Mother rotors and fibrillatory conduction: a mechanism of atrial fibrillation
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and the major cardiac cause of stroke. Recent studies in patients with paroxysmal AF have shown that the arrhythmia is triggered by focal sources localized usually in one of the cardiac veins. However, in chronic AF, the prevai...
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Veröffentlicht in: | