Sudden Infant Death Syndrome Siblings Research Articles

Sleep disordered breathing in SIDS siblings and infants with Apparent Life Threatening Event

Sleep disordered breathing in SIDS siblings and infants with Apparent Life Threatening Event

Jerold Francis Lucey, MD (1926-2017)

We note with sadness the death of Jerry Lucey, a friend, mentor, and colleague. His name is familiar to all pediatricians though his life work and contributions as an outstanding clinician, neonatologist, investigator, advocate, educator, and editor. Dr Lucey was an internationally renowned neonatologist at the University of Vermont College of Medicine since 1956. He made numerous contributions to the care of premature infants, specifically advances in phototherapy and oxygen monitoring, and the promotion of randomized trials among neonatal units. He was the recipient of numerous awards in recognition of his outstanding qualities of scholarship and advocacy on behalf of children. In his role as the Editor of Pediatrics, Dr Lucey established policies and standards that have served to guide us all. His vision of having Pediatrics embrace the global medical community led to the establishment in that journal of a strong international science and clinical practice presence. Of specific note was his commitment to the highest ethical standards in research and publication. This is perhaps best exemplified by his response to an article published in Pediatrics in 1972, which had linked sudden infant death syndrome (SIDS) and breathing abnormalities.1Steinschneider A. Prolonged apnea and sudden infant death syndrome: clinical and laboratory observations.Pediatrics. 1972; 50: 646-654PubMed Google Scholar Several children from one family with apparent SIDS served as the basis for this study; they were later shown to be victims of medical child abuse. The published hypothesis of a genetic predisposition to SIDS, as well as a causal association between SIDS and infantile apnea, led to the use of home cardiorespiratory monitors to prevent SIDS. This widely cited report triggered not only parental anxiety but countess hours of fruitless investigation into the relationship between apnea and SIDS.2Consensus Statement National Institutes of Health Consensus Development Conference on infantile apnea and home monitoring, September 29, 1986–October l, 1986.Pediatrics. 1987; 79: 292-300PubMed Google Scholar, 3Firstman R. Talen J. The death of innocents. Bantam Books, New York (NY)1997Google Scholar, 4Duffy P. Bryan M.H. Home apnea monitoring in “near miss” sudden infant death syndrome (SIDS) and siblings of SIDS victims.Pediatrics. 1982; 70: 69-74PubMed Google Scholar Despite the fact that this article was accepted before Dr Lucey's tenue as editor, he addressed the issue head on, apologized for the mistake, and stated that the article was flawed and should never have been published.5Lucey J.F. A very important erratum? — 20 years later.Pediatrics. 1994; 93: 944Google Scholar Dr Lucey's dedication to the highest ethical standards is an enduring legacy. In 1990, he joined the editors of several general pediatric journals to express concern about ethical transgressions—such as the duplication of data in papers submitted to several journals (self-plagiarism) and the practice of dividing a study into several short reports (the “least publishable unit”)—in a constructive effort to maintain the quality of the pediatric literature.6Bier D.M. Fulginiti V.A. Garfunkel J.M. Lucey J.M. Spranger J. Valman B. et al.Duplicate publication and related problems.J Pediatr. 1990; 117: 903Abstract Full Text PDF Scopus (4) Google Scholar In 2009, Dr Lucey and the editors of the major US general pediatric journals met at the annual Pediatric Academic Societies meeting to initiate a workshop entitled “Ethics in Publishing”; this on-going workshop remains important and highly relevant today. Dr Lucey will be missed by all who have benefited from his contributions—his patients, his students, as well as pediatricians worldwide.

