Mutation Analysis Ion Channel Genes Ventricular Fibrillation Survivors with Coronary Artery Disease
Background: Observations from population‐based studies demonstrated a strong genetic component of sudden cardiac death. The aim of this study was to test the hypothesis that ion channel genes mutations are more common in ventricular fibrillation (VF) survivors with coronary artery disease (CAD) comp...
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| Veröffentlicht in: | Pacing and clinical electrophysiology 2011-06, Vol.34 (6), p.742-749 |
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| creator | NOVOTNY, TOMAS KADLECOVA, JITKA RAUDENSKA, MARTINA BITTNEROVA, ALEXANDRA ANDRSOVA, IRENA FLORIANOVA, ALENA VASKU, ANNA NEUGEBAUER, PETR KOZAK, MILAN SEPSI, MILAN KRIVAN, LUBOMIR GAILLYOVA, RENATA SPINAR, JINDRICH |
| description | Background: Observations from population‐based studies demonstrated a strong genetic component of sudden cardiac death. The aim of this study was to test the hypothesis that ion channel genes mutations are more common in ventricular fibrillation (VF) survivors with coronary artery disease (CAD) compared to controls.
Methods: The entire coding sequence of KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 genes was analyzed in 45 (five females) CAD individuals—survivors of documented VF and in 90 matched healthy controls. In another control group of 141 matched patients with CAD without malignant arrhythmias, the exons containing rare coding variants found in the VF survivors were sequenced.
Results: The carrier frequency of all the rare sequence variants was significantly higher in the VF survivors (8/45, 17.8%) than in CAD controls (3/141, 2.2%, P = 0.001). In VF survivors, four coding variants in eight individuals were found. Three in KCNH2 gene: R148W and GAG186del are novel; P347S was previously related to long QT syndrome. In SCN5A gene, P2006A variant was found in five unrelated males. This variant has been demonstrated previously to have small effect on sodium channel kinetics. No rare coding variants were found in the healthy controls. The P2006A variant was found in three CAD controls.
Conclusion: The prevalence of selected, rare coding variants in five long QT genes was significantly higher in cases versus controls, confirming a mechanistic role for these genes among a subgroup of patients with coronary disease and VF. (PACE 2011; 742–749) |
| doi_str_mv | 10.1111/j.1540-8159.2011.03045.x |
| format | Article |
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Methods: The entire coding sequence of KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 genes was analyzed in 45 (five females) CAD individuals—survivors of documented VF and in 90 matched healthy controls. In another control group of 141 matched patients with CAD without malignant arrhythmias, the exons containing rare coding variants found in the VF survivors were sequenced.
Results: The carrier frequency of all the rare sequence variants was significantly higher in the VF survivors (8/45, 17.8%) than in CAD controls (3/141, 2.2%, P = 0.001). In VF survivors, four coding variants in eight individuals were found. Three in KCNH2 gene: R148W and GAG186del are novel; P347S was previously related to long QT syndrome. In SCN5A gene, P2006A variant was found in five unrelated males. This variant has been demonstrated previously to have small effect on sodium channel kinetics. No rare coding variants were found in the healthy controls. The P2006A variant was found in three CAD controls.
