Estimating sleep time from non-EEG-based PSG signals in the diagnosis of sleep-disordered breathing.

PURPOSE: The purpose of this study was to use non-EEG PSG signals to estimate TST in order to diagnose SDB with a greater sensitivity than type 3 device methodology that relies on TRT. METHODS: Movement patterns were obtained from the thoracoabdominal signals of adult PSG recordings (n = 60) in the laboratory and the home. Parameters obtained allowed, with 95% certainty, identification of sleep and wake based on the duration of movements and quiescent time (Qd). Snoring, apneas, and hypopneas indicated sleep with 100% certainty. The method was tested in a different set of PSG recordings (n = 80). RESULTS: Subjects lay awake and immobile for longer in the laboratory (QdLAB = 27.4 (12.1, 62.0), QdHOME = 16.0 s (8.0, 36.0); p < 0.0001) but asleep and immobile for longer at home (QdLAB = 65.2 (23.0, 121.4), QdHOME = 95.0 s (44.5, 247.5); 0.005). Only 5% of wake Qd periods were >173 s in the laboratory and >105 s at home. In both locations, 95% of movements during sleep were <10 s. Experimental TST values were 21 min shorter than EEG-defined TST and, combined with fewer scored respiratory events, produced AHI values that were 1.6 events/h lower than the reference. The experimental TST increased the sensitivity of SDB diagnosis from 73 to 97%. CONCLUSIONS: In the sleep laboratory, subjects are immobile for longer periods when awake and for shorter periods when asleep. The experimental TST was similar to EEG-defined TST and could be used to diagnose SDB with a much higher sensitivity than the type 3 method.

Hypertension, snoring, and obstructive sleep apnoea during pregnancy: a cohort study.

OBJECTIVE: To assess the frequency of obstructive sleep apnoea among women with and without hypertensive disorders of pregnancy. DESIGN: Cohort study. SETTING: Obstetric clinics at an academic medical centre. POPULATION: Pregnant women with hypertensive disorders (chronic hypertension, gestational hypertension, or pre-eclampsia) and women who were normotensive. METHODS: Women completed a questionnaire about habitual snoring and underwent overnight ambulatory polysomnography. MAIN OUTCOME MEASURES: The presence and severity of obstructive sleep apnoea. RESULTS: Obstructive sleep apnoea was found among 21 of 51 women with hypertensive disorders (41%), but in only three of 16 women who were normotensive (19%, chi-square test, P=0.005). [Author correction added on 16 June 2014, after first online publication: Results mentioned in the abstract were amended.] Non-snoring women with hypertensive disorders typically had mild obstructive sleep apnoea, but >25% of snoring women with hypertensive disorders had moderate to severe obstructive sleep apnoea. Among women with hypertensive disorders, the mean apnoea/hypopnoea index was substantially higher in snorers than in non-snorers (19.9±34.1 versus 3.4±3.1, P=0.013), and the oxyhaemoglobin saturation nadir was significantly lower (86.4±6.6 versus 90.2±3.5, P=0.021). Among women with hypertensive disorders, after stratification by obesity, the pooled relative risk for obstructive sleep apnoea in snoring women with hypertension compared with non-snoring women with hypertension was 2.0 (95% CI 1.4-2.8). CONCLUSIONS: Pregnant women with hypertension are at high risk for unrecognised obstructive sleep apnoea. Although longitudinal and intervention studies are urgently needed, given the known relationship between obstructive sleep apnoea and hypertension in the general population, it would seem pertinent that hypertensive pregnant women who snore should be tested for obstructive sleep apnoea, a condition believed to cause or promote hypertension.

Clinical guidelines for oral appliance therapy in the treatment of snoring and obstructive sleep apnoea.

The purpose of this review is to provide guidelines for the use of oral appliances (OAs) for the treatment of snoring and obstructive sleep apnoea (OSA) in Australia. A review of the scientific literature up to June 2012 regarding the clinical use of OAs in the treatment of snoring and OSA was undertaken by a dental and medical sleep specialists team consisting of respiratory sleep physicians, an otolaryngologist, orthodontist, oral and maxillofacial surgeon and an oral medicine specialist. The recommendations are based on the most recent evidence from studies obtained from peer reviewed literature. Oral appliances can be an effective therapeutic option for the treatment of snoring and OSA across a broad range of disease severity. However, the response to therapy is variable. While a significant proportion of subjects have a near complete control of the apnoea and snoring when using an OA, a significant proportion do not respond, and others show a partial response. Measurements of baseline and treatment success should ideally be undertaken. A coordinated team approach between medical practitioner and dentist should be fostered to enhance treatment outcomes. Ongoing patient follow-up to monitor treatment efficacy, OA comfort and side effects are cardinal to long-term treatment success and OA compliance.