Algorithms for sleep–wake identification using actigraphy: a comparative study and new results

The aim of this study was to investigate two new scoring algorithms employing artificial neural networks and decision trees for distinguishing sleep and wake states in infants using actigraphy and to validate and compare the performance of the proposed algorithms with known actigraphy scoring algorithms. The study employed previously recorded longitudinal physiological infant data set from the Collaborative Home Infant Monitoring Evaluation (CHIME) study conducted between 1994 and 1998 [http://dccwww.bumc.bu.edu/ChimeNisp/Main_Chime.asp; Sleep26 (1997) 553] at five clinical sites around the USA. The original CHIME data set contains recordings of 1079 infants <1 year old. In our study, we used the overnight polysomnography scored data and ankle actimeter (Alice 3) raw data for 354 infants from this data set. The participants were heterogeneous and grouped into four categories: healthy term, preterm, siblings of SIDS and infants with apparent life-threatening events (apnea of infancy). The selection of the most discriminant actigraphy features was carried out using Fisher's discriminant analysis. Approximately 80% of all the epochs were used to train the artificial neural network and decision tree models. The models were then validated on the remaining 20% of the epochs. The use of artificial neural networks and decision trees was able to capture potentially nonlinear classification characteristics, when compared to the previously reported linear combination methods and hence showed improved performance. The quality of sleep-wake scoring was further improved by including more wake epochs in the training phase and by employing rescoring rules to remove artifacts. The large size of the database (approximately 337,000 epochs for 354 patients) provided a solid basis for determining the efficacy of actigraphy in sleep scoring. The study also suggested that artificial neural networks and decision trees could be much more routinely utilized in the context of clinical sleep search.

Cry features in siblings of SIDS

To examine the acoustic features of crying demonstrated by infants whose older sibling died of sudden infant death syndrome (SIDS) and compare these features to a nonrisk group of infants. Pain-induced crying episodes were collected from a group of healthy term (HT) infants and siblings of SIDS infants. One complete crying episode was obtained from each infant and analyzed acoustically with regard to durational and spectral features. The cries of SIDS siblings were found to be significantly higher in pitch and reflected hyperadductory vocal fold vibratory behaviour compared to the HT group. There were no group differences with regard to durational features of crying. The laryngeal behaviour of infant crying, as inferred via acoustic analyses, differs between HT infants and siblings of SIDS infants. Accordingly, acoustic features of infant crying may serve as an additional diagnostic marker in the identification of children who may be at risk for SIDS.

Are substitutions in the first hypervariable region of the mitochondrial DNA displacement-loop in sudden infant death syndrome due to maternal inheritance?

To investigate whether all substitutions in the first hypervariable region (HVR1) in sudden infant death syndrome (SIDS) can be recovered along the maternal line of the family (inherited), or whether SIDS victims have new substitutions compared to maternal relatives (somatic mutations) that may be related to environmental factors. Seventy-one SIDS/mother pairs, including 11 families with SIDS, mother and mother's relatives and/or SIDS siblings, were studied. The HVR1 sequence was recorded in the base-pair range 16056-16400. The recorded HVR1 sequence was compared with the Cambridge sequence, and differences were recorded as substitutions. The substitution pattern in the SIDS victims was compared with the pattern found in family members along the maternal line. All the substitutions found in SIDS victims could be traced in the maternal line of the family; in 5 cases this was observed through three generations, and in 3 cases through four generations. In patients with known mitochondrial (mt) DNA disease, a large number of sequence variants have been found in the D-loop region. Substitutions in the D-loop may be part of a haplotype with mutations elsewhere in the mtDNA. HVR1 substitutions in SIDS victims are hereditary and not due to somatic mutations.

Are substitutions in the first hypervariable region of the mitochondrial DNA displacement‐loop in sudden infant death syndrome due to maternal inheritance?

