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PubMed2005

Effects of antihypertensives on arterial responses associated with obstructive sleep apneas.

BACKGROUND: Many patients with obstructive sleep apnea syndrome (OSAS) have complicated with hypertension and may be prescribed with antihypertension medications to control their blood pressure. But whether antihypertension medications can also decrease arterial stiffness or control the blood pressure increasing following obstructive events is not well described. This study aimed to investigate whether antihypertensive medications can ameliorate the changes in arterial stiffness and blood pressure associated with OSA. METHODS: Sixty-one OSAS patients [13 women, 48 men, mean age (53.4 +/- 12.3) years], 26 normotensive patients (N), 7 hypertensive patients on no antihypertension medications (H), and 28 hypertensive patients on various combination antihypertension therapy (HM), were prospectively diagnosed with standard nocturnal polysomnography. Beat-to-beat blood pressure was continuously recorded from the radial artery by applanation tonometry during baseline sleep. As a measure of arterial stiffness, arterial augmentation index (AAI) was calculated as the ratio of augmented systolic blood pressure (SBP) to pulse pressure and expressed as a percentage for the following conditions: awakening, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events (apnea or hypopnea), and the first 15 cardiac cycles following event termination ("post apnea") for all events with nadir O2 saturation <or= 89%. RESULTS: Systolic blood pressure (SBP) post-apnea [(142.74 +/- 13.06) mmHg (N), (137.06 +/- 26.56) mmHg (H), (136.94 +/- 14.1) mmHg (HM)] was significantly increased from awakening [(135.76 +/- 14.76) mmHg (N), (135.58 +/- 23.17) mmHg (H), (129.77 +/- 14.00) mmHg (HM)], early apnea [(130.53 +/- 12.65) mmHg (N), (124.47 +/- 24.97) mmHg (H), (126.04 +/- 13.12) mmHg (HM)], and late apnea [(129.8 +/- 12.68) mmHg (N), (124.78 +/- 25.15) mmHg (H), (124.48 +/- 13.82) mmHg (HM)] respectively (P < 0.001, repeated measures ANOVA). AAI was significantly increased for the N group (P < 0.001) from awakening to late apnea [(10.45 +/- 2.62)% vs (14.43 +/- 3.21)%] and from early apnea to late apnea [(10.61 +/- 2.34)% vs (14.43 +/- 3.21)%], and also for H group (P < 0.05) from awakening to late apnea [(11.23 +/- 3.87)% vs (16.32 +/- 8.02)%] and from early apnea to late apnea [(11.75 +/- 3.79)% vs (16.32 +/- 8.02)%]. Meanwhile, no significant differences in AAI among awakening, early apnea, late apnea, and post-apnea conditions were found in HM group. CONCLUSIONS: The current data demonstrate that systemic blood pressure increases significantly during the post-apneic phase of OSAS, compared with that during awakening and intra-apnea phases even with the use of combined antihypertensive therapy which could normalize BP during awakening in the hypertensive patients. However, increases in arterial stiffness during obstructive events could be ameliorated by combined antihypertension medications.

Adult↗
PubMed2000

Kinesthetic stimulation for treating apnea in preterm infants.

BACKGROUND: This section is under preparation and will be included in the next issue. OBJECTIVES: Main question: in preterm infants with apnea, does the use of kinesthetic stimulation lead to clinically important reductions in clinical apnea and bradycardia (>50% reduction in number of episodes), use of mechanical ventilation (IPPV) or continuous positive airways pressure (CPAP), and neurodevelopmental disability, without clinically important side effects. SEARCH STRATEGY: The standard search strategy of the Neonatal Review Group was used. This included searches of the Oxford Database of Perinatal Trials, Cochrane Controlled Trials Register, MEDLINE, previous reviews including cross references, abstracts, conferences, symposia proceedings, expert informants, and journal handsearching mainly in the English language. SELECTION CRITERIA: All trials using random or quasi-random patient allocation in which kinesthetic stimulation in preterm infants was compared to placebo or no treatment for apnea of prematurity were included. DATA COLLECTION AND ANALYSIS: Standard methods of the Cochrane Collaboration and its Neonatal Review Group were used with separate evaluation of trial quality, data extraction by both authors and synthesis of data using relative risk and weighted mean difference. As all three trials were crossover trials, the data were extracted from all exposure periods and combined where appropriate. Measures of severity of apnea as well as the response to treatment were consistent with an evaluation of 'clinical apnea', as defined by the American Academy of Pediatrics (Nelson 1978). MAIN RESULTS: Three crossover studies (Korner 1978, Tuck 1982 and Jirapaet 1993) were identified that compared a form of kinesthetic stimulation to control for the treatment of apnea of prematurity. Clinically significant apnea: None of the three studies showed an important reduction (>50%) in clinical apnea. Using a lower threshold (>25%), the study by Korner 1978 found less apnea and bradycardia in infants receiving kinesthetic stimulation. Tuck 1982 demonstrated reductions in the frequencies of apneas (> 12 seconds) associated with bradycardia (< 100 bpm), apneas associated with hypoxia (TcP02 < 50 mmHg), and apneas requiring stimulation in infants on the rocking bed. Individual patient data were not available from the author to determine if there was an important reduction in clinical apnea. No outcome could be extracted from the study by Jirapaet 1993 that was consistent with the definition of clinically important apnea. Other events: No significant differences were found in the incidence of infants requiring resuscitation, IPPV, CPAP or respiratory stimulants whilst receiving treatment. Adverse events such as death, intraventricular hemorrhage and neurodevelopmental follow up were not reported. REVIEWER'S CONCLUSIONS: There is insufficient evidence to recommend kinesthetic stimulation as treatment for clinically significant apnea of prematurity. Previous reviews have suggested that kinesthetic stimulation is not effective at preventing apnea of prematurity (Henderson-Smart and Osborn 1998) and is not as effective as theophylline at treating clinically significant apnea of prematurity (Osborn and Henderson-Smart 1998).