Increasing hospitalizations for serious skin infections in New Zealand children, 1990-2007.

The incidence of serious skin infections in New Zealand children is significantly higher than in comparative countries. This study aimed to describe the epidemiology of these infections and identify changes in disease distribution over time. Discharge data were analysed for all children admitted to a New Zealand public hospital with a serious skin infection during the period 1990-2007. Patient and admission variables were compared between 1990-1999 and 2000-2007. The incidence of serious skin infections almost doubled from 298·0/100,000 in 1990 to 547·3/100,000 in 2007. The highest rates were observed in boys, preschool-aged children, Maori and Pacific children, those living in deprived neighbourhoods, urban areas and northern regions. Over time there were disproportionate increases in infection rates in Maori and Pacific children and children from highly deprived areas. Serious skin infections are an increasing problem for New Zealand children. Worsening ethnic and socioeconomic health inequalities may be contributing to increasing rates.

Repeated enzyme immunoassays have limited utility in diagnosing Clostridium difficile.

Many clinical laboratories use enzyme immunoassays (EIA) to diagnose Clostridium difficile-associated disease (CDAD). Clinicians frequently order three EIAs to "rule out" CDAD. We performed a retrospective cohort study to determine the clinical utility of repeating EIA testing to diagnose CDAD. We reviewed all EIAs performed by our laboratory during 2005, determined the total number of tests per patient and per testing episode, and calculated the relative negative predictive value (NPV) of one EIA compared to > or =2 EIAs. The laboratory performed 2,938 EIAs, of which 253 (8.6%) tests were positive. Most patients (85%) were diagnosed by the first EIA performed. Of >1,000 testing episodes that included > or =2 EIAs within 7 days, only 15 patients had a positive second or third test after negative initial testing. The relative NPV of the first EIA was 97.4%. These data suggest that using newer generation EIAs, repeated testing is of limited benefit in diagnosing CDAD.

nCPAP improves abnormal autonomic function in at-risk-for-SIDS infants with OSA.

We evaluated cardiovascular autonomic control and arousability during sleep in infants with obstructive sleep apnea (OSA) before and after 10 +/- 4 (mean +/- SD) days of treatment with nasal continuous positive airway pressure (nCPAP). Six OSA infants and 12 age-matched control infants were studied with polygraphic sleep studies at the age of 13 +/- 4 wk. During the study, 45 degrees head-up tilt tests were performed in slow-wave and rapid eye movement sleep. Blood pressure (BP) and heart rate (HR) were continuously monitored. All OSA infants had decreased initial BP and HR responses, followed by hypotension in two and hypertension in two. OSA infants displayed higher arousal thresholds in response to the tilt in rapid eye movement sleep (P < 0.005) and higher baseline HR (P < 0.05) than controls. nCPAP treatment normalized BP and HR responses as well as arousal thresholds to tilting and stabilized HR levels. OSA in infants may be linked with cardiovascular autonomic control disturbances and decreased arousability during sleep. These defects are improved by control of OSA with nCPAP.

Lactation is associated with an increase in slow-wave sleep in women.

Major physiological changes occur following parturition and the onset of lactation, including the withdrawal of oestrogen and progesterone, with a consequent increase in circulating prolactin (PRL). Changes in other circulating hormones are well known to alter sleep architecture in other circumstances. We therefore aimed to assess whether sleep architecture is altered in fully lactating women as a result of hormonal changes associated with lactation. A descriptive comparison study was undertaken on 12 fully breastfeeding women (B/F), 12 age-matched control women (CTRL), and seven postnatal women who had chosen to bottle-feed their infants (BOTTLE). Maternal age, infant age and body mass index (BMI) were similar between all three groups. We performed overnight polysomnography utilizing the Portable Compumedics P-series. The total sleep time (TST) and rapid eye movement (REM) sleep time were similar in the three groups of women. However, B/F women demonstrated a marked increase in slow wave sleep (SWS), 182 +/- 41 min compared with CTRL (86 +/- 22 min, P < 0.001 compared with B/F) and BOTTLE subjects (63 +/- 29 min, P < 0.001 compared with B/F). There was a compensatory reduction in light non-rapid eye movement (NREM) sleep in B/F when compared with CTRL and BOTTLE. The most likely explanation for the altered sleep architecture noted to occur in women who are fully breastfeeding their infants is an increase in circulating PRL, which occurs in lactating women. Enhanced SWS may be another important factor to support breastfeeding in the postnatal period.