Aim: To investigate whether all substitutions in the first hypervariable region (HVR1) in sudden infant death syndrome (SIDS) can be recovered along the maternal line of the family (inherited), or whether SIDS victims have new substitutions compared to maternal relatives (somatic mutations) that may be related to environmental factors. Methods: Seventy‐one SIDS/mother pairs, including 11 families with SIDS, mother and mother's relatives and/or SIDS siblings, were studied. The HVR1 sequence was recorded in the base‐pair range 16056‐16400. The recorded HVR1 sequence was compared with the Cambridge sequence, and differences were recorded as substitutions. The substitution pattern in the SIDS victims was compared with the pattern found in family members along the maternal line. Results: All the substitutions found in SIDS victims could be traced in the maternal line of the family; in 5 cases this was observed through three generations, and in 3 cases through four generations. Discussion: In patients with known mitochondrial (mt) DNA disease, a large number of sequence variants have been found in the D‐loop region. Substitutions in the D‐loop may be part of a haplotype with mutations elsewhere in the mtDNA. Conclusion: HVR1 substitutions in SIDS victims are hereditary and not due to somatic mutations.

Effect of home monitoring on a high-risk population.

A large cohort of infants (8,998) at high risk for sudden and unexpected death was followed with home cardiorespiratory monitoring over a five-year period. These infants included premature infants (23-36 weeks post-conceptual age), SIDS siblings, and infants who experienced an Apparent Life-Threatening Event. The overall SIDS rate in this high-risk population was 0.55/1,000, a rate significantly less than the 0.85 deaths/1,000 reported in the "general population" of Georgia over this same time period. In addition, we report our experience with using home monitors as a diagnostic tool, as well as how monitors can actually be cost-effective. Editorial opinions, and lay press summaries of the CHIME study (JAMA, May 2, 2001) imply that home cardiorespirtory monitors are of little value. Despite the fact that the study never made this claim, many clinicians are now referring to this study as evidence that home monitoring is ineffective and not needed. This article disputes those misconceptions about home cardiorespiratory monitors based on our experience with a large high-risk population of infants.

Low melatonin production in infants with a life‐threatening event

This study compares the urinary excretion of the main melatonin metabolite, 6‐sulfatoxymelatonin (6SMT), in infants who have and have not experienced a life‐threatening event (ALTE). 6SMT was assessed in the following groups of infants: 15 infants with ALTE for whom home monitoring had been recommended, 15 infants who had had an abrupt cyanotic apneic event but did not require mouth‐to‐mouth resuscitation, 15 siblings of those who had died from sudden infant death syndrome (SIDS), and 35 age‐matched healthy comparison infants. All 80 infants were between 48 and 58 weeks of postconceptional age. On a double‐blind basis, the total amount of 6SMT excreted over 24 hours and the diurnal rhythm in the rate of 6SMT excretion were assessed using urine samples taken from disposable diapers (nappies). The mean daily excretion of 6SMT was significantly lower in the ALTE (1588ng/24 hour) than in the comparison infants (3961 ng/24 hour). No such difference was found between the infants with a cyanotic apneic event (3268 ng/24 hour) and the SIDS siblings (2962 ng/24 hour). The diurnal 6SMT rhythms in the ALTE infants were characterized by lower 24‐hour mean and amplitude values, whereas the time of peak and nadir excretion rates (07:15 to 08:45 hours and 14:45 to 16:15 hours respectively) was similar in all four infant groups. Follow‐up of the ALTE infants, performed 6 to 8 weeks later (59 to 66 weeks of postconceptional age), revealed that 6SMT excretion increased in all of them, suggesting a delayed ontogeny rather than permanent deficiency of melatonin production in ALTE.

The implications of a relationship between prolonged QT interval and the sudden infant death syndrome.