Apnea↗
PubMed2006

Complex sleep apnea syndrome: is it a unique clinical syndrome?

STUDY OBJECTIVES: Some patients with apparent obstructive sleep apnea hypopnea syndrome (OSAHS) have elimination of obstructive events but emergence of problematic central apneas or Cheyne-Stokes breathing pattern. Patients with this sleep-disordered breathing problem, which for the sake of study we call the "complex sleep apnea syndrome," are not well characterized. We sought to determine the prevalence of complex sleep apnea syndrome and hypothesized that the clinical characteristics of patients with complex sleep apnea syndrome would more nearly resemble those of patients with central sleep apnea syndrome (CSA) than with those of patients with OSAHS. DESIGN: Retrospective review SETTING: Sleep disorders center. PATIENTS OR PARTICIPANTS: Two hundred twenty-three adults consecutively referred over 1 month plus 20 consecutive patients diagnosed with CSA. INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Prevalence of complex sleep apnea syndrome, OSAHS, and CSA in the 1-month sample was 15%, 84%, and 0.4%, respectively. Patients with complex sleep apnea syndrome differed in gender from patients with OSAHS (81% vs 60% men, p < .05) but were otherwise similar in sleep and cardiovascular history. Patients with complex sleep apnea syndrome had fewer maintenance-insomnia complaints (32% vs 79%; p < .05) than patients with CSA but were otherwise not significantly different clinically. Diagnostic apnea-hypopnea index for patients with complex sleep apnea syndrome, OSAHS, and CSA was 32.3 +/- 26.8, 20.6 +/- 23.7, and 38.3 +/- 36.2, respectively (p = .005). Continuous positive airway pressure suppressed obstructive breathing, but residual apnea-hypopnea index, mostly from central apneas, remained high in patients with complex sleep apnea syndrome and CSA (21.7 +/- 18.6 in complex sleep apnea syndrome, 32.9 +/- 30.8 in CSA vs 2.14 +/- 3.14 in OSAHS; p < .001). CONCLUSIONS: Patients with complex sleep apnea syndrome are mostly similar to those with OSAHS until one applies continuous positive airway pressure. They are left with very disrupted breathing and sleep on continuous positive airway pressure. Clinical risk factors don't predict the emergence of complex sleep apnea syndrome, and best treatment is not known.

Adult↗
PubMed2001

Patterns of EEG frequency, movement, heart rate, and oxygenation after isolated short apneas in infants.

Patterns of events occurring at the end of apneas have rarely been reported in infants. No previous studies have compared these patterns to those of spontaneous events during sleep. We examined 163 isolated apneas in 17 infants (47 +/- 4 wk postconceptional age) who underwent polysomnography for suspected upper airway problems. Mean apnea duration was 6.5+/-1.5 s (range, 5 to 11.5 s), 78% of apneas occurred in active sleep, and 67% of apneas were obstructive. We recorded the occurrence of body movement or augmented breath and analyzed changes in EEG frequency > or = 1 s, heart rate, and oxygen saturation value at the end of apneas and of a control ventilatory period defined as a period of breathing equal in duration to the apnea and preceding the apnea by 1 min. We found that 7.9% of apneas and 11.6% of control periods were followed by an augmented breath and that 14.1% of apneas and 0.5% of control periods were followed by a body movement. The percentages of motor events or no event differed significantly after the apneas (p = 0.008) compared with the control periods. A significant increase in EEG frequency was observed at the end of the apneas compared with the control periods (p < 0.04). EEG frequency increased after 61% of the apneas. Neither heart rate nor oxygen saturation value changed after the control periods. Heart rate decreased significantly after the apneas not followed by a motor event (p = 0.02) but not after the apneas followed by a body movement. We conclude that 1) at termination of isolated apneas in infants, a motor event was rare, whereas an EEG frequency increase was common; 2) event patterns at apnea termination differed from those at control period termination.

