) one of its early symptoms. It is important to have available a drug treatment that will effectively control blood pressure (BP) without exacerbating symptoms of SA. Twelve patients with SA and HT were investigated in a double-blind, comparative trial. Patients were randomly allocated to either metoprolol (M) 100 mg daily or cilazapril (C) 2.5 mg daily. Polysomnographic measurements under standardized conditions including intraarterial BP monitoring were taken on two consecutive nights each before and after the 1-week treatment. Values in the M group were (mean ± 95% CI) systolic BP 161 ± 2.1 vs. 148 ± 2.2 mm Hg (p < 0.01); diastolic BP 98 ± 1.8 vs. 93 ± 1.8 mm Hg (p < 0.01); and HR 73 ± 1.2 vs. 65 ± 1.1 beats/min (p < 0.01). Corresponding figures for the C group were systolic BP 140 ± 2.1 vs. 127 ± 2.1 mm Hg (p < 0.01); diastolic BP 95 ± 1.7 vs. 78 ± 1.7 mm Hg (p < 0.01); and HR 82 ± 1.1 vs. 79 ± 1.2 beats/min (p < 0.01). Whereas C reduced both BP and HR in all sleep phases, M produced no changes during REM sleep. SA activity was 45 (range 15–91) vs. 34 (range 2–57) apneas per hour of sleep in the M group and 54 (range 21–84) vs. 40 (range 8–72) apneas per hour in the C group (p < 0.01). There were no changes in total sleep time or in the proportions of non-REM to REM sleep. Both M and C reduce nocturnal BP in SA patients, but the effect of C is seen in all sleep phases. C has a more favorable effect on the disturbed nocturnal blood pressure of SA patients.

Mean blood pressure, pulse pressure and grade of hypertension in untreated hypertensive patients with sleep-related breathing disorder.

Objective To test the hypothesis that sleep-related breathing disorder (SRBD) is associated with increasing severity of cardiovascular risk markers. Design A cross-sectional study of sleep laboratory patients. Setting University Hospital Sleep Disorders Centre. Patients We studied 591 patients referred for a sleep study, all of them without a history of systemic hypertension. Interventions Clinical interview, two unattended sleep studies, and assessment of office blood pressure, cholesterol concentration, alcohol and nicotine consumption and daytime blood gases. Main outcome measure Post-hoc analysis of different cardiovascular risk markers: mean blood pressure, pulse pressure, and the type and grade of systemic hypertension. Results Patients were classified as normotensive (blood pressure < 140/90 mmHg, n = 228) or hypertensive (blood pressure ⩾ 140/90 mmHg, n = 363) according to office blood pressure measurements. Mixed (systolic and diastolic) hypertension was the most common type of hypertension (n = 182), followed by isolated diastolic hypertension (n = 101), borderline isolated systolic hypertension (n = 70), and isolated systolic hypertension (n = 10). The frequency of mixed hypertension increased with SRBD activity (P < 0.05) and respiratory disturbance index (RDI; the number of breathing disorders per hour of estimated sleep time) was increased in those with mixed hypertension compared with those with normotension (24.8 compared with15.7;t test:P < 0.01). In hypertensive patients classified as having grades 1–3 of hypertension (n = 265, 80 and 18, respectively), there was a progressive increase in RDI (18.9, 27.2 and 30.3, respectively, P < 0.01). Mean blood pressure increased significantly with RDI. Pulse pressure increased significantly with age (P < 0.001), but was unrelated to the degree of SRBD. Conclusion We conclude that mean blood pressure and the severity of hypertension, but not pulse pressure, increase with the severity of the SRBD.