* Abbreviations: SIDS = : sudden infant death syndrome • ECG = : electrocardiogram • LQTS = : long QT syndrome We read with interest the article on the proposed association of prolonged QT interval and the sudden infant death syndrome (SIDS) by Schwartz et al.1 Recognizing the previous failures to determine cause(s) for SIDS and the risks of changing practice in response to one study, we wish to take this opportunity to place the findings of the study in perspective and reflect on directions that might be pursued. Although the mechanism for SIDS (the most common cause of death from 1 month to 1 year of age) remains unknown, certain factors, such as smoking during pregnancy and sleep position of the infant lter the risk of SIDS.2–7 The hypothesis that there is a relationship between SIDS and prolonged QT has been previously raised by Schwartz8 and other authors,9–12 and disputed by some,13–15 but the recent data by Schwartz et al1 are the most compelling to date. Schwartz et al obtained electrocardiogram (ECG) recordings 3 to 4 days after birth in 34 443 newborn infants, 24 of whom died within the first year after birth with a diagnosis of SIDS. The authors found that these 24 infants had an average QT interval (corrected for heart rate) that was longer than in 9725 randomly selected living infants and longer than in 10 infants who died of other causes. Accordingly, this report raises several important questions. What is the cause of the long QT interval in the infants? Schwartz et al1 suggest that the prolonged QT might be caused by: a) different rates of development of the right and left sympathetic nerves rendering the infant susceptible to an arrhythmia during sudden increases in sympathetic activity8 ,16 ,17; or b) mutation in one of the genes encoding sodium or potassium channels, as has been identified … Address correspondence to George Lister, MD, Department of Pediatrics, Yale University School of Medicine, 333 Cedar St, PO Box 208064, New Haven, CT 06520-8064.

Maternal smoking, birthweight and gestational age in sudden infant death syndrome (SIDS) babies and their surviving siblings.

To evaluate the effect of maternal smoking on intrauterine growth of babies who died of sudden infant death syndrome (SIDS), birthweights of SIDS infants and their surviving siblings were compared with birthweights of infants in sibships were all infants survived the first year of life. We studied 184,349 mothers with at least two births registered in the population-based Swedish Medical Birth Registry during 1983-91. The mother being the unit of analysis, birthweight and gestational age of her infants were the repeated measures used in a repeated measures analysis of variance. Mothers whose first two infants survived at least 1 year, smoked less than mothers of SIDS infants, 25 and 41% (P < 0.01). Overall, SIDS mothers did not smoke more while pregnant with the SIDS infant than while pregnant with the surviving sibling. SIDS siblings weighted, on average, 90 g less than infants in non-affected sibships. SIDS babies were even lighter, 193 g, and had 3.8 days shorter mean gestational age, compared with same birth-order babies in non-affected sibships. After adjustment for gestational age, the birthweight difference changed only slightly for SIDS siblings, while the difference for SIDS infants was reduced from 193 to 110 g. Further adjustment for smoking reduced the birthweight difference for SIDS siblings, from 74 to 50 g, and SIDS infants, from 110 to 82 g. Intrauterine growth retardation of sibships with a SIDS baby is explained only partly by maternal smoking. The even lower birthweight of the SIDS baby, resulting from shorter gestational age, cannot be explained by smoking, suggesting pregnancy factors specific to the SIDS baby and not to its siblings.

Fetal Growth Retardation in Sudden Infant Death Syndrome (SIDS) Babies and Their Siblings

To evaluate the intrauterine growth potential of infants that die from sudden infant death syndrome (SIDS), the authors compared SIDS infants with their surviving siblings. The SIDS sibships themselves were also compared with sibships where all infants survived. Data from the population-based Medical Birth Registry of Norway, with 1.3 million births during 1967-1988, were used. From the birth cohorts, 1,984 SIDS cases were identified. All births were linked into sibships. The mean birth weight and gestational age were calculated across sibships of different sizes for first to fourth birth order. In a further analysis, birth weights were standardized to adjust for gestational age. Mothers of SIDS infants give birth to smaller babies in general. SIDS infants weighed, on average, 85 g less at birth than their siblings and 164 g less compared with babies in nonaffected sibships. When birth weights were standardized for gestational age, most of the weight difference between SIDS infants and siblings was due to a shorter gestational age of SIDS infants, while the difference between surviving siblings of SIDS infants and births from nonaffected sibships remained. All births in sibships with a SIDS infant were intrauterine growth retarded. This may reflect factors that contribute to SIDS risk (such as maternal smoking). The factors that contribute to shorter gestational age and further slowing of growth in the SIDS infants may specifically influence the SIDS infant and not its siblings.