Electroencephalography↗
PubMed2000

Adverse effects of nicotine and interleukin-1beta on autoresuscitation after apnea in piglets: implications for sudden infant death syndrome.

OBJECTIVES: Maternal cigarette smoking is established as a major dose-dependent risk factor for sudden infant death syndrome (SIDS). Both prenatal and postnatal exposures to constituents of tobacco smoke are associated with SIDS, but no mechanism of death attributable to nicotine has been found. Breastfeeding gives a substantial increase in absorbed nicotine compared with only environmental tobacco smoke when the mother smokes, because the milk:plasma concentration ratio of nicotine is 2.9 in smoking mothers. Furthermore, many SIDS victims have a slight infection and a triggered immune system before their death, thus experiencing a release of cytokines like interleukin-1beta (IL-1beta) that may depress respiration. Because apneas in infancy are associated with SIDS, we have tested the hypothesis that postnatal exposure to tobacco constituents and infections might adversely affect an infant's ability to cope with an apneic episode. This is performed by investigating the acute effects of nicotine and IL-1beta on apnea by laryngeal reflex stimulation and on the subsequent autoresuscitation. DESIGN: Thirty 1-week-old piglets (+/-1 day) were sedated with azaperone. A tracheal and an arterial catheter were inserted during a short halothane anesthesia. The piglets were allowed a 30-minute stabilization period before baseline values were recorded and they were randomized to 4 pretreatment groups (avoiding siblings in the same group): 1) immediate infusion of 10 pmol IL-1beta intravenously/kg (IL-1beta group; n = 8); 2) slow infusion of 5 microg nicotine intravenously/kg 5 minutes later (NIC group; n = 8); 3) both IL-1beta and NIC combined (NIC + IL-1beta group; n = 6); or 4) placebo by infusion of 1 ml .9% NaCl (CTR group; n = 8). Fifteen minutes later, apnea was induced by insufflation of .1 ml of acidified saline (pH = 2) in the subglottic space 5 times with 5-minute intervals, and variables of respiration, heart rate, blood pressure, and blood gases were recorded. RESULTS: Stimulation of the laryngeal chemoreflex by insufflation of acidified saline in the subglottic space produced apneas, primarily of central origin. This was followed by a decrease in heart rate, a fall in blood pressure, swallowing, occasional coughs, and finally autoresuscitation with gasping followed by rapid increase in heart rate, rise in blood pressure, and (in the CTR group) an increase of respiratory rate. Piglets pretreated with nicotine had more spontaneous apneas, and repeated spontaneous apneas caused an inability to perform a compensatory increase of the respiratory rate after induced apnea. This resulted in a lower SaO(2) than did CTR at 2 minutes after apnea (data shown as median [interquartile range]: 91% [91-94] vs 97% [94-98]). The pretreatment with IL-1beta caused prolonged apneas in piglets and an inability to hyperventilate causing a postapneic respiratory rate similar to the NIC. When nicotine and IL-1beta were combined, additive adverse effects on respiratory control and autoresuscitation compared with CTR were observed: NIC + IL-1beta had significantly more spontaneous apneas the last 5 minutes before induction of apnea (2 [.3-3] vs 0 [0-0]). Apneas were prolonged (46 seconds [39-51] vs 26 seconds [22-31]) and followed by far more spontaneous apneas the following 5 minutes (6.6 [4.0-7.9] vs.5 [.2- .9]). Instead of normal hyperventilation after apnea, a dramatic decrease in respiratory rate was seen (at 20 seconds: -45% [-28 to -53] vs +29% [+24-+50], and at 60 seconds: -27% [-23 to -32] vs +3% [-2-+6), leading to SaO(2) below 90% 3 minutes after end of apnea: 89% (87-93) versus 97% (95-98). These prolonged adverse effects on ventilation were reflected in lowered PaO(2), elevated PaCO(2) and lowered pH 2 minutes, and even 5 minutes, after induction of apnea. CONCLUSIONS: Nicotine interferes with normal autoresuscitation after apnea when given in doses within the range of what the child of a smoking mother could receive through environmental t

Animals↗
PubMed2003

Spleen volume and blood flow response to repeated breath-hold apneas.

