Factors Predisposing to the Development of Atrial Fibrillation
Identifieur interne : 001877 ( Istex/Corpus ); précédent : 001876; suivant : 001878Factors Predisposing to the Development of Atrial Fibrillation
Auteurs : Samuel LévySource :
- Pacing and Clinical Electrophysiology [ 0147-8389 ] ; 1997-10.
English descriptors
- KwdEn :
Abstract
Atrial fibrillation (AF) is in most patients (approximately 70%) associated with organic heart disease including valvular heart disease, coronary artery disease, hypertension, hypertrophic cardiomyopathy, dilated cardiomyopathy, and congenital heart disease, mostly atrial septal defect in adults. In many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (without mitral regurgitation), calcifications of the mitral annulus, atrial myxoma, pheochomocytoma, and idiopathic dilated right atrium may present with AF. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so‐called “lone AF”, in about 30% of cases. The term “idiopathic AF” implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolff‐Parkinson‐White syndrome), only to mention a few of other uncommon causes of AF. The autonomous nervous system may contribute to the occurrence of AF in some patients. AF occurs commonly. In patients with valvular heart disease, AF is common, particularly when the mitral valve is involved. The occurrence of AF is unrelated to the severity of mitral stenosis or mitral regurgitation but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, AF occurs predominantly in older patients, males, and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. The risk of the development of AF, in an individual patient, is often difficult to assess. Increasing age, presence of valvular heart disease, and congestive heart failure increase the risk of atrial fibrillation.
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DOI: 10.1111/j.1540-8159.1997.tb06115.x
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In many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (without mitral regurgitation), calcifications of the mitral annulus, atrial myxoma, pheochomocytoma, and idiopathic dilated right atrium may present with AF. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so‐called “lone AF”, in about 30% of cases. The term “idiopathic AF” implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolff‐Parkinson‐White syndrome), only to mention a few of other uncommon causes of AF. The autonomous nervous system may contribute to the occurrence of AF in some patients. AF occurs commonly. In patients with valvular heart disease, AF is common, particularly when the mitral valve is involved. The occurrence of AF is unrelated to the severity of mitral stenosis or mitral regurgitation but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, AF occurs predominantly in older patients, males, and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. The risk of the development of AF, in an individual patient, is often difficult to assess. Increasing age, presence of valvular heart disease, and congestive heart failure increase the risk of atrial fibrillation.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>SAMUEL LÉVY</name><affiliations><json:string>University of Marseille, School of Medicine, Chief Cardiology Division, Hopital Nord, Marseille, France</json:string><json:string>Address for reprints: Professor Samuel Lévy, M.D., Division of Cardiology, Hôpital Nord, 13015 Marseille, France. Fax: 33‐4‐9196‐2162.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>atrial fibrillation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>predisposing factors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>valvular heart disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>coronary artery disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cardiomyopathy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>heart failure</value></json:item></subject><articleId><json:string>PACE2670</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Atrial fibrillation (AF) is in most patients (approximately 70%) associated with organic heart disease including valvular heart disease, coronary artery disease, hypertension, hypertrophic cardiomyopathy, dilated cardiomyopathy, and congenital heart disease, mostly atrial septal defect in adults. In many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (without mitral regurgitation), calcifications of the mitral annulus, atrial myxoma, pheochomocytoma, and idiopathic dilated right atrium may present with AF. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so‐called “lone AF”, in about 30% of cases. The term “idiopathic AF” implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolff‐Parkinson‐White syndrome), only to mention a few of other uncommon causes of AF. The autonomous nervous system may contribute to the occurrence of AF in some patients. AF occurs commonly. In patients with valvular heart disease, AF is common, particularly when the mitral valve is involved. The occurrence of AF is unrelated to the severity of mitral stenosis or mitral regurgitation but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, AF occurs predominantly in older patients, males, and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. The risk of the development of AF, in an individual patient, is often difficult to assess. Increasing age, presence of valvular heart disease, and congestive heart failure increase the risk of atrial fibrillation.</abstract><qualityIndicators><score>7.443</score><pdfVersion>1.6</pdfVersion><pdfPageSize>568 x 793 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>2012</abstractCharCount><pdfWordCount>2943</pdfWordCount><pdfCharCount>18434</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>283</abstractWordCount></qualityIndicators><title>Factors Predisposing to the Development of Atrial Fibrillation</title><refBibs><json:item><author><json:item><name>S Lévy</name></json:item><json:item><name>P Novella</name></json:item><json:item><name>PH Ricard</name></json:item></author><host><volume>6</volume><pages><last>74</last><first>69</first></pages><author></author><title>J Cardiovasc Electrophysiol</title></host><title>Paroxysmal atrial fibrillation: A need for classification</title></json:item><json:item><author><json:item><name>N. 