Sleep disordered breathing and pregnancy.

Many changes in the respiratory system occur during pregnancy, particularly during the third trimester, which can alter respiratory function during sleep, increasing the incidence and severity of sleep disordered breathing. These changes include increased ventilatory drive and metabolic rate, reduced functional residual capacity and residual volume, increased alveolar-arterial oxygen gradients, and changes in upper airway patency. The clinical importance of these changes is indicated by the increased incidence of snoring during pregnancy, which is likely also to reflect an increased incidence of obstructive sleep apnoea/hypopnoea syndrome. For the respiratory physician asked to review a pregnant patient, the possibility of sleep disordered breathing should always be considered. This review first examines the normal physiological changes of pregnancy and their relationship to sleep disordered breathing, and then summarises the current knowledge of sleep disordered breathing in pregnancy.

Relationship between craniofacial abnormalities and sleep-disordered breathing in Marfan's syndrome.

OBJECTIVES: To examine the prevalence and nature of craniofacial abnormalities in patients with Marfan's syndrome and to investigate the relationship between craniofacial abnormalities and obstructive sleep apnea (OSA) severity in these patients. DESIGN: Cross-sectional. SETTING: Marfan's syndrome clinic in a tertiary teaching hospital. PATIENTS: Fifteen consecutive adult patients (7 men and 8 women; mean [+/- SD] age, 34.8 +/- 13.2 years) who had Marfan's syndrome. MEASUREMENTS AND RESULTS: Apneic status was determined from standard overnight polysomnography testing. Measurements from standardized lateral cephalometric radiographs were compared to normative data. Thirteen patients had OSA, which was defined as an apnea/hypopnea index (AHI) of > 5 episodes per hour (mean AHI, 22 +/- 15 episodes per hour). A high prevalence of craniofacial abnormalities was found with significant gender differences for some of the variables. Significant abnormalities for the entire group were bimaxillary retrusion, a reduced maxillary length, an increased total anterior face height, a long lower anterior face height, an obtuse gonial angle, a steep mandibular plane, a reduced posterior nasal airway height, a reduced posterior airway space, and an increased distance from the mandibular plane to the hyoid bone. Univariate analysis revealed significant correlations among the total anterior face height, the upper anterior and posterior face heights, the mandibular length, and AHI. There was a significant correlation between the rank of the number of cephalometric abnormalities per patient and AHI in those patients with OSA. CONCLUSIONS: Craniofacial abnormalities are common in patients with Marfan's syndrome. The relationship between some cephalometric parameters and apnea severity suggests a potential role of craniofacial structure in the pathogenesis of OSA in these patients.

Hemodynamic responses to obstructive respiratory events during sleep are augmented in women with preeclampsia.

Preeclampsia is the most common disease of pregnancy, occurring in up to 10% of the pregnant population. The cause of the disease is as yet undetermined; however, most of the clinical effects are commonly attributed to damage to the endothelial layer, leading to increased pressor activity of all the maternal blood vessels. Therefore, we suspected that if obstructive sleep apnea (OSA) coexisted with preeclampsia in pregnancy, the hemodynamic effects of the OSA would be markedly potentiated. To test this hypothesis, we performed full sleep studies and overnight beat-to-beat blood pressure (BP) monitoring. The control patient group included 10 pregnant women with OSA and no evidence of hypertensive disease either before or during their current pregnancy. The test group included 10 women with preeclampsia and coexisting OSA. The pressor responses to obstructive respiratory events during sleep were enhanced in preeclamptic patients compared with control OSA patients (21+/-2/12+/-1 mm Hg and 38+/-5/25+/-4 mm Hg above baseline in control OSA and preeclamptic OSA patients, respectively, P = .005/.005). In contrast, there was no difference in heart rate responses between the two groups of subjects (34+/-5 beats/min and 49+/-13 beats/min above baseline in control and preeclamptic patient groups, respectively, P = .326). We suggest that the augmented pressor responses in preeclamptic women occur as a result of maternal endothelial damage induced by the preeclampsia disease process. These findings may have important implications in the management of preeclamptic patients.