The purpose of this study was 1) to answer whether the reduction in spleen size in breath-hold apnea is an active contraction or a passive collapse secondary to reduced splenic arterial blood flow and 2) to monitor the spleen response to repeated breath-hold apneas. Ten trained apnea divers and 10 intact and 7 splenectomized untrained persons repeated five maximal apneas (A1-A5) with face immersion in cold water, with 2 min interposed between successive attempts. Ultrasonic monitoring of the spleen and noninvasive cardiopulmonary measurements were performed before, between apneas, and at times 0, 10, 20, 40, and 60 min after the last apnea. Blood flows in splenic artery and splenic vein were not significantly affected by breath-hold apnea. The duration of apneas peaked after A3 (143, 127, and 74 s in apnea divers, intact, and splenectomized persons, respectively). A rapid decrease in spleen volume ( approximately 20% in both apnea divers and intact persons) was mainly completed throughout the first apnea. The spleen did not recover in size between apneas and only partly recovered 60 min after A5. The well-known physiological responses to apnea diving, i.e., bradycardia and increased blood pressure, were observed in A1 and remained unchanged throughout the following apneas. These results show rapid, probably active contraction of the spleen in response to breath-hold apnea in humans. Rapid spleen contraction and its slow recovery may contribute to prolongation of successive, briefly repeated apnea attempts.

Adult↗
PubMed1999

Influence of pulmonary capillary wedge pressure on central apnea in heart failure.

BACKGROUND: Recent studies suggest that acute pulmonary congestion induces hyperventilation and that hyperventilation-related hypocapnia leads to ventilatory control instability and central sleep apnea. Whether chronic pulmonary congestion due to congestive heart failure (CHF) is associated with central apnea is unknown. We hypothesized that CHF patients with central apnea would have greater pulmonary capillary wedge pressure (PCWP) than patients without central apnea and that PCWP would correlate with central apnea severity. METHODS AND RESULTS: Seventy-five stable CHF patients underwent right heart catheterization and, on the basis of overnight sleep studies, were divided into central apnea (n=33), obstructive apnea (n=20), or nonapnea groups (apnea-hypopnea index [AHI] <5 events per hour). Mean PCWP was significantly greater in the central than in the obstructive and nonapnea groups (mean+/-SEM [range]: 22. 8+/-1.2 [11 to 38] versus 12.3+/-1.2 [4 to 21] versus 11.5+/-1.5 [3 to 28] mm Hg, respectively; P<0.001). Within the central apnea group, PCWP correlated with the frequency and severity of central apnea (AHI: r=0.47, P=0.006) and degree of hypocapnia (PaCO2: r=-0.42, P=0. 017). Intensive medical therapy in 7 patients with initially high PCWP and central apneas reduced both PCWP (29.0+/-2.6 [20 to 38] to 22.0+/-1.8 [17 to 27] mm Hg; P<0.001) and central apnea frequency (AHI) (38.5+/-7.7 [7 to 62] to 18.5+/-5.3 [1 to 31] events per hour; P=0.005). CONCLUSIONS: PCWP is elevated in CHF patients with central apneas compared with those with obstructive apnea or without apnea. Moreover, a highly significant relationship exists between PCWP, hypocapnia, and central apnea frequency and severity.

Adolescent↗
PubMed1991

Sleep apnea in acromegaly.

OBJECTIVE: To provide information on the nature, prevalence, and severity of sleep apnea in patients with acromegaly. DESIGN: Consecutive case series. SETTING: Tertiary referral hospital. PATIENTS: Fifty-three patients with acromegaly were consecutively referred: 33 patients were referred because of clinical suspicion of sleep apnea and 20 patients were referred without suspected apnea. MEASUREMENTS: Sleep studies as well as growth hormone and insulin-like growth factor 1 (IGF-1) measurements were done. MAIN RESULTS: Thirty-one patients (93%; 95% Cl, 85% to 100%) referred because of suspicion of sleep apnea had sleep apnea compared with 12 patients (60%; Cl, 37% to 83%) referred without suspected sleep apnea. Patients with sleep apnea did not have biochemical evidence of increased disease activity (random growth hormone, 12.7 +/- 4.4 micrograms/L; mean growth hormone at 24-hour sampling, 10.8 +/- 8.4 micrograms/L; IGF-1, 90.0 +/- 7.5 nmol/L) compared with patients without sleep apnea (random growth hormone, 14.2 +/- 4.9 micrograms/L, P greater than 0.2; mean growth hormone, 12.4 +/- 3.5 micrograms/L, P greater than 0.2; IGF-1, 90.0 +/- 10.0 nmol/L, P greater than 0.2). Central sleep apnea was the predominant type of apnea in 33% (Cl, 18% to 47%) of patients and was associated with higher random growth hormone and IGF-1 levels than was obstructive apnea (random growth hormone, 23.4 +/- 3.9 compared with 8.8 +/- 3.1 micrograms/L, P less than 0.001; IGF-1, 126 +/- 17.5 compared with 72.5 +/- 7.5 nmol/L, P less than 0.01). CONCLUSIONS: Sleep apnea is common in acromegaly. The rate of central sleep apnea was unexpectedly high in patients with acromegaly, and biochemical evidence of increased disease activity was associated with the presence of central apnea rather than with the degree of sleep apnea. Altered respiratory control is a possible mechanism producing sleep apnea in acromegaly.

