Background The sudden infant death syndrome (SIDS) is multifactorialin origin, but its causes remain unknown. We previously proposedthat prolongation of the QT interval on the electrocardiogram,possibly resulting from a developmental abnormality in cardiacsympathetic innervation, may increase the risk of life-threateningventricular arrhythmias and contribute to this devastating disorder.We prospectively tested this hypothesis.
Methods Between 1976 and 1994, we recorded electrocardiogramson the third or fourth day of life in 34,442 newborns and followedthem prospectively for one year. The QT interval was analyzedwith and without correction for the heart rate.
Results One-year follow-up data were available for 33,034 ofthe infants. There were 34 deaths, of which 24 were due to SIDS.The infants who died of SIDS had a longer corrected QT interval(QTc) than did the survivors (mean [±SD], 435±45vs. 400±20 msec, P<0.01) and the infants who diedfrom causes other than SIDS (393±24 msec, P<0.05).Moreover, 12 of the 24 SIDS victims but none of the other infantshad a prolonged QTc (defined as a QTc greater than 440 msec).When the absolute QT interval was determined for similar cardiac-cyclelengths, it was found that 12 of the 24 infants who died ofSIDS had a QT value exceeding the 97.5th percentile for thestudy group as a whole. The odds ratio for SIDS in infants witha prolonged QTc was 41.3 (95 percent confidence interval, 17.3to 98.4).
Conclusions Prolongation of the QT interval in the first weekof life is strongly associated with SIDS. Neonatal electrocardiographicscreening may permit the early identification of a substantialpercentage of infants at risk for SIDS, and the institutionof preventive measures may therefore be possible.
The incidence of the sudden infant death syndrome (SIDS) hasrecently declined.1 This trend followed the identification ofseveral behavioral risk factors and their subsequent modificationthrough public-education campaigns.2 Nonetheless, SIDS remainsthe leading cause of death in the first year of life after theneonatal period, and effective preventive measures are stilllacking because of the poor understanding of the mechanismsunderlying the disorder. SIDS has devastating psychosocial consequencesfor the affected families.3 There is a consensus that the causeof SIDS is multifactorial,4 but despite the many hypothesesproposed,5 none have yet been proved.
Most cases of SIDS probably result from a temporary defect inthe neural control of either respiratory or cardiac functionthat may initiate a lethal sequence of events.6 In 1976 oneof us proposed that a developmental abnormality in cardiac sympatheticinnervation may predispose some infants to lethal arrhythmiasin the first year of life.7 Specifically, it was suggested thatan imbalance in the sympathetic nervous system may result inprolongation of the QT interval on the electrocardiogram andin potentially lethal ventricular arrhythmias.8
To test the hypothesis of a relation between prolongation ofthe QT interval and SIDS, we designed a multiyear, prospectivestudy based on the recording of a standard electrocardiogramin three-to-four-day-old infants (the Multicenter Italian Studyof Neonatal Electrocardiography and SIDS). Given the low incidenceof SIDS (0.5 to 2 cases per 1000 live births), we prospectivelycollected neonatal electrocardiograms in a very large populationof infants born in the period from 1976 through 1994 and followedthe infants for one year to determine the incidence of deathdue to SIDS or to other causes. We now report the final resultsof this 19-year study.
Methods
Study Population
Electrocardiograms were recorded in 34,442 neonates born innine maternity hospitals (listed in the Appendix) between October1976 and December 1994. Almost all the infants were healthyand born at full term, because most very premature and sicknewborns were transferred to intensive care units before electrocardiographycould be performed.
Electrocardiography
Twelve-lead electrocardiograms were recorded at a paper speedof 25 mm per second with Hewlett–Packard 1504 A and 1511A recorders in the first part of the study and, since 1989,with a Marquette MAC PC recorder. All the recordings were madeon the third or fourth day of life in order to avoid the variabilityof the QT interval that is maximal during the first two daysof life.9 RR and QT intervals were usually measured in leadII from five nonconsecutive beats, and the corrected QT interval(QTc) was calculated by dividing the QT interval by the squareroot of the RR interval (Bazett's formula).10 We analyzed theelectrocardiograms of all infants who died and those of a randomsample of 9725 surviving infants (4867 boys and 4858 girls).Since the heart rate is elevated in the neonatal period, Bazett'sformula may not be appropriate for correcting the QT intervalfor short cardiac-cycle lengths. Accordingly, we also dividedthe RR intervals into 17 categories with progressively increasingvalues (in increments of 20 msec); for each category we calculatedthe percentile distribution of the corresponding absolute valuesof the QT interval (from the 2.5th to the 97.5th percentile).
