Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence

Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The ge...
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Autor*in:	Ioakeimidis, Nikolaos S. [verfasserIn] Papamitsou, Theodora Meditskou, Soultana Iakovidou-Kritsi, Zafiroula

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Sudden infant death Long QT syndrome Prevalence

Anmerkung:	© The Author(s) 2017

Übergeordnetes Werk:	Enthalten in: Journal of biological research - Thessaloniki - London : BioMed Central, 2014, 24(2017), 1 vom: 14. März
Übergeordnetes Werk:	volume:24 ; year:2017 ; number:1 ; day:14 ; month:03

Links:	Volltext

DOI / URN:	10.1186/s40709-017-0063-1

Katalog-ID:	SPR037862243

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520			\|a Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants.
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allfields	10.1186/s40709-017-0063-1 doi (DE-627)SPR037862243 (SPR)s40709-017-0063-1-e DE-627 ger DE-627 rakwb eng Ioakeimidis, Nikolaos S. verfasserin aut Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants. Sudden infant death (dpeaa)DE-He213 Long QT syndrome (dpeaa)DE-He213 Prevalence (dpeaa)DE-He213 Papamitsou, Theodora aut Meditskou, Soultana aut Iakovidou-Kritsi, Zafiroula aut Enthalten in Journal of biological research - Thessaloniki London : BioMed Central, 2014 24(2017), 1 vom: 14. März (DE-627)796585997 (DE-600)2783839-0 2241-5793 nnns volume:24 year:2017 number:1 day:14 month:03 https://dx.doi.org/10.1186/s40709-017-0063-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2017 1 14 03
spelling	10.1186/s40709-017-0063-1 doi (DE-627)SPR037862243 (SPR)s40709-017-0063-1-e DE-627 ger DE-627 rakwb eng Ioakeimidis, Nikolaos S. verfasserin aut Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants. Sudden infant death (dpeaa)DE-He213 Long QT syndrome (dpeaa)DE-He213 Prevalence (dpeaa)DE-He213 Papamitsou, Theodora aut Meditskou, Soultana aut Iakovidou-Kritsi, Zafiroula aut Enthalten in Journal of biological research - Thessaloniki London : BioMed Central, 2014 24(2017), 1 vom: 14. März (DE-627)796585997 (DE-600)2783839-0 2241-5793 nnns volume:24 year:2017 number:1 day:14 month:03 https://dx.doi.org/10.1186/s40709-017-0063-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2017 1 14 03
allfields_unstemmed	10.1186/s40709-017-0063-1 doi (DE-627)SPR037862243 (SPR)s40709-017-0063-1-e DE-627 ger DE-627 rakwb eng Ioakeimidis, Nikolaos S. verfasserin aut Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants. Sudden infant death (dpeaa)DE-He213 Long QT syndrome (dpeaa)DE-He213 Prevalence (dpeaa)DE-He213 Papamitsou, Theodora aut Meditskou, Soultana aut Iakovidou-Kritsi, Zafiroula aut Enthalten in Journal of biological research - Thessaloniki London : BioMed Central, 2014 24(2017), 1 vom: 14. März (DE-627)796585997 (DE-600)2783839-0 2241-5793 nnns volume:24 year:2017 number:1 day:14 month:03 https://dx.doi.org/10.1186/s40709-017-0063-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2017 1 14 03
allfieldsGer	10.1186/s40709-017-0063-1 doi (DE-627)SPR037862243 (SPR)s40709-017-0063-1-e DE-627 ger DE-627 rakwb eng Ioakeimidis, Nikolaos S. verfasserin aut Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants. Sudden infant death (dpeaa)DE-He213 Long QT syndrome (dpeaa)DE-He213 Prevalence (dpeaa)DE-He213 Papamitsou, Theodora aut Meditskou, Soultana aut Iakovidou-Kritsi, Zafiroula aut Enthalten in Journal of biological research - Thessaloniki London : BioMed Central, 2014 24(2017), 1 vom: 14. März (DE-627)796585997 (DE-600)2783839-0 2241-5793 nnns volume:24 year:2017 number:1 day:14 month:03 https://dx.doi.org/10.1186/s40709-017-0063-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2017 1 14 03
allfieldsSound	10.1186/s40709-017-0063-1 doi (DE-627)SPR037862243 (SPR)s40709-017-0063-1-e DE-627 ger DE-627 rakwb eng Ioakeimidis, Nikolaos S. verfasserin aut Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2017 Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants. Sudden infant death (dpeaa)DE-He213 Long QT syndrome (dpeaa)DE-He213 Prevalence (dpeaa)DE-He213 Papamitsou, Theodora aut Meditskou, Soultana aut Iakovidou-Kritsi, Zafiroula aut Enthalten in Journal of biological research - Thessaloniki London : BioMed Central, 2014 24(2017), 1 vom: 14. März (DE-627)796585997 (DE-600)2783839-0 2241-5793 nnns volume:24 year:2017 number:1 day:14 month:03 https://dx.doi.org/10.1186/s40709-017-0063-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2017 1 14 03
language	English
source	Enthalten in Journal of biological research - Thessaloniki 24(2017), 1 vom: 14. März volume:24 year:2017 number:1 day:14 month:03
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authorswithroles_txt_mv	Ioakeimidis, Nikolaos S. @@aut@@ Papamitsou, Theodora @@aut@@ Meditskou, Soultana @@aut@@ Iakovidou-Kritsi, Zafiroula @@aut@@
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author	Ioakeimidis, Nikolaos S.
spellingShingle	Ioakeimidis, Nikolaos S. misc Sudden infant death misc Long QT syndrome misc Prevalence Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence
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topic_title	Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence Sudden infant death (dpeaa)DE-He213 Long QT syndrome (dpeaa)DE-He213 Prevalence (dpeaa)DE-He213
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title	Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence
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title_full	Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence
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title_sort	sudden infant death syndrome due to long qt syndrome: a brief review of the genetic substrate and prevalence
title_auth	Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence
abstract	Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants. © The Author(s) 2017
abstractGer	Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants. © The Author(s) 2017
abstract_unstemmed	Abstract The pathophysiological mechanisms which lead to sudden infant death syndrome (SIDS) are not completely understood. Cardiac channelopathies are a well-established causative factor with long QT syndrome (LQTS) being the most frequent one, accounting for approximately 12% of SIDS cases. The genetic substrate of the above arrhythmogenic syndrome has been thoroughly described but only specific gene mutations or polymorphisms have been identified as SIDS causative. The review will focus on the prevalence of LQTS-induced SIDS or near-SIDS cases and the mutations held responsible. A literature search was performed in PubMed and Scopus electronic databases. Search terms used were: long QT syndrome, channelopathies, QT prolongation, cardiac ion channels. The above-mentioned search terms were always combined with the term: sudden infant death syndrome. Study types considered eligible were: case–control, family pedigree analysis, case reports. The prevalence of LQTS-induced SIDS according to six broad genetic studies ranges from 3.9 to 20.6%, with an average of 12%. Since LQTS can be effectively managed, LQTS-related SIDS cases could be prevented, provided that a screening method is efficient enough to detect all the affected infants. © The Author(s) 2017
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title_short	Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence
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Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence

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