Acromegaly↗
PubMed2005

[Effects of antihypertensives on arterial responses associated with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To investigate whether antihypertensive medications ameliorate the changes in arterial stiffness and blood pressure associated with obstructive sleep apnea-hypopnea syndrome (OSAHS). METHODS: Sixty-one OSAHS patients (13 female, 48 male, mean age 53 +/- 12 years), among which 26 were normotensive (N group), 7 hypertensive on no antihypertension medications (H group), and 28 hypertensive on various combination antihypertension therapy (HM group), were prospectively diagnosed with standard nocturnal polysomnography. Beat-to-beat blood pressure was continuously recorded from the radial artery by applanation tonometry. Arterial stiffness was measured by arterial augmentation index (AAI). The following conditions:awake, early apnea, late apnea and post apnea for all events with nadir O(2) saturation < or = 89% were analyzed. RESULTS: Systolic blood pressures (SBP) post-apnea [N group (143 +/- 13) mm Hg, H group (137 +/- 27) mm Hg, HM group (137 +/- 14) mm Hg] were significantly increased from awake [N group (136 +/- 15) mm Hg, H group (136 +/- 23) mm Hg, HM group (130 +/- 14) mm Hg], early apnea [N group (131 +/- 13) mm Hg, H group (124 +/- 25) mm Hg, HM group (126 +/- 13) mm Hg], and late apnea [N group (130 +/- 13) mm Hg, H group (125 +/- 25) mm Hg, HM group (124 +/- 14) mm Hg] respectively (P < 0.01, repeated measures ANOVA). AAI was significantly increased for the N group (P < 0.01) from awake to late apnea [(10.5 +/- 2.6)% vs (14.4 +/- 3.2)%] and from early apnea to late apnea [(10.6 +/- 2.3)% vs (14.4 +/- 3.2)%], and also for H group (P < 0.05) from awake to late apnea [(11.2 +/- 3.9)% vs (16.3 +/- 8.0)%)] and from early apnea to late apnea [(11.8 +/- 3.8)% vs (16.3 +/- 8.0)%]. Meanwhile, no significant differences in AAI among awake, early apnea, late apnea, and post-apnea conditions were found in HM group. CONCLUSIONS: Systemic blood pressure increases significantly during the post-apneic phase of OSAHS even with the combined antihypertensive therapy which normalizes awake BP in the hypertensive patients. However, increases in arterial stiffness during obstructive events can be ameliorated by combined antihypertension medications, in contrast to increased arterial stiffness seen in normotensive OSAHS patients or hypertensive OSAHS patients on no such medications.

Adult↗
PubMed1982

Periodic apnea in the full-term infant: individual consistency, sex differences, and state specificity.

The occurrence of periodic apnea (apnea during periodic breathing) was studied in 27 normal, full-term infants during the first five weeks of life. The rate and mean length of apnea were analyzed both with respect to sleep state and with respect to respiratory pattern, ie, periodic vs nonperiodic breathing. The rate of apnea was found to vary according to sleep state and the pattern of breathing. The highest apnea rates were nonperiodic apneas in active sleep. Periodic apnea rates were relatively low in both active and quiet sleep; however, this type of apnea was consistently observed from weeks 2 through 5. The proportion of apneas that are periodic is much higher in quiet sleep than in active sleep. Rates of periodic and nonperiodic apnea were more consistently correlated in active sleep than in quiet sleep. The mean length of periodic apnea was found to be significantly greater than the mean length of nonperiodic apnea in both sleep states, a difference that reflected a greater positive skew in the distribution of the nonperiodic apnea lengths. This variation in length between periodic and nonperiodic apnea explains, in part, the increased mean length in quiet sleep compared with active sleep. There were significant individual differences over weeks in both forms of apnea in active sleep and in quiet sleep. Female infants were observed to have higher rates of nonperiodic apnea than male infants in active sleep, although no significant differences in the distribution of lengths were obtained.