Follow-Up
Information on survival at one year was obtained either by telephoneor by mail through the census bureau for the cities where theinfants' families resided. In cases of death, all the relevantrecords were analyzed. The diagnosis of SIDS was based on anadequate negative postmortem examination (i.e., on the absenceof evidence of other causes of death) and on traditional criteria.11
Statistical Analysis
The distribution of values for the heart rate, QT interval,and QTc was assessed, and percentile values (from the 2.5thto the 97.5th percentile) were calculated. Differences in electrocardiographicmeasurements between groups were assessed by analysis of varianceand Student's t-test with Bonferroni's correction, or by theKruskal–Wallis test for non-normally distributed values.The frequency of outcomes was compared by means of chi-squareanalysis and Fisher's exact test. Odds ratios and 95 percentconfidence intervals were calculated for all variables understudy. A multiple logistic-regression analysis was performed,including the effects of sex, QTc, and heart rate. Data arepresented as means ±SD. A two-sided P value below 0.05was considered to indicate statistical significance.
Results
Electrocardiographic Characteristics
Of the 34,442 infants enrolled, one-year follow-up data wereavailable for 33,034 (96 percent; 16,538 boys and 16,496 girls).The remaining 1408 were lost to follow-up when their familiesmoved.
The distribution of values for the heart rate, QT interval,and QTc was normal (P<0.001). The mean heart rate was 135±20beats per minute, the mean PR interval was 113±23 msec,the duration of the QRS complex was 57±7 msec, and theQT interval was 274±28 msec. The mean QTc was 400±20msec, confirming our earlier observation based on data on 3946infants,12 and it did not differ significantly between boysand girls (401±19 and 400±20 msec, respectively).The 97.5th percentile for the QTc among the infants was 440msec, 2 SD above the mean. Consequently, we considered a QTcgreater than 440 msec to be prolonged.
Incidence of Death Due to SIDS and Other Causes
During the one year of follow-up, there were 34 deaths: 24 dueto SIDS and 10 due to other causes. The number of deaths fromcauses other than SIDS was low, probably because most of theinfants who were sick at birth did not enter the study. Theincidence of SIDS in this population was 0.7 per 1000, similarto that reported for Italy.6
Characteristics of Infants Who Died
Table 1 shows the characteristics of the infants who died ofSIDS and those who died of other causes. The distribution ofboys and girls was similar among survivors and infants who diedof causes other than SIDS; the slight excess of boys among theinfants who died of SIDS (15 of 24 infants [62 percent]) wasnot statistically significant (odds ratio for death among boysas compared with girls, 1.7; 95 percent confidence interval,0.7 to 3.8). Most deaths due to SIDS (18 of 24 [75 percent])occurred in the second or third month of life, as is typicalof this disease, whereas other deaths occurred either duringthe first or after the third month of life. No victim of SIDShad a family history consistent with the long-QT syndrome.
Table 1. Characteristics of the Infants Who Died of SIDS and Those Who Died of Other Causes.
Electrocardiographic Findings
The mean heart rate among the infants who died of SIDS was 136±20beats per minute and did not differ from that among the infantswho died of other causes (140±21 beats per minute, Pnot significant) or among the survivors (135±20 beatsper minute, P not significant). The mean QTc was 435±45msec in the group of infants who died of SIDS, significantlylonger than that among the infants with other causes of death(393±24 msec, P<0.05) and that of the survivors (400±20msec, P<0.01) (Figure 1). More important, the analysis ofthe individual values for QTc in the two groups of infants whodied (Figure 1) showed that 12 of the 24 infants who died ofSIDS (50 percent) had a QTc greater than 440 msec, whereas allthe infants who died from other causes had a QTc shorter than440 msec. Among the infants who died of SIDS, no significantdifference was found in the duration of the QT interval betweenpremature and full-term babies (439±26 and 433±50msec, respectively). Furthermore, these findings were similarin our analysis of the relation between the absolute QT intervalsand RR intervals. As Figure 2 shows, the individual values in12 of the 24 infants who died of SIDS (50 percent) were at orabove the 97.5th percentile, whereas all the values in the infantswho died of other causes were below the 90th percentile.
Figure 1. Mean QT Interval Corrected for Heart Rate (QTc) in 9725 Infants Who Were Alive at One Year, 24 Infants Who Died of SIDS, and 10 Infants Who Died of Other Causes.
The horizontal line represents the value of QTc at the 97.5th percentile for the entire study population. The circles represent individual values for QTc, and the bars indicate the SD. The mean QTc for the infants who died of SIDS was significantly longer than that for the infants who were alive at one year (P<0.01) and that of the infants who died of other causes (P<0.05).
Figure 2. Relation between the Duration of the QT Interval and the Length of the Cardiac Cycle.
The curves represent the percentiles for uncorrected QT intervals at the corresponding range of values for the RR interval. The circles represent individual values for the 24 infants who died of SIDS and the 10 who died of other causes.
The absolute risk of SIDS in infants with a normal QTc was 0.037percent; by contrast, that of infants with a prolonged QTc was1.53 percent (odds ratio, 41.3; 95 percent confidence interval,17.3 to 98.4). Among the victims of SIDS, the incidence of aprolonged QTc was similar in boys (8 of 15 infants [53 percent])and girls (4 of 9 [44 percent]), despite a trend toward longerQTc values among boys (439±51 vs. 422±31 msec,P not significant). As compared with infants of the same sexwith a normal QTc, boys with a QTc above 440 msec had an oddsratio for SIDS of 46.9 (95 percent confidence interval, 15.4to 144.2), and girls with a QTc above 440 msec had an odds ratioof 33.0 (95 percent confidence interval, 7.4 to 141.7). Multiplelogistic-regression analysis, including the effect of sex, heartrate, and QTc, showed that only the QTc was a significant predictorof SIDS (P<0.001).
Discussion
This large, prospective study of more than 33,000 infants bornduring a 19-year period demonstrates that prolongation of theQT interval on the electrocardiogram is an important risk factorfor SIDS. This finding points to pathogenetic mechanisms thatmay be involved in a large proportion of cases of SIDS and alsosuggests rational preventive strategies.
The "Normal" Neonatal Electrocardiogram
We collected a large body of electrocardiographic data recordedin the first week of life, which contribute to the definitionof normal electrocardiographic standards for newborns. Mostprevious studies have been of older infants or have includedfewer electrocardiograms.9,13,14,15 In the study by Southallet al., which is an exception to this pattern,16 most electrocardiogramswere recorded before the third day, when there is still markedvariability in the QT interval in individual subjects.
The mean heart rate and QTc were similar to those previouslyreported during the first week of life.9,13,14 Among adults,women have a longer QTc than men,17 but in a previous studyof neonates, we found no difference according to sex.18 Fornewborns, unlike adults,19 a QTc of 440 msec should be consideredthe upper limit of normal for both males and females.
Prolongation of the QT Interval and SIDS
Our results show that QTc measured on the third or fourth dayof life is prolonged in infants who subsequently die of SIDSas compared with infants who survive for at least one year andalso as compared with infants who die of other causes. The oddsratio for SIDS among infants with a QTc greater than 440 msecwas approximately 41, and in boys it was approximately 47. Consequently,a prolonged QT interval in the first week of life representsan important risk factor, and this information may be usefulin the early identification of infants at risk for SIDS. Theother traditional risk factors, such as sleeping in a proneposition, maternal smoking, and bed sharing, have odds ratiosmarkedly lower than those we observed with prolongation of theQT interval.20,21
The original hypothesis that prolongation of the QT intervalmay have a role in the pathogenesis of SIDS was prematurelydiscarded on the basis of a series of apparently negative results.16,22,23,24,25However, most of those studies were performed in very smallpopulations or focused on infants assumed to be at increasedrisk for SIDS, such as the siblings of SIDS victims23,25 orinfants who had had so-called near-miss or aborted SIDS.22,23,24As discussed in detail elsewhere,4,26 conclusions drawn fromthese studies are not relevant to the assessment of the riskof SIDS associated with prolongation of the QT interval, forseveral reasons. Among the infants considered at risk for SIDS,even assuming that risk increases by a factor of 5 to 10, theprobability of SIDS would approximate 10 per 1000, which wouldimply a 99 percent rate of false positives. In a populationof infants most of whom will not die of SIDS, the absence ofa prolonged QT interval obviously has no implications.
Southall et al.16 prospectively studied 7254 infants, 15 ofwhom subsequently died of SIDS, and compared the mean valuesfor QTc between those who died and the survivors. Even thoughthey concluded that there was no significant difference betweenvictims of SIDS and controls, 6 of the 15 infants who died ofSIDS (40 percent) had a QTc exceeding the 90th percentile forthe study population, with an odds ratio of 6. The combinedresults of the study by Southall et al.16 and our study, whichtogether involved more than 40,000 infants, suggest that evenat a very conservative estimate, probably not less than 30 to35 percent of infants who subsequently die of SIDS can be expectedto have a prolonged QT interval in the first week of life.
The possibility that inadequate shortening of the QT intervalduring increases in the heart rate may be involved in SIDS wassuggested by Sadeh et al.,27 on the basis of nighttime findingsin 5 of 10 infants who subsequently died of SIDS. However, thisfinding was not confirmed when the analysis of the same infantswas extended to the entire 24-hour period.28
Prolongation of the QT Interval and Susceptibility to Lethal Arrhythmias
Our finding of a strong association between SIDS and prolongationof the QT interval, a marker of reduced cardiac electrical stability,29suggests that some infants may have an increased susceptibilityto life-threatening arrhythmias. Prolongation of the QT intervalfavors the occurrence of lethal arrhythmias and is associatedwith an increased risk of sudden death in several clinical conditions30,31,32and even in apparently healthy persons.33 We have shown thatthe QTc increases during the second month of life and returnsto the values recorded at birth by the sixth month.12 Thesedata agree with the epidemiologic observation that SIDS is rareduring the first month of life, has a peak incidence duringthe second and third months, and declines after the fourth.5,6Thus, there is a tendency, which in some infants may becomeexcessive, toward a reduction in cardiac electrical stabilityduring the period when the incidence of SIDS is highest.
In the population we studied, the fact that many infants withprolonged QT intervals did not die of SIDS indicates that otherfactors in the postnatal period contribute to the lethal event.This assumption is consistent with the concept that prolongationof the QT interval acts as an arrhythmogenic substrate, whichrequires a trigger for the development of life-threatening arrhythmias.Prolongation of the QT interval, even in neonates,34 is almostalways associated with increased dispersion of ventricular repolarization,a factor that favors arrhythmias — particularly when sympatheticactivity is augmented.8 The likelihood that life-threateningarrhythmia will develop in an infant with an arrhythmogenicsubstrate — that is, with prolongation of the QT interval— depends on the presence of adequate triggers, such asthe release of catecholamines or factors (such as drug therapy)that further prolong the QT interval.
Potential Causes of Prolongation of the QT Interval in Infants
Why is the QT interval prolonged in some newborns? Two mechanismsmay be proposed. The first, based on the hypothesis proposedby one of us,7 suggests that prolongation of the QT intervalmay depend on developmental alterations in cardiac sympatheticinnervation.35,36 The sympathetic innervation of the heart continuesto develop after birth and becomes functionally complete byapproximately the sixth month of life.37 The right and leftsympathetic nerves may occasionally develop at different ratesand lead temporarily to a harmful imbalance.8,36 A sudden increasein sympathetic activity may trigger lethal arrhythmias in suchelectrically unstable hearts. Infants with these characteristicswould be particularly vulnerable during the first year of life,and their higher risk of SIDS could be identified by the observationof a prolonged QT interval.
A second possibility involves a genetic abnormality. Some victimsof SIDS may have a variant of the congenital long-QT syndrome.This disorder is characterized by prolongation of the QT intervaland a high risk of sudden death, mostly under stressful conditionsbut also during sleep; it is usually familial but may be sporadic.30,38Four of the genes responsible for the long-QT syndrome havebeen identified, and they all encode sodium and potassium channels.39However, SIDS is not a familial disease. What is relevant toSIDS is that in sporadic cases of the long-QT syndrome, spontaneousmutations have been found. Infants with spontaneous mutationsthat affected one of the ionic currents controlling ventricularrepolarization would also have a prolonged QT interval. Someof them might die because of ventricular fibrillation duringthe first few months of life,40 and if no electrocardiogramwere available, they would be labeled as having died of SIDS.Others might begin to have syncopal episodes during childhoodand would then be diagnosed as having sporadic cases of thelong-QT syndrome.
There is an additional genetic possibility. In some familieswith the long-QT syndrome, penetrance is so low that both parentsand all siblings of clinically affected patients may have acompletely normal QT interval and nonetheless be gene carriers.41In such a case, if the affected infant died suddenly withoutan electrocardiogram having been recorded, the examination ofthe family would reveal no prolongation of the QT interval.Without molecular diagnosis, the death would be ascribed toSIDS.