Predicting sleep-disordered breathing in patients with cystic fibrosis.

STUDY OBJECTIVES: To examine predictors of sleep-disordered breathing in patients with cystic fibrosis (CF) and moderate-to-severe lung disease using a comprehensive evaluation of both sleep and daytime function. DESIGN: Cross-sectional analysis of sleep studies, lung function, respiratory muscle strength, and evening and morning arterial blood gas measurements in patients with stable CF. A questionnaire addressing sleep quality was administered. Forward stepwise regression analysis was used to identify the parameters that best predict sleep-related desaturation, hypercapnia, and respiratory disturbance. SETTING: Sleep investigation unit and lung function laboratory. PATIENTS: Thirty-two patients with CF and FEV(1) < 65% predicted, in stable clinical condition. Patients were aged 27 +/- 8 years (mean +/- 1 SD) with FEV(1) of 36 +/- 10% predicted, evening PaO(2) of 68 +/- 8 mm Hg, and PaCO(2) of 43 +/- 5 mm Hg. RESULTS: Evening PaO(2) (p < 0.0001) and morning PaCO(2) (p < 0.01) were predictive of the average minimum oxyhemoglobin saturation per 30-s epoch of sleep (r(2) = 0.74; p < 0.0001). Evening PaO(2) (p < 0.001) was predictive of the rise in transcutaneous carbon dioxide (TcCO(2)) seen from non-rapid eye movement (NREM) to rapid eye movement (REM) sleep (r(2) = 0.37; p < 0.001). In addition, there was some relationship between expiratory respiratory muscle strength and the REM respiratory disturbance index (r(2) = 0.22; p < 0.01). CONCLUSION: Evening PaO(2) was found to contribute significantly to the ability to predict both sleep-related desaturation and the rise in TcCO(2) from NREM sleep to REM sleep in this subgroup of patients with CF.

Noninvasive pressure preset ventilation for the treatment of Cheyne-Stokes respiration during sleep.

Cheyne-Stokes respiration (CSR) during sleep is common in patients with congestive heart failure (CHF). This pattern of breathing fragments sleep, leading to daytime symptoms of sleepiness and fatigue. It was hypothesized that by controlling CSR with noninvasive pressure preset ventilation (NPPV), there would be a decrease in sleep fragmentation and an improvement in sleep quality. Nine patients (eight males, one female; mean +/- SD 65 +/- 11 yrs) with symptomatic CSR diagnosed on overnight polysomnography (apnoea/hypopnoea index (AHI) 49 +/- 10 x h(-1), minimum arterial oxygen saturation (Sa,O2, 77 +/- 7%) and CHF (left ventricular ejection fraction 25 +/- 8%) were studied. After a period of acclimatization to NPPV (variable positive airway pressure (VPAP) II ST, Sydney, NSW, Australia and bilevel positive airway pressure (BiPAP), Murraysville, PA, USA), sleep studies were repeated on therapy. NPPV almost completely abolished CSR in all patients with a reduction in AHI from 49 +/- 10 to 6 +/- 5 x h(-1) (p<0.001). Residual respiratory events were primarily due to upper airway obstruction at sleep on-set. Arousal index was markedly decreased from 42 +/- 6 to 17 +/- 7 x h(-1) (p <0.001). Sleep architecture showed a trend toward improvement with a reduction in stage 1 and 2 (79 +/- 7% during the diagnostic night versus 72 +/- 10% during NPPV, (p=0.057)), whilst sleep efficiency, slow-wave sleep (SWS), and rapid eye movement (REM) were not altered. Controlling Cheyne-Stokes respiration with noninvasive pressure preset ventilation resulted in reduced arousal and improved sleep quality in the patients with congestive heart failure. Noninvasive pressure preset ventilation should be considered a potential therapy for Cheyne-Stokes respiration in congestive heart failure in those patients who do not respond or fail to tolerate nasal continuous positive airway pressure therapy.

Cardiovascular responses to three simple, provocative tests of autonomic activity in sleeping infants.

