The QT Interval in Aborted Sudden Infant Death Syndrome Infants

Abstract

SummaryThe QT interval was measured in 12 normal and 7 aborted sudden infant death syndrome (SIDS) infants in rapid eye movement (REM) and quiet sleep at monthly intervals through the age of 4 months. An accuracy of better than 2 msec was assured by high resolution of the digitized signal and calibration of each Q T measurement'with an accurately ge-nerated time code. In contrast to current speculations, the QT index was significantly smaller in the infants with aborted SIDS than in the normal infants in both REM and quiet sleep ( P < 0.05). In addition, as in normal infants, the QT, was smaller in REM than in quiet sleep ( P < 0.01).Although these results offer no support for the hypothesis that SIDS results from prolongation of the QT interval, they suggest that aborted SIDS infants have a functional abnormality in the autonomic nervous system. requiring vigorous physical stimulation for resuscitation; mouthto-mouth resuscitation was required in five. At the time of the episode, four of the seven infants were clearly asleep; the level of consciousness was not known in the remaining three infants. Detailed clinical and laboratory assessment failed to reveal an explanation for the aborted SIDS episode. The laboratory evaluation included hematologic profile, serum glucose, calcium, magnesium, sodium, potassium, and chloride, acid-base and blood gas analysis, a chest x-ray, a conventional 12-lead electrocardiogram, an electroencephalogram, and a roentgenographic study i f the upper gastrointestinal tract after swallowing barium. Although the precise relationship between massive gastroesophageal reflux and the cardiorespiratory collapse of the aborted SIDS episode is not well understood, we excluded four infants with massive gastroesophageal reflux because their recurrent aborted SIDS episodes were eliminated by thickening the feedings and placing the infants SpeculationWe suggest that 1) the shortening of the QT interval in the aborted SIDS infants results from a uniform increase in the sympathetic outflow to the cardiac ventricles or an increase in circulating levels of catecholamines; and 2) an imbalance between the left and the right sympathetic outtlow to the ventricles of aborted SlDS infants, as has been previously hypothesized, is not likely since the QT, was not larger in REM sleep, a sleep state in which an increase in sympathetic activity occurs.Experimentally induced imbalance in the sympathetic outflow to the ventricles causes prolongation of the QT interval (24,25). Such a prolongation of the QT interval is associated with increased vulnerability to ventricular arrhythmias and sudden death. The clinical counterpart of these experimental observations is the long QT syndrome in which infants, as well as adults, die suddenly and unexpectedly after physical or emotional stress (8,16, 17). Recently, it has been postulated that infants dying in the first few months of life of the SIDS might have an asymmetrical development of the sympathetic innervation of the ventricles, causing an imbalance in the ventric...

Prolongation of the QT Interval and the Sudden Infant Death Syndrome

“…20,21 The original hypothesis that prolongation of the QT interval may have a role in the pathogenesis of SIDS was prematurely discarded on the basis of a series of apparently negative results. 16,[22][23][24][25] However, most of those studies were performed in very small populations or focused on infants assumed to be at increased risk for SIDS, such as the siblings of SIDS victims 23,25 or infants who had had so-called nearmiss or aborted SIDS. [22][23][24] As discussed in detail elsewhere, 4,26 conclusions drawn from these studies are not relevant to the assessment of the risk of SIDS associated with prolongation of the QT interval, for several reasons.…”

“…16,[22][23][24][25] However, most of those studies were performed in very small populations or focused on infants assumed to be at increased risk for SIDS, such as the siblings of SIDS victims 23,25 or infants who had had so-called nearmiss or aborted SIDS. [22][23][24] As discussed in detail elsewhere, 4,26 conclusions drawn from these studies are not relevant to the assessment of the risk of SIDS associated with prolongation of the QT interval, for several reasons. Among the infants considered at risk for SIDS, even assuming that risk increases by a factor of 5 to 10, the probability of SIDS would approximate 10 per 1000, which would imply a 99 percent rate of false positives.…”

QTc and R-R Intervals in Victims of the Sudden Infant Death Syndrome

“…Simi¬ lar increases in neonatal heart rate have been observed in the subsequent siblings of SIDS victims8 and "nearmiss" infants. 9 Although the elevation of heart rate observed in the current report is insufficient to provide a means for early identification of the "at-risk" infant, this observation adds to the growing body of knowledge indi¬ cating that SIDS victims do have a chronic abnormality which has subtle manifestations within the first few days of life.710"17 This observation also reinforces the need for more intensive studies directed at the perinatal period to more fully understand those factors that predispose an infant for SIDS. The findings in this study are con¬ sistent with those of previous reports in demonstrating that age is associated with an increase in QTc interval and a decrease in R-R interval and that the QTc interval tends to be longer during NREM sleep.4·8·18·19…”

Cardiac Ion Channelopathies and the Sudden Infant Death Syndrome

“…Further evidence for a role of a functional abnormality in the autonomic nervous system came from the study by Haddad et al [76], who measured the QT interval in 7 near-miss SIDS victims and 12 control infants. Again, in contrast with the hypothesis of Schwartz [74], no QT prolongation was observed.…”