Clinical Implications
Our data, which document a significant association between prolongationof the QT interval and SIDS, also raise two further issues.One is the potential value of routine neonatal screening byelectrocardiography; the other is the treatment strategy forthe infants who are found to have a prolonged QTc. Screeningmay be warranted, because it is likely to identify some infantsat high risk for SIDS. However, formal cost-effectiveness studieswill be required before such a practice is implemented. Ourstudy contains no data to justify new therapeutic recommendations.However, the identification of a mechanism that may be involvedin the pathogenesis of SIDS allows some cautious speculation.
The lethal arrhythmias associated with prolongation of the QTinterval are almost always torsade-de-pointes ventricular tachycardiadue to early after-depolarizations and are usually triggeredby sudden increases in sympathetic activity.8 In the first yearof life, such an increase may be elicited often by a numberof conditions, including sudden noise, exposure to cold, rapid-eye-movementsleep, apnea leading to a chemoreceptive reflex, and arousal.5In the long-QT syndrome, antiadrenergic interventions are quitebeneficial.30 It is plausible that infants with a prolongedQT interval, who are at high risk for SIDS on the basis of ourdata, could be protected by the careful administration of beta-blockersduring the first year of life.
Even if our hypothesis were proved to be correct, however, suchidentification and treatment would not be a simple task. Thelow incidence of SIDS contributes to the low positive predictivevalue of QT-interval prolongation. Thus, not only would a largenumber of infants need to be screened to identify those withprolongation of the QT interval, but also 100 infants wouldhave to be treated in order to save 2 lives. Additional informationis needed to identify infants at risk for SIDS more precisely,so that preventive interventions can be targeted effectively.
Supported by a grant (16736) from the Consiglio Nazionale delleRicerche.
We are indebted to Pinuccia De Tomasi for expert editorial support.
* Centers and investigators participating in the study are listedin the Appendix.
Source Information
From the Department of Cardiology, Policlinico San Matteo Istituto di Ricovero e Cura a Carattene Scientifico and the University of Pavia, Pavia (P.J.S.); Centro di Fisiologia Clinica e Ipertensione, University of Milan and Ospedale Maggiore Istituto di Ricovero e Cura a Carattene Scientifico, Milan (M.S.-B., A.S., F.G.); the Cardiology Department A. De Gasperis, Ospedale Niguarda Ca' Granda, Milan (P.A.); the Pediatrics Institute, University of Ferrara, Ferrara (G.B.); Ospedale Galmarini, Tradate (R.G.); the Department of Pediatrics, University of Pavia, Pavia (E.D.M.); the Department of Experimental and Clinical Cardiology G. Salvatore–Catanzaro, University of Reggio Calabria, Catanzaro (F.P.); and Ospedale Regina Elena, Milan (D.R., P.S.) — all in Italy.
Address reprint requests to Dr. Schwartz at the Department of Cardiology, Policlinico San Matteo IRCCS, Piazzale Golgi, 2, Pavia 27100, Italy.
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Appendix
The following centers and investigators participated in theMulticenter Italian Study of Neonatal Electrocardiography andSIDS: University of Milan, Milan (coordinating center) —P.J. Schwartz, M. Stramba-Badiale, A. Segantini, F. Grancini,P. Careddu, V. Carnelli, M. Facchini, M. Montemerlo, M. Frediani,S. Guffanti, M. Negrini, F. Palla, N. Porta, P. Rusinenti, andT. Varisco; Ospedale Regina Elena, Milan — D. Rosti andP. Salice; Ospedale Galmarini, Tradate — R. Giorgettiand G. Poggio; Ospedale Niguarda, Milan — P. Austoni;University of Ferrara, Ferrara — G. Bosi; University ofReggio Calabria, Catanzaro: F. Perticone; University of Rome,Rome — S. Pelargonio; University of Pavia, Pavia —E.D. Marni; Ospedale Regina Margherita, Turin — M.G. Broveglio-Ferri;University of Florence, Florence — G. Mainardi.
Prolongation of the QT Interval and the Sudden Infant Death Syndrome
Guntheroth W. G., Spiers P. S., Dancey D. R., Redelmeier D. A., Rosenthal E., Scholz T. D., Yoldi A., Sena F., Gutierrez L., Schwartz P. J., Stramba-Badiale M., Friedman R. A., Towbin J. A.
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N Engl J Med 1998;
339:1161-1163, Oct 15, 1998.
Correspondence
Prolongation of the QT Interval and SIDS
Beinder E., Grancay T., Hofbeck M., Skinner J., Phoon C. K., Schwartz P. J., Priori S. G., Stramba-Badiale M.
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N Engl J Med 2000;
343:1896-1897, Dec 21, 2000.
Correspondence
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