Conclusion: The prevalence of selected, rare coding variants in five long QT genes was significantly higher in cases versus controls, confirming a mechanistic role for these genes among a subgroup of patients with coronary disease and VF. (PACE 2011; 742–749)</description><identifier>ISSN: 0147-8389</identifier><identifier>EISSN: 1540-8159</identifier><identifier>DOI: 10.1111/j.1540-8159.2011.03045.x</identifier><identifier>PMID: 21410720</identifier><language>eng</language><publisher>Malden, USA: Blackwell Publishing Inc</publisher><subject>Aged ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Biological and medical sciences ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Comorbidity ; Coronary Artery Disease - genetics ; Coronary Artery Disease - mortality ; Coronary heart disease ; Czech Republic - epidemiology ; DNA Mutational Analysis ; Emergency and intensive care: neonates and children. Prematurity. Sudden death ; Female ; Genetic Predisposition to Disease - epidemiology ; Genetic Predisposition to Disease - genetics ; Heart ; Humans ; Incidence ; Intensive care medicine ; ion channel ; Male ; Medical sciences ; Middle Aged ; mutation ; Polymorphism, Single Nucleotide - genetics ; Potassium Channels - genetics ; Risk Assessment ; Risk Factors ; sudden death ; Survival Analysis ; Survival Rate ; Survivors ; ventricular fibrillation ; Ventricular Fibrillation - genetics ; Ventricular Fibrillation - mortality</subject><ispartof>Pacing and clinical electrophysiology, 2011-06, Vol.34 (6), p.742-749</ispartof><rights>2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4375-54466f78d4710bb75b62bcf6538a6ccf00d044a388057c935ec35f019687e55a3</citedby><cites>FETCH-LOGICAL-c4375-54466f78d4710bb75b62bcf6538a6ccf00d044a388057c935ec35f019687e55a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1540-8159.2011.03045.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1540-8159.2011.03045.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24242599$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21410720$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NOVOTNY, TOMAS</creatorcontrib><creatorcontrib>KADLECOVA, JITKA</creatorcontrib><creatorcontrib>RAUDENSKA, MARTINA</creatorcontrib><creatorcontrib>BITTNEROVA, ALEXANDRA</creatorcontrib><creatorcontrib>ANDRSOVA, IRENA</creatorcontrib><creatorcontrib>FLORIANOVA, ALENA</creatorcontrib><creatorcontrib>VASKU, ANNA</creatorcontrib><creatorcontrib>NEUGEBAUER, PETR</creatorcontrib><creatorcontrib>KOZAK, MILAN</creatorcontrib><creatorcontrib>SEPSI, MILAN</creatorcontrib><creatorcontrib>KRIVAN, LUBOMIR</creatorcontrib><creatorcontrib>GAILLYOVA, RENATA</creatorcontrib><creatorcontrib>SPINAR, JINDRICH</creatorcontrib><title>Mutation Analysis Ion Channel Genes Ventricular Fibrillation Survivors with Coronary Artery Disease</title><title>Pacing and clinical electrophysiology</title><addtitle>Pacing Clin Electrophysiol</addtitle><description>Background: Observations from population‐based studies demonstrated a strong genetic component of sudden cardiac death. The aim of this study was to test the hypothesis that ion channel genes mutations are more common in ventricular fibrillation (VF) survivors with coronary artery disease (CAD) compared to controls.
Methods: The entire coding sequence of KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 genes was analyzed in 45 (five females) CAD individuals—survivors of documented VF and in 90 matched healthy controls. In another control group of 141 matched patients with CAD without malignant arrhythmias, the exons containing rare coding variants found in the VF survivors were sequenced.
Results: The carrier frequency of all the rare sequence variants was significantly higher in the VF survivors (8/45, 17.8%) than in CAD controls (3/141, 2.2%, P = 0.001). In VF survivors, four coding variants in eight individuals were found. Three in KCNH2 gene: R148W and GAG186del are novel; P347S was previously related to long QT syndrome. In SCN5A gene, P2006A variant was found in five unrelated males. This variant has been demonstrated previously to have small effect on sodium channel kinetics. No rare coding variants were found in the healthy controls. The P2006A variant was found in three CAD controls.