Whereas defective cardiovascular autonomic control has been implicated in the sudden infant death syndrome, relatively little is known about the normal development of autonomic control, due to the inability to measure blood pressure in infants noninvasively. We studied 12 normal infants [age: 13 +/- 2 (SD) wk] using a noninvasive method of continuous blood pressure recording and examined the cardiovascular responses to 45 degrees head-up tilting, a modified cold face test, and a loud noise. In head-up tilting, in both slow-wave sleep and rapid eye movement sleep, all infants displayed a rapid biphasic heart rate response (mean increase of 16% and mean decrease of 21%) and blood pressure response (mean increase of 16% and mean decrease of 16%), with a return to pretest values within 20 s. Both ice and noise caused a less pronounced biphasic response. In conclusion, at 3 mo, infants show the adult pattern of response to postural challenge. The short latency of the response suggests that neural inputs, apart from baroreceptors, are involved in the initial phase of the response.

Low-flow oxygen and bilevel ventilatory support: effects on ventilation during sleep in cystic fibrosis.

We measured ventilation in all sleep stages in patients with cystic fibrosis (CF) and moderate to severe lung disease, and compared the effects of low-flow oxygen (LFO2) and bilevel ventilatory support (BVS) on ventilation and gas exchange during sleep. Thirteen subjects, age 26 +/- 5.9 yr (mean +/- 1 SD), body mass index (BMI) 20 +/- 3 kg/m2, FEV1 32 +/- 11% predicted, underwent three sleep studies breathing, in random order, room air (RA), LFO2, and BVS +/- O2 with recording of oxyhemoglobin saturation (SpO2) (%) and transcutaneous carbon dioxide (TcCO2) (mm Hg). During RA and LFO2 studies, patients wore a nasal mask with a baseline continuous positive airway pressure (CPAP) of 4 to 5 cm H2O. Minute ventilation (V I) was measured using a pneumotachograph in the circuit and was not different between wake and non-rapid eye movement (NREM) sleep on any night. However, V I was reduced on the RA and LFO2 nights from awake to rapid eye movement (REM) (p < 0.01) and from NREM to REM (p < 0.01). On the BVS night there was no significant difference in V I between NREM and REM sleep. Both BVS and LFO2 improved nocturnal SpO2, especially during REM sleep (p < 0.05). The rise in TcCO2 seen with REM sleep with both RA and LFO2 was attenuated with BVS (p < 0.05). We conclude that BVS leads to improvements in alveolar ventilation during sleep in this patient group.

Pre-eclampsia is associated with marked alterations in sleep architecture.

STUDY OBJECTIVES: Pre-eclampsia is currently the predominant cause of maternal and fetal morbidity and mortality. Diurnal blood pressure variation is flattened or reversed in pre-eclampsia; however, sleep has not been extensively investigated in this disease. Our objective was therefore to study sleep architecture in this group of patients. STUDY DESIGN: Full polysomnography using the Compumedics Sleepwatch System or Compumedics p-series. SETTING: NA. PATIENTS: 25 pre-eclamptic patients and 17 primigravidas with normal pregnancies and no history of cardiovascular disease or sleep disorder. With the exception of one subject, all pre-eclamptics were taking clonidine (a known suppressant of rapid eye movement-REM-sleep) for control of their hypertension. INTERVENTIONS: NA. RESULTS: Pre-eclamptic subjects had markedly altered sleep architecture, with a markedly increased percentage of time spent in slow-wave sleep (SWS) (21 * 2% versus 43 * 3%, p<0.001). There was a longer latency to rapid eye movement (REM) sleep (92 * 11 mins vs. 205 * 23 mins in control and pre-eclamptic subjects, respectively, p<0.001) and reduced time spent in REM (18 * 1% and 10 * 2% in control and pre-eclamptic subjects, respectively, p<0.001). CONCLUSIONS: While the increased REM latency and decreased REM time are most likely due to clonidine, this is unlikely to also account for the increased SWS. Two possible explanations for this include cerebral edema and release of cytokines, which are known to alter sleep structure.

Nasal continuous positive airway pressure reduces sleep-induced blood pressure increments in preeclampsia.

Preeclampsia is the predominant cause of admissions to neonatal intensive care. The diurnal blood pressure pattern is flattened or reversed in preeclampsia. We hypothesized that snoring and partial upper airway obstruction contribute to nocturnal rises in blood pressure. We tested this hypothesis by controlling sleep- induced upper airway flow limitation and snoring with nasal positive pressure. Eleven women with preeclampsia underwent two consecutive polygraphic sleep studies with simultaneous beat-to-beat blood pressure monitoring. Average blood pressure for the night overall and in each sleep stage was calculated. Sleep architecture was similar on the two study nights. Sleep-induced partial upper airway flow limitation occurred in all patients in the initial study. Autosetting nasal continuous positive airway pressure (CPAP) applied at a mean maximal pressure of 6 +/- 1 cm H(2)O eliminated flow limitation throughout sleep on the treatment night. Blood pressure was markedly reduced on the treatment night [(128 +/- 3)/(73 +/- 3)] when compared with the initial nontreatment study night [(146 +/- 6)/(92 +/- 4)], p = (0.007)/(0.002). We conclude that partial upper airway obstruction during sleep in women with preeclampsia is associated with increments in blood pressure, which can be eliminated with the use of nasal CPAP.

Treatment of obstructive sleep apnea syndrome in children.

Obstructive sleep apnea (OSA) has been identified and recorded in paediatric patients, the potential mechanisms for OSA include anatomical abnormalities that lead to a narrowed airway space, reduced muscle tone and abnormal central ventilatory control. Several treatments have been developed and are routinely used to treat OSA in infants and children. Nasal mask continuous positive airway pressure (CPAP) is an effective non-invasive treatment that prevents the majority of obstructive events, reverses sleep disturbances, improves daytime performance and is associated with increased growth in patients with failure to thrive. Surgery to correct underlying anatomical abnormalities is frequently used and usually results in an improvement in symptoms and in some cases, it is curative. Other forms of treatment include pharmacological interventions, positioning and nasopharyngeal intubation.

Influence of maxillary morphology on nasal airway resistance in Marfan's syndrome.

High nasal airway resistance (NAR) has been reported in Marfan's syndrome, and this appears to contribute to the development of obstructive sleep apnoea in these patients. The cause of high NAR in Marfan's syndrome is unknown, but these patients characteristically have a narrow maxilla, which could have an influence on nasal dimensions. The aim of this study was to define the mechanism(s) mediating high NAR in Marfan's syndrome. Five patients with Marfan's syndrome (mean age 29+/-4 (SEM) years) were compared with an equivalent number of normal control subjects (31+/-1 years). NAR was measured by posterior rhinomanometry, before and after topical decongestant, nasal stenting, or both. Dental impressions were taken to evaluate maxillary arch morphology, allowing measurement of the following lateral distances: inter-canine (ICD), inter-premolar (IPD), and inter-molar (IMD). NAR (at a flow of 500 ccm/s) was considerably higher in patients compared with controls at baseline (0.93+/-0.08 vs 0.35+/-0.08 Pa/ccm/s, p < 0.001), and following decongestant and/or stenting. The maxillary arch was considerably narrower in patients. There were strong inverse correlations between the lateral maxillary dimensions and NAR after nasal decongestant, with or without stenting. These results indicate a strong association between maxillary width and NAR, and suggest that maxillary constriction is the dominant mechanism for the high NAR in Marfan's syndrome. The therapeutic implications of this finding warrant further investigation.

Obstructive sleep apnea in infants: relation to family history of sudden infant death syndrome, apparent life-threatening events, and obstructive sleep apnea.

OBJECTIVES: Familial aggregation of obstructive sleep apnea (OSA) has been shown to be associated with sudden infant death syndrome (SIDS) and apparent life-threatening events (ALTE) in infants. We wanted to determine the incidence of OSA in infants with siblings with ALTE and SIDS referred to our sleep clinic and to ascertain whether OSA was more common in infants who have family histories of SIDS, ALTE, and OSA. STUDY DESIGN: We studied 125 infants (mean age, 11.5 +/- 0.6 weeks) who were separated into 2 groups on the basis of their family history; polysomnographic studies were performed on each infant. RESULTS: Twenty infants had a multiple family history of SIDS, ALTE, or OSA (group 1), whereas the other 105 infants (group 2) had only one case of SIDS or ALTE within the family and no known history of OSA. We found that 19 of 20 infants in group 1 had OSA, whereas only 31 of 105 infants in group 2 had OSA (chi-squared analysis, P <.05). The OSA recorded was more frequent in infants of group 1 than in those of group 2. Follow-up studies in some infants with OSA demonstrated a progressive decrease in OSA, which resolved between 6 and 12 months of age. CONCLUSION: We conclude that infants of families with multiple histories of SIDS, ALTE, and OSA are more likely to have OSA than infants of families with only one case of SIDS or ALTE.