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Prospective study including 251 patients</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>20</volume><publisherId><json:string>PACE</json:string></publisherId><pages><total>5</total><last>2674</last><first>2670</first></pages><issn><json:string>0147-8389</json:string></issn><issue>10</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1540-8159</json:string></eissn><title>Pacing and Clinical Electrophysiology</title><doi><json:string>10.1111/(ISSN)1540-8159</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>engineering, biomedical</json:string><json:string>cardiac & cardiovascular systems</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>cardiovascular system & hematology</json:string></scienceMetrix></categories><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1111/j.1540-8159.1997.tb06115.x</json:string></doi><id>76E0A6803DB551B9B1F27073E282420C7B553ADB</id><score>0.20566048</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/76E0A6803DB551B9B1F27073E282420C7B553ADB/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/76E0A6803DB551B9B1F27073E282420C7B553ADB/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/76E0A6803DB551B9B1F27073E282420C7B553ADB/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Factors Predisposing to the Development of Atrial Fibrillation</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1997</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Factors Predisposing to the Development of Atrial Fibrillation</title><author xml:id="author-1"><persName><forename type="first">SAMUEL</forename><surname>LÉVY</surname></persName><affiliation>University of Marseille, School of Medicine, Chief Cardiology Division, Hopital Nord, Marseille, France</affiliation><affiliation>Address for reprints: Professor Samuel Lévy, M.D., Division of Cardiology, Hôpital Nord, 13015 Marseille, France. Fax: 33‐4‐9196‐2162.</affiliation></author></analytic><monogr><title level="j">Pacing and Clinical Electrophysiology</title><idno type="pISSN">0147-8389</idno><idno type="eISSN">1540-8159</idno><idno type="DOI">10.1111/(ISSN)1540-8159</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1997-10"></date><biblScope unit="volume">20</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="2670">2670</biblScope><biblScope unit="page" to="2674">2674</biblScope></imprint></monogr><idno type="istex">76E0A6803DB551B9B1F27073E282420C7B553ADB</idno><idno type="DOI">10.1111/j.1540-8159.1997.tb06115.x</idno><idno type="ArticleID">PACE2670</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Atrial fibrillation (AF) is in most patients (approximately 70%) associated with organic heart disease including valvular heart disease, coronary artery disease, hypertension, hypertrophic cardiomyopathy, dilated cardiomyopathy, and congenital heart disease, mostly atrial septal defect in adults. In many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (without mitral regurgitation), calcifications of the mitral annulus, atrial myxoma, pheochomocytoma, and idiopathic dilated right atrium may present with AF. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so‐called “lone AF”, in about 30% of cases. The term “idiopathic AF” implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolff‐Parkinson‐White syndrome), only to mention a few of other uncommon causes of AF. The autonomous nervous system may contribute to the occurrence of AF in some patients. AF occurs commonly. In patients with valvular heart disease, AF is common, particularly when the mitral valve is involved. The occurrence of AF is unrelated to the severity of mitral stenosis or mitral regurgitation but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, AF occurs predominantly in older patients, males, and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. The risk of the development of AF, in an individual patient, is often difficult to assess. Increasing age, presence of valvular heart disease, and congestive heart failure increase the risk of atrial fibrillation.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>atrial fibrillation</term></item><item><term>predisposing factors</term></item><item><term>valvular heart disease</term></item><item><term>coronary artery disease</term></item><item><term>cardiomyopathy</term></item><item><term>heart failure</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/76E0A6803DB551B9B1F27073E282420C7B553ADB/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1540-8159</doi><issn type="print">0147-8389</issn><issn type="electronic">1540-8159</issn><idGroup><id type="product" value="PACE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="PACING CLINICAL ELECTROPHYSIOLOGY">Pacing and Clinical Electrophysiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="10010"><doi origin="wiley">10.1111/pace.1997.20.issue-10</doi><numberingGroup><numbering type="journalVolume" number="20">20</numbering><numbering type="journalIssue" number="10">10</numbering></numberingGroup><coverDate startDate="1997-10">October 1997</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0267000" status="forIssue"><doi origin="wiley">10.1111/j.1540-8159.1997.tb06115.x</doi><idGroup><id type="unit" value="PACE2670"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="tocHeading1">CLINICAL APPLICATIONS</title></titleGroup><eventGroup><event type="firstOnline" date="2006-06-30"></event><event type="publishedOnlineFinalForm" date="2006-06-30"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:HeaderRef result:HeaderRef" date="2010-04-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-06"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="2670">2670</numbering><numbering type="pageLast" number="2674">2674</numbering></numberingGroup><correspondenceTo>Address for reprints: Professor Samuel Lévy, M.D., Division of Cardiology, Hôpital Nord, 13015 Marseille, France. Fax: 33‐4‐9196‐2162.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:PACE.PACE2670.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received February 20, 1997; revised April 24, 1997; accepted April 28, 1997.</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="27"></count><count type="linksCrossRef" number="2"></count></countGroup><titleGroup><title type="main">Factors Predisposing to the Development of Atrial Fibrillation</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>SAMUEL</givenNames><familyName>LÉVY</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="FR"><unparsedAffiliation>University of Marseille, School of Medicine, Chief Cardiology Division, Hopital Nord, Marseille, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">atrial fibrillation</keyword><keyword xml:id="k2">predisposing factors</keyword><keyword xml:id="k3">valvular heart disease</keyword><keyword xml:id="k4">coronary artery disease</keyword><keyword xml:id="k5">cardiomyopathy</keyword><keyword xml:id="k6">heart failure</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Atrial fibrillation (AF) is in most patients (approximately 70%) associated with organic heart disease including valvular heart disease, coronary artery disease, hypertension, hypertrophic cardiomyopathy, dilated cardiomyopathy, and congenital heart disease, mostly atrial septal defect in adults. In many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (without mitral regurgitation), calcifications of the mitral annulus, atrial myxoma, pheochomocytoma, and idiopathic dilated right atrium may present with AF. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so‐called “lone AF”, in about 30% of cases. The term “idiopathic AF” implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolff‐Parkinson‐White syndrome), only to mention a few of other uncommon causes of AF. The autonomous nervous system may contribute to the occurrence of AF in some patients. AF occurs commonly. In patients with valvular heart disease, AF is common, particularly when the mitral valve is involved. The occurrence of AF is unrelated to the severity of mitral stenosis or mitral regurgitation but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, AF occurs predominantly in older patients, males, and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. The risk of the development of AF, in an individual patient, is often difficult to assess. Increasing age, presence of valvular heart disease, and congestive heart failure increase the risk of atrial fibrillation.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Factors Predisposing to the Development of Atrial Fibrillation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Factors Predisposing to the Development of Atrial Fibrillation</title></titleInfo><name type="personal"><namePart type="given">SAMUEL</namePart><namePart type="family">LÉVY</namePart><affiliation>University of Marseille, School of Medicine, Chief Cardiology Division, Hopital Nord, Marseille, France</affiliation><affiliation>Address for reprints: Professor Samuel Lévy, M.D., Division of Cardiology, Hôpital Nord, 13015 Marseille, France. Fax: 33‐4‐9196‐2162.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1997-10</dateIssued><edition>Received February 20, 1997; revised April 24, 1997; accepted April 28, 1997.</edition><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">27</extent></physicalDescription><abstract lang="en">Atrial fibrillation (AF) is in most patients (approximately 70%) associated with organic heart disease including valvular heart disease, coronary artery disease, hypertension, hypertrophic cardiomyopathy, dilated cardiomyopathy, and congenital heart disease, mostly atrial septal defect in adults. In many chronic conditions, determining whether AF is the result or is unrelated to the underlying heart disease, remains unclear. The list of possible etiologies also include cardiac amyloidosis, hemochromatosis and endomyocardial fibrosis. Other heart diseases, such as mitral valve prolapse (without mitral regurgitation), calcifications of the mitral annulus, atrial myxoma, pheochomocytoma, and idiopathic dilated right atrium may present with AF. Atrial fibrillation may occur in the absence of detectable organic heart disease, the so‐called “lone AF”, in about 30% of cases. The term “idiopathic AF” implies the absence of any detectable etiology including hyperthyroidism, chronic obstructive lung disease, overt sinus node dysfunction, and overt or concealed preexcitation (Wolff‐Parkinson‐White syndrome), only to mention a few of other uncommon causes of AF. The autonomous nervous system may contribute to the occurrence of AF in some patients. AF occurs commonly. In patients with valvular heart disease, AF is common, particularly when the mitral valve is involved. The occurrence of AF is unrelated to the severity of mitral stenosis or mitral regurgitation but is more common in patients with enlarged left atrium and congestive heart failure. In patients with coronary artery disease, AF occurs predominantly in older patients, males, and patients with left ventricular dysfunction. Important predictive factors of AF include hypertension, left ventricular hypertrophy and diabetes. The risk of the development of AF, in an individual patient, is often difficult to assess. Increasing age, presence of valvular heart disease, and congestive heart failure increase the risk of atrial fibrillation.</abstract><subject lang="en"><genre>keywords</genre><topic>atrial fibrillation</topic><topic>predisposing factors</topic><topic>valvular heart disease</topic><topic>coronary artery disease</topic><topic>cardiomyopathy</topic><topic>heart failure</topic></subject><relatedItem type="host"><titleInfo><title>Pacing and Clinical Electrophysiology</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0147-8389</identifier><identifier type="eISSN">1540-8159</identifier><identifier type="DOI">10.1111/(ISSN)1540-8159</identifier><identifier type="PublisherID">PACE</identifier><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>2670</start><end>2674</end><total>5</total></extent></part></relatedItem><identifier type="istex">76E0A6803DB551B9B1F27073E282420C7B553ADB</identifier><identifier type="DOI">10.1111/j.1540-8159.1997.tb06115.x</identifier><identifier type="ArticleID">PACE2670</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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