Female↗
PubMed1988

Neonatal apnea: diagnosis by nurse versus computer.

In an effort to characterize significant neonatal apnea and evaluate the nursing diagnosis of apnea, apnea type and frequency were determined in 27 infants by continuous computer recording of heart rate, respiratory impedance, end-tidal CO2, and either or both transcutaneous oxygen and pulse oximetry. Of the 1,266 recorded apneas, 46% were central, 44% were mixed, and 10% were obstructive. Mixed apnea was associated with a longer mean duration and greater mean decrease in heart rate than central apnea. Apnea duration was positively correlated with both a decrease in heart rate and oxygen saturation (P less than .001), and a lower baseline saturation was associated with a greater decrease in oxygen saturation during apnea (P = .002). Theophylline therapy had no effect on apnea duration or oxygen desaturation but resulted in a decrease in the mean heart rate decrease associated with apnea. Overall, nurses diagnosed 54% of all apneic episodes and were significantly poorer at detecting mixed and obstructive events. Nursing detection of apnea improved with increasing apnea duration and was always associated with a greater decrease in heart rate. Nurses diagnosed significantly fewer mixed apnea following theophylline therapy. Improved monitoring techniques, particularly for mixed and obstructive apnea, are essential to increase apnea detection in the nursery.

Apnea↗
PubMed1994

Epidemiology of obstructive sleep apnea.

Sleep-disturbed breathing, which includes apneas, hypopneas, and oxygen desaturations, occurs in asymptomatic individuals and increases with age. Obstructive apnea is the most frequent type of respiratory disturbance documented by polysomonography, the gold standard test for assessing sleep-disturbed breathing. Many of the prevalence studies done to date have had one or more methodological weaknesses, including selection biases, varying definitions of obstructive sleep apnea, failure to distinguish types of apneas, failure to control for confounding variables, and small sample size. Although there is consensus on the definitions of sleep-disturbed breathing, the appropriate number of apneas and hypopneas for diagnosing clinically significant obstructive sleep apnea is uncertain. While the cutoff of five or more apneas and hypopneas per hour is historically considered abnormal, the origins of this number are vague, and the longevity of those who have this value on polysomnography is not necessarily reduced. This is particularly true among those without symptoms of obstructive sleep apnea syndrome, which include excessive daytime sleepiness, snoring, nocturnal awakenings, and morning headaches. Investigators should be careful to distinguish symptomatic study subjects from asymptomatic subjects, and to exclude central apneas in calculating their estimates. In addition, various studies have used different definitions of sleep apnea syndrome, making comparisons of point estimates difficult. It would be more appropriate for researchers to estimate morbidity and mortality indices with confidence intervals, using several different cutoff points. Subject selection in all studies should follow a two-stage sampling procedure. All subjects with symptoms compatible with obstructive sleep apnea syndrome and a subsample of asymptomatic individuals should be studied with all-night polysomnography. If portable monitoring is used, the validity and reproducibility of this diagnostic method should be assessed. Subjects with significant comorbidity should be excluded from prevalence studies. Factors that clearly increase the risk of sleep-disturbed breathing and obstructive sleep apnea and its related symptoms include age, structural abnormalities of the upper airway, sedatives and alcohol, and probably family history. Although endocrine changes such as growth hormone, thyroid hormone, and progesterone deficiency also have been suggested as risk factors for exacerbating obstructive sleep apnea syndrome, there is minimal epidemiologic evidence to support this. Case-control studies are recommended to assess the relation of endocrine factors to obstructive sleep apnea syndrome in a rigorous fashion. A limited number of mortality studies have suggested decreased survival in persons with the obstructive sleep apnea syndrome, possibly primarily due to vascular-related disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2005

Association between atrial fibrillation and central sleep apnea.