Aberrant temporal patterning of slow-wave sleep in siblings of SIDS victims

We assessed the patterning of slow-wave EEG activity during sleep in siblings of sudden infant death syndrome (SIDS) victims over the first 6 months of life. Twelve hour overnight physiologic recordings were obtained from 25 apparently healthy subsequent siblings of SIDS victims and 25 control infants at 1 week, and 1, 2, 3, 4 and 6 months of age. The EEG activity was electronically bandpass filtered, leaving primarily activity ranging from 0.5 to 2.5 Hz (the delta frequency), and the filtered traces were full-wave rectified and integrated over 1 min periods. The recordings were divided into four 3 h segments beginning at sleep onset, and the mean integrated delta activity during quiet sleep was determined for each segment of the night. At 3 and 4 months postnatal age, SIDS siblings displayed increased integrated delta amplitude in the early morning hours relative to control infants. Most SIDS deaths occur in the early morning hours during the 2–4 month age range. We thus speculate that increased delta activity may be indicative of increased arousal thresholds in the early morning, which may contribute to SIDS deaths.

The ventilatory response to carbon dioxide in high risk infants

Purpose: To examine the ventilatory response to inspired carbon dioxide in infants considered to be at risk for sudden infant death syndrome or apnea. Design: Clinical data measurement. Setting: Infant apnea evaluation program of a university division of neonatology. Patients: Fifty nine infants were full term characterized by the following diagnoses; siblings of infants who had died from sudden infant death syndrome (SIDS) ( n = 7), apparent life threatening event (ALTE) ( n = 24), apnea/cyanosis in the newborn nursery ( n = 21), and controls [7]. Sixty-nine infants were preterm and consisted of patients suffering from idiopathic apnea ( n = 61), and bronchopulmonary dysplasia ( n = 8). Measurements: The ventilatory response to carbon dioxide was measured with a computerized waveform analyzer. Main results: Among full term infants no significant differences in the ventilatory slope in response to CO 2 was seen. The range of mean slope was 19.4 ± 7.6 in siblings of SIDS and 36 ± 17 in control infants. Greater number of sibling of SIDS had slopes less than 20 ml/kg/min/mmHg in comparison to control infants. Sibling of SIDS had less increase in minute ventilation and inspiratory flow in response to CO 2 administration in comparison to control infants. Preterm infants had similar slopes with a mean of 33 ml/kg/min/mmHg in infants with idiopathic apnea and 28 ml/kg/min/mmHg in infants with bronchopulmonary dysplasia. Conclusions: The large intragroup variability in the ventilatory response to inspired CO 2, confirming previously reported data, compromises the benefit of this test. Thus, ventilatory response to CO 2 administration is not useful in unselected patients at risk of SIDS or apnea.

Breathing, transcutaneous blood gases, and CO2 response in SIDS siblings and control infants during sleep.

Age-related changes of 20 variables describing breathing patterns, transcutaneous blood gases, and estimated CO2 response during sleep were examined in a cross-sectional study of 30 healthy control infants and 150 healthy siblings of sudden infant death syndrome victims within the first 18 mo of life. Whole-night measurements were performed using noninvasive respiratory induction plethysmography and transcutaneous blood gas electrodes. Each candidate for the study was extensively screened and found to be healthy. Mean transcutaneous PCO2 (PtcCO2, median 40.3 Torr) and maximum PtcCO2 (median 44.8 Torr), as well as the estimated ventilatory response to inhalation of 2% CO2 in air during regular breathing, causing a 20-36% increase of ventilation per Torr PtcCO2, were not related to postnatal age. In contrast, paradoxical breathing decreased from 49.5 to 0% of total sleep time (TST), periodic breathing from 5.5 to 0% TST, and respiratory rate during regular breathing from 40 to 22 breaths/min; the portion of regular breathing increased from 32 to 55% TST and mean and minimum transcutaneous PO2 from 65.4 and 47 to 69.7 and 52 Torr with increasing stability. The largest changes occurred in the first 6 mo of life. Maximum apnea duration (9.5 s, maximum 16 s), mean apnea duration (3.74 s, breathing pauses > or = 2 s), and time spent apneic per hour of irregular breathing (199 s/h) were not related to age. The comparison of data from siblings and controls showed similarities in the above-mentioned variables. No significant differences were found among the groups. Also a comparison of 30 pairs of siblings and controls, matched for age, gender, birth, and actual body weight, did not show significant differences. The present study extends the knowledge of development of breathing control beyond the first 6 mo of life.

