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

Weinstein, Steven L.; Steinschneider, Alfred

doi:10.1001/archpedi.1985.02140120033023

Cited by 13 publications

(10 citation statements)

References 13 publications

(1 reference statement)

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“…28 It is critical to note that this study was performed while the infants were kept at a room temperature of 900 F. Heating modifies the sympathetic tone and may revert to normal a neurally mediated QT prolongation.…”

mentioning

confidence: 99%

The quest for the mechanisms of the sudden infant death syndrome: doubts and progress.

Schwartz¹

1987

Circulation

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mentioning

confidence: 99%

The quest for the mechanisms of the sudden infant death syndrome: doubts and progress.

Schwartz¹

1987

Circulation

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“…However, these results could not be confirmed by other investigators [69,70,71,72] (Table 2) and therefore considerable discussion arose. In 1998 the working group of Schwartz [73] published a new investigation of more than 34,000 infants where an ECG was performed during the first week of life.…”

Section: Disturbances Of Rhythmogenic Functionmentioning

confidence: 79%

Pathological changes of the heart in sudden infant death

Bajanowski

Ortmann

Teige

et al. 2003

International Journal of Legal Medicine

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There are more than 120 different theories on the possible causes of sudden infant death (SID). In particular, dysfunctions of the central nervous system, cardiorespiratory insufficiency due to infections including atypical immune reactions, and cardiac dysregulation have been discussed during the previous decade. Reports on disturbances of the cardiac rhythmogenic function due to LQTS were among the most speculative. Based on gross histological, immunohistochemical and molecular genetic investigations of SID cases, the most important and most frequent findings of the heart are shown. The significance of different types of myocarditis, hypoxia-related changes, disturbances of the rhythmogenic function, cardiomyopathy, and other changes is discussed with regard to the cause of death. In conclusion, most of the changes reported in the literature are not sufficient to explain the cause of death. Problems in the diagnosis are shown which influence the classification of these disturbances as well as the classification of SID.

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“…No prolongation of the QT interval was apparent in this group. In a subsequent study, Weinstein and Steinschneider [86] found that none of the eight infants who subsequently died of SIDS had a prolonged QTc interval. However, the RR interval during REM sleep was significantly shorter in these future SIDS victims than in control subjects, as in the aforementioned study by Leistner et al [77] on infants with aborted SIDS.…”

Section: Clinical Associationsmentioning

confidence: 99%

Cardiac Ion Channelopathies and the Sudden Infant Death Syndrome

Wilders

2012

ISRN Cardiology

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The sudden infant death syndrome (SIDS) causes the sudden death of an apparently healthy infant, which remains unexplained despite a thorough investigation, including the performance of a complete autopsy. The triple risk model for the pathogenesis of SIDS points to the coincidence of a vulnerable infant, a critical developmental period, and an exogenous stressor. Primary electrical diseases of the heart, which may cause lethal arrhythmias as a result of dysfunctioning cardiac ion channels (“cardiac ion channelopathies”) and are not detectable during a standard postmortem examination, may create the vulnerable infant and thus contribute to SIDS. Evidence comes from clinical correlations between the long QT syndrome and SIDS as well as genetic analyses in cohorts of SIDS victims (“molecular autopsy”), which have revealed a large number of mutations in ion channel-related genes linked to inheritable arrhythmogenic syndromes, in particular the long QT syndrome, the short QT syndrome, the Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia. Combining data from population-based cohort studies, it can be concluded that at least one out of five SIDS victims carries a mutation in a cardiac ion channel-related gene and that the majority of these mutations are of a known malignant phenotype.

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

Cited by 13 publications

References 13 publications

The quest for the mechanisms of the sudden infant death syndrome: doubts and progress.

The quest for the mechanisms of the sudden infant death syndrome: doubts and progress.

Pathological changes of the heart in sudden infant death

Cardiac Ion Channelopathies and the Sudden Infant Death Syndrome

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