Conclusion: The prevalence of selected, rare coding variants in five long QT genes was significantly higher in cases versus controls, confirming a mechanistic role for these genes among a subgroup of patients with coronary disease and VF. (PACE 2011; 742–749)</description><subject>Aged</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Comorbidity</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary Artery Disease - mortality</subject><subject>Coronary heart disease</subject><subject>Czech Republic - epidemiology</subject><subject>DNA Mutational Analysis</subject><subject>Emergency and intensive care: neonates and children. Prematurity. Sudden death</subject><subject>Female</subject><subject>Genetic Predisposition to Disease - epidemiology</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Heart</subject><subject>Humans</subject><subject>Incidence</subject><subject>Intensive care medicine</subject><subject>ion channel</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>mutation</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Potassium Channels - genetics</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>sudden death</subject><subject>Survival Analysis</subject><subject>Survival Rate</subject><subject>Survivors</subject><subject>ventricular fibrillation</subject><subject>Ventricular Fibrillation - genetics</subject><subject>Ventricular Fibrillation - mortality</subject><issn>0147-8389</issn><issn>1540-8159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkEFv0zAUxy0EYmXwFZAviFOy59qOnQtSla1l0iiTGHC0HNfRXFJn2MnWfnucpZQr9uHZ8u_9_fRDCBPISVoX25xwBpkkvMznQEgOFBjP9y_Q7PTwEs2AMJFJKssz9CbGLQAUCXuNzuaEERBzmCHzZeh17zqPF163h-givk6X6l57b1u8st5G_MP6PjgztDrgpauDa9up59sQHt1jFyJ-cv09rrrQeR0OeBF6m8qli1ZH-xa9anQb7btjPUffl1d31efs5uvqulrcZIZRwTPOWFE0Qm6YIFDXgtfFvDZNwanUhTENwAYY01RK4MKUlFtDeQOkLKSwnGt6jj5OuQ-h-z3Y2Kudi8amYb3thqikIISTUhaJlBNpQhdjsI16CG6XJlcE1GhYbdUoUo0i1WhYPRtW-9T6_vjJUO_s5tT4V2kCPhwBHY1um6C9cfEfx9LmZZm4TxP35Fp7-O8B1O2iuhqPKSCbAlzs7f4UoMMvVYgkVP1crxS_K2_XcLlUa_oH0fOl-g</recordid><startdate>201106</startdate><enddate>201106</enddate><creator>NOVOTNY, TOMAS</creator><creator>KADLECOVA, JITKA</creator><creator>RAUDENSKA, MARTINA</creator><creator>BITTNEROVA, ALEXANDRA</creator><creator>ANDRSOVA, IRENA</creator><creator>FLORIANOVA, ALENA</creator><creator>VASKU, ANNA</creator><creator>NEUGEBAUER, PETR</creator><creator>KOZAK, MILAN</creator><creator>SEPSI, MILAN</creator><creator>KRIVAN, LUBOMIR</creator><creator>GAILLYOVA, RENATA</creator><creator>SPINAR, JINDRICH</creator><general>Blackwell Publishing Inc</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201106</creationdate><title>Mutation Analysis Ion Channel Genes Ventricular Fibrillation Survivors with Coronary Artery Disease</title><author>NOVOTNY, TOMAS ; KADLECOVA, JITKA ; RAUDENSKA, MARTINA ; BITTNEROVA, ALEXANDRA ; ANDRSOVA, IRENA ; FLORIANOVA, ALENA ; VASKU, ANNA ; NEUGEBAUER, PETR ; KOZAK, MILAN ; SEPSI, MILAN ; KRIVAN, LUBOMIR ; GAILLYOVA, RENATA ; SPINAR, JINDRICH</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4375-54466f78d4710bb75b62bcf6538a6ccf00d044a388057c935ec35f019687e55a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aged</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Comorbidity</topic><topic>Coronary Artery Disease - genetics</topic><topic>Coronary Artery Disease - mortality</topic><topic>Coronary heart disease</topic><topic>Czech Republic - epidemiology</topic><topic>DNA Mutational Analysis</topic><topic>Emergency and intensive care: neonates and children. Prematurity. Sudden death</topic><topic>Female</topic><topic>Genetic Predisposition to Disease - epidemiology</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Heart</topic><topic>Humans</topic><topic>Incidence</topic><topic>Intensive care medicine</topic><topic>ion channel</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>mutation</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Potassium Channels - genetics</topic><topic>Risk Assessment</topic><topic>Risk Factors</topic><topic>sudden death</topic><topic>Survival Analysis</topic><topic>Survival Rate</topic><topic>Survivors</topic><topic>ventricular fibrillation</topic><topic>Ventricular Fibrillation - genetics</topic><topic>Ventricular Fibrillation - mortality</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NOVOTNY, TOMAS</creatorcontrib><creatorcontrib>KADLECOVA, JITKA</creatorcontrib><creatorcontrib>RAUDENSKA, MARTINA</creatorcontrib><creatorcontrib>BITTNEROVA, ALEXANDRA</creatorcontrib><creatorcontrib>ANDRSOVA, IRENA</creatorcontrib><creatorcontrib>FLORIANOVA, ALENA</creatorcontrib><creatorcontrib>VASKU, ANNA</creatorcontrib><creatorcontrib>NEUGEBAUER, PETR</creatorcontrib><creatorcontrib>KOZAK, MILAN</creatorcontrib><creatorcontrib>SEPSI, MILAN</creatorcontrib><creatorcontrib>KRIVAN, LUBOMIR</creatorcontrib><creatorcontrib>GAILLYOVA, RENATA</creatorcontrib><creatorcontrib>SPINAR, JINDRICH</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Pacing and clinical electrophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NOVOTNY, TOMAS</au><au>KADLECOVA, JITKA</au><au>RAUDENSKA, MARTINA</au><au>BITTNEROVA, ALEXANDRA</au><au>ANDRSOVA, IRENA</au><au>FLORIANOVA, ALENA</au><au>VASKU, ANNA</au><au>NEUGEBAUER, PETR</au><au>KOZAK, MILAN</au><au>SEPSI, MILAN</au><au>KRIVAN, LUBOMIR</au><au>GAILLYOVA, RENATA</au><au>SPINAR, JINDRICH</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mutation Analysis Ion Channel Genes Ventricular Fibrillation Survivors with Coronary Artery Disease</atitle><jtitle>Pacing and clinical electrophysiology</jtitle><addtitle>Pacing Clin Electrophysiol</addtitle><date>2011-06</date><risdate>2011</risdate><volume>34</volume><issue>6</issue><spage>742</spage><epage>749</epage><pages>742-749</pages><issn>0147-8389</issn><eissn>1540-8159</eissn><abstract>Background: Observations from population‐based studies demonstrated a strong genetic component of sudden cardiac death. The aim of this study was to test the hypothesis that ion channel genes mutations are more common in ventricular fibrillation (VF) survivors with coronary artery disease (CAD) compared to controls.
Methods: The entire coding sequence of KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 genes was analyzed in 45 (five females) CAD individuals—survivors of documented VF and in 90 matched healthy controls. In another control group of 141 matched patients with CAD without malignant arrhythmias, the exons containing rare coding variants found in the VF survivors were sequenced.
Results: The carrier frequency of all the rare sequence variants was significantly higher in the VF survivors (8/45, 17.8%) than in CAD controls (3/141, 2.2%, P = 0.001). In VF survivors, four coding variants in eight individuals were found. Three in KCNH2 gene: R148W and GAG186del are novel; P347S was previously related to long QT syndrome. In SCN5A gene, P2006A variant was found in five unrelated males. This variant has been demonstrated previously to have small effect on sodium channel kinetics. No rare coding variants were found in the healthy controls. The P2006A variant was found in three CAD controls.
Conclusion: The prevalence of selected, rare coding variants in five long QT genes was significantly higher in cases versus controls, confirming a mechanistic role for these genes among a subgroup of patients with coronary disease and VF. (PACE 2011; 742–749)</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>21410720</pmid><doi>10.1111/j.1540-8159.2011.03045.x</doi><tpages>8</tpages></addata></record> |
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| subjects | Aged Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences Cardiac dysrhythmias Cardiology. Vascular system Comorbidity Coronary Artery Disease - genetics Coronary Artery Disease - mortality Coronary heart disease Czech Republic - epidemiology DNA Mutational Analysis Emergency and intensive care: neonates and children. Prematurity. Sudden death Female Genetic Predisposition to Disease - epidemiology Genetic Predisposition to Disease - genetics Heart Humans Incidence Intensive care medicine ion channel Male Medical sciences Middle Aged mutation Polymorphism, Single Nucleotide - genetics Potassium Channels - genetics Risk Assessment Risk Factors sudden death Survival Analysis Survival Rate Survivors ventricular fibrillation Ventricular Fibrillation - genetics Ventricular Fibrillation - mortality |
| title | Mutation Analysis Ion Channel Genes Ventricular Fibrillation Survivors with Coronary Artery Disease |
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