Hypercapnic and hypoxic ventilatory and cardiac responses in school-aged siblings of sudden infant death syndrome victims

Siblings of sudden infant death syndrome (SIDS) victims have been shown to have abnormal ventilatory patterns and altered responses to respiratory stimuli during infancy. To evaluate whether these abnormalities persist, we studied ventilatory responses in 20 older SIDS siblings (9.8 +/- 0.9 (mean +/- SEM) years of age) and 20 control subjects (10.2 +/- 0.9 years of age). To evaluate hypercapnic ventilatory responses, we had subjects rebreathe 5% carbon dioxide and 95% oxygen until end-tidal carbon dioxide tension reached 65 mm Hg. Instantaneous minute ventilation, mean inspiratory flow, and respiratory rate were calculated breath by breath. Hypercapnic responses did not differ between SIDS siblings (2.08 +/- 0.14 L/min per mm Hg) and control subjects (1.90 +/- 0.10 L/min per mm Hg; not significant). To assess hypoxic ventilatory responses, we asked subjects to rebreathe 13% oxygen and 7% carbon dioxide, with the balance nitrogen, at mixed-venous end-tidal carbon dioxide tension, until arterial oxygen saturation by pulse oximetry fell to 75%. No differences in hypoxic ventilatory responses were found between the SIDS siblings (-1.39 +/- 0.15 L/min/% saturation) and the control subjects (-1.22 +/- 0.17 L/min/% saturation; not significant). The mean inspiratory flow, tidal volume, respiratory rate, and heart rate responses to hypercapnia and hypoxia were also similar in the two groups. We conclude that there is no difference in hypercapnic and hypoxic ventilatory and cardiac responses, as assessed by rebreathing techniques, between school-aged SIDS siblings and control subjects. We speculate that in SIDS siblings the control of breathing is immature during infancy and that they achieve maturity of control and resolution of breathing abnormalities with time.

Parental Reports of Apnea and Bradycardia: Temporal Characteristics and Accuracy

A prospective examination was made of the temporal course of parental observations in response to a monitor alarm of apnea (apnea setting of 20 seconds) or bradycardia (bradycardia setting of 80 beats per minute). Data were obtained from 155 subsequent sudden infant death syndrome siblings followed up at home, during the first 20 weeks of life, on an apnea/bradycardia monitor with an attached event recorder. In addition, parental reports were compared to an objective recording of the pattern of cardiorespiratory activity surrounding each monitor alarm. Only those parental observations were considered which reported the infant to be asleep with no apparent equipment malfunction following an apnea alarm (with or without pallor, cyanosis, or the provision of external stimulation) or a low heart rate alarm associated with pallor, cyanosis, or stimulation. Observations were analyzed within each of five age periods (less than 29, 29 through 56, 57 through 84, 85 through 112, 113 through 140 days). The percentage of infants reported to have prolonged apnea, prolonged apnea with stimulation, or bradycardia with stimulation was found to decrease with age. An examination of the linked event recordings failed to document an episode of apnea as long as 15 seconds for any of the reported episodes of apnea. Furthermore, bradycardia as long as 5 seconds in duration could be documented in only 3 of 422 reported episodes of bradycardia. These results indicate the potential for considerable error when total reliance is placed on parental observations and point to the necessity for objective event recordings when using home monitors in the clinical management of at-risk infants.