BACKGROUND: We previously described an association between atrial fibrillation and central sleep apnea in a group of patients with congestive heart failure. We hypothesized that the prevalence of atrial fibrillation might also be increased in patients with central sleep apnea in the absence of other cardiac disease. METHODS AND RESULTS: We compared the prevalence of atrial fibrillation in a series of 60 consecutive patients with idiopathic central sleep apnea (apnea-hypopnea index > 10 events per hour, > 50% central events) with that in 60 patients with obstructive sleep apnea (apnea-hypopnea index > 10, > 50% obstructive events) and 60 patients without sleep apnea (apnea-hypopnea index < 10), matched for age, sex, and body mass index. Subjects with a history of congestive heart failure, coronary artery disease, or stroke were excluded from the study. The prevalence of atrial fibrillation among patients with idiopathic central sleep apnea was found to be significantly higher than the prevalence among patients with obstructive sleep apnea or no sleep apnea (27%, 1.7%, and 3.3%, respectively, P < .001). However, hypertension was most common and oxygen desaturation most extreme among patients with obstructive sleep apnea. CONCLUSIONS: We conclude that there is a markedly increased prevalence of atrial fibrillation among patients with idiopathic central sleep apnea in the absence of congestive heart failure. Moreover, the high prevalence of atrial fibrillation among patients with idiopathic central sleep apnea is not explainable by the presence of hypertension or nocturnal oxygen desaturation, since both of these were more strongly associated with obstructive sleep apnea.

Arrhythmias, Cardiac↗
PubMed1994

Cardiovascular effects of periodic obstructive and central apneas in dogs.

Patients with sleep apnea may experience two types of apnea, central and obstructive. We compared cardiovascular effects of these two types of apnea matched for changes in arterial blood gas tensions and periodicity. In 12 anesthetized, closed chest dogs, obstructive apneas were induced by completely occluding the endotracheal tube at end-expiration for 1 min and allowing 1 min of spontaneous ventilation. Central apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on with the same periodicity as obstructive apneas. During both types of apnea, changes in arterial PO2 and PCO2 were approximately the same. During obstructive apneas, mean blood pressure (BP) and cardiac output (CO) did not change significantly, heart rate (HR) decreased by 27% (p < 0.001), and stroke volume increased by 7.8 ml (p < 0.005). During central apnea, BP did not change, but HR and CO decreased by far more than with obstructive apneas: 44% (p < 0.001) and 27% (p < 0.05) respectively, and stroke volume increased by 5.0 ml (p < 0.05). During obstructive apneas, right atrial pressure increased, as did right heart blood volume. During central apneas, both right atrial pressure and left atrial pressure increased, as did pulmonary blood volume. We conclude that: (1) HR decreases are more severe during central apnea, most likely due to lack of respiratory mechanoreceptor input; (2) CO decreases more with central compared with obstructive apnea due to the heart rate response; (3) HR-induced cardiac dysfunction with central apnea could lead to pulmonary vascular congestion.

Animals↗
PubMed1993

Obstructive sleep apnea and the kidney.

Recent studies of obstructive sleep apnea and its comorbidity with other systemic diseases have stimulated interest in the relationship of apnea to renal disease and hypertension. Polysomnographic sleep studies in patients on dialysis who complain of day-time fatigue or sleepiness reveal significant apnea in up to 73% of those studied. Abnormalities in respiratory controller mechanisms from chronic hypocarbia, metabolic acidosis, and uremic toxins have been blamed for the occurrence of apnea in this setting. Proteinuria and sometimes nephrotic syndrome have been recognized in morbidly obese patients with sleep apnea syndrome. Renal biopsies of such patients have shown glomerulomegaly and focal segmental sclerosis. It is postulated that these lesions may result from increased glomerular filtration and blood flow. Elevated urine output, sodium and chloride excretion, and atrial natriuretic peptide have been well demonstrated in obstructive apnea patients and correct to control levels with treatment of the apnea. Both acute (with each apnea) and chronic daytime blood pressure elevation are frequently observed in sleep apnea patients, and occult sleep apnea is postulated as one possible cause of "primary" hypertension in middle-aged men. In younger patients, such hypertension seems to be more reversible with the elimination of apnea. In older patients, however, the cure of systemic hypertension cannot be guaranteed with the elimination of the apnea, and asymptomatic apnea patients tend not to tolerate the bother and discomfort of apnea treatment with nasal continuous positive airway pressure. Therefore, aside from a careful history regarding sleep symptomatology, polysomnographic studies of clinic populations with primary hypertension to search for apnea as a cause cannot be recommended.

Aged↗
PubMed1998

Effect of a prosthetic appliance for treatment of sleep apnea syndrome on masticatory and tongue muscle activity.