Risk to SIDS siblings

Risk to SIDS siblings

Polysomnographic Sleep and Waking States Are Similar in Subsequent Siblings of SIDS and Control Infants During the First Six Months of Life

Twenty-five subsequent siblings of infants who died of Sudden Infant Death Syndrome (SIDS) underwent 12-h overnight polygraphic recordings during the first week of life and at 1, 2, 3, 4, and 6 months of age. The polygraphic tracings from these infants were compared with those from 25 infants without a family history of SIDS. One dozen sleep and waking parameters were examined including state transition probabilities, the ratio between quiet sleep (QS) and active sleep (AS), the incidence and duration of sustained states and the stability of an infant's sleep and waking during the first half year of life. Variability within and between infants was marked with a reduction of variability in measures of QS at 3 months and of AS at 4 months of age. The similarities between subsequent siblings of SIDS and control infants far outweighted the differences. However, subsequent siblings exhibited a tendency, once asleep, to remain asleep longer than controls. This finding was observed in a comparison of 20 infants in each group. When five infants were added to each group, infants in both groups tended to awaken equally from QS, but once in AS the subsequent siblings tended to proceed into QS instead of awaken as the controls did.

Infants at risk for sudden infant death syndrome (SIDS): differential prediction for three siblings of SIDS infants.

The outcome for three siblings of SIDS (SSIDS) infants was predicted, using as a risk model the sleep and respiratory characteristics of a SIDS victim studied extensively during the neonatal period. The SIDS infant had shown unstable state organization and deviant respiration patterns, including a deficit of brief apneic pauses. Like the SIDS infant, the SSIDS infants and a group of 16 normal infants were observed in the home for 7-hr periods when they were 2, 3, 4, and 5 weeks old. Two of the infants showed normal sleep and respiratory characteristics, and they were predicted to develop without respiratory dysfunction. In contrast, the third infant showed a pattern of deviancies similar to the SIDS infant; and at 4 months, she had prolonged apneic episodes, requiring resuscitation on two occasions. The findings are consistent with the notion of subtle central nervous system (CNS) dysfunction in SIDS risk infants from the time of birth.

Night sleep heart rate patterns recorded by cardioneumography at home in normal and at-risk for SIDS infants

It has been reported that infants at higher than normal epidemiological risk for the sudden infant death syndrome (SIDS) have abnormal cardiac autonomic activity. A prospective work was performed using cardiopneumographic recordings (CPG) in order to evaluate heart rate (HR) and heart rate variability (HRV) patterns in sleeping normal control infants (C) and in infants at-risk for SIDS in their normal environment at home. One hundred appropriate-for-gestational age full-term infants were studied: 28 C, 48 SIDS siblings (SS), and 24 near-miss for SIDS (NM) within the first 2 weeks following the first detected apparent life-threatening event. The three groups of infants were comparable with respect to gestational and conceptional ages, birthweights, sex distribution and socio-economic backgrounds. CPG were done over two successive nights. Records were visually analysed for sleep states (quiet: QS, and combined active + indeterminate sleep: AIS) and wakefulness (W) coding. Periods of W were not analysed. An automatic programme allowed us to study HR minute-by-minute, and to assess whether HR and HRV patterns were specific to a certain part of the night, records were divided into three periods (2200-0040 h, 0041-0320 h, and 0321-0600 h). In C and SS groups, the HR was significantly lower in the 2nd night-period than in the 1st and 3rd periods in both QS and AIS (P less than 0.05). In the NM group this difference was only observed during AIS (P less than 0.05). During the three night-periods the HR was significantly elevated in AIS as compared to QS (at least P less than 0.05) in all infant groups except the NM group during the 2nd night-period. During QS the HR was significantly higher in NM than in C and SS groups (P less than 0.02). During AIS the HR did not differ between infant groups. HRV was significantly lower in the NM group during QS in the three night-periods (P less than 0.05). There was no difference in the HR and HRV patterns between C and SS groups with respect to sleep states and night period. We concluded that following the first detected apparent life-threatening event differences in the HR and HRV patterns can be demonstrated when sleeping NM infants are compared with both C and SS infants especially during QS in different night periods studied by CPG at home.