STATEMENT OF PROBLEM: The efficiency of an appliance for treatment of sleep apnea shows inordinate interindividual difference. The mechanism of its therapeutic effects remains unresolved. PURPOSE: This study examined the effect of the device on sleep apnea, and masticatory and tongue muscles. MATERIAL AND METHODS: Fifteen patients with sleep apnea syndrome were evaluated polysomnographically, with and without the appliance. Electromyograms (EMG) of genioglossal, masseter, and lateral pterygoid muscles were recorded and EMG amplitudes measured before, during, and after the apneas. Apneas were classified into three types: obstructive, central, and mixed. RESULTS: During obstructive apneas, muscles showed significantly lower EMG amplitudes; whereas during central apneas, no decrease in the mean EMG amplitude was observed. EMG amplitudes increased after insertion of the device. EMG amplitudes during obstructive apneas were significantly increased in the genioglossal (p < 0.03, t test) and lateral pterygoid muscles (p < 0.03) by the device. Obstructive and mixed apneas per hour were significantly reduced by the appliance; however, in contrast, central apneas showed slightly increased. The apnea index decreased significantly (p < 0.002) by the device owing to the paucity of central apneas. CONCLUSIONS: The apnea appliance activated masticatory and tongue muscles during sleep and prevented the upper airway from collapsing. The prosthetic appliance was useful in the treatment of sleep apnea syndrome.

Aged↗
PubMed1985

Obesity and hormonal factors in sleep and sleep apnea.

The presence of obesity, defined as weight 20 per cent or more above ideal body weight or increased body fat content, significantly increases risk of pulmonary, cardiovascular, metabolic, and gastrointestinal problems. Obesity is a major cause of shortened life expectancy. While obesity is not essential for the development of the obstructive sleep apnea syndrome, a significant percentage of patients with obstructive sleep apnea are obese. When evaluating these patients who have obstructive sleep apnea, it is important to search diligently for medical problems that are commonly found among the obese. While there is an increased incidence of obese patients among those who have obstructive sleep apnea, the exact reason for this is uncertain. The study of endorphins and enkephalins may expand our understanding of obesity, ventilatory regulation, and obstructive sleep apnea. This may, in fact, enable us to understand better the interrelationship between obesity and obstructive sleep apnea. The role that thyroid hormone, testosterone, and progesterone play in obstructive sleep apnea has also been reviewed. Patients who have obstructive sleep apnea should not be treated with testosterone. All patients given testosterone should be observed quite closely for the possible signs and symptoms of obstructive sleep apnea. Progesterone seems to be of some help in patients who have obesity hypoventilation syndrome. Its effectiveness in patients with obstructive sleep apnea is less clear. The obesity hypoventilation syndrome as described by Burwell is relatively uncommon. Many of the manifestations of the obesity hypoventilation syndrome, however, are found in patients with obstructive sleep apnea. The recognition that the symptoms stem from underlying obstructive sleep apnea offers great potential for therapy. Weight reduction is valuable therapy for patients with obesity and pulmonary dysfunction, obesity and obstructive sleep apnea, and obesity hypoventilation syndrome. Weight reduction and weight maintenance, while difficult, are essential in patients with obesity, obesity and obstructive sleep apnea, and the hypoventilation syndrome. Obesity should be viewed as a medical problem deserving medical attention and long-term medical follow-up.

Adult↗
PubMed1999

Recent weight gain in patients with newly diagnosed obstructive sleep apnea.

OBJECTIVE: Patients with obstructive sleep apnea are often obese. Obesity may contribute to both sleep apnea itself and to the cardiovascular risk associated with sleep apnea. Weight loss in obese patients with sleep apnea may alleviate symptoms and decrease the severity of sleep apnea. Whether patients with obstructive sleep apnea are indeed predisposed to recent weight gain, as compared with similarly obese subjects without sleep apnea, is not known. PATIENTS AND METHODS: We compared 1-year weight histories in 53 male and female patients newly diagnosed with obstructive sleep apnea, compared with 24 controls matched for gender, age, body mass index, and percent body fat. Sleep apnea patients had never been treated. Control subjects were proven to be free of sleep-disordered breathing by overnight polysomnography. RESULTS: Patients with obstructive sleep apnea (n = 53) had a significant recent weight gain of 7.4 +/- 1.5 kg compared with a weight loss of 0.5 +/- 1.7 kg (P = 0.001) in similarly obese controls (n = 24). Male patients with obstructive sleep apnea (n = 28) had a history of significant weight gain (6.8 +/- 2.3 kg) over the year preceding the study compared with male control subjects (n = 13), in whom average weight fell by 0.58 +/- 2.4 kg (P = 0.03). Female patients (n = 25) with obstructive sleep apnea had an 8.0 +/- 1.9 kg weight gain compared with female controls (n = 11) who had a history of weight loss of 0.46 +/- 2.6 kg (P = 0.02). CONCLUSION: These findings support the concept that patients with obstructive sleep apnea may be susceptible to increasing obesity in the period preceding the diagnosis of obstructive sleep apnea.

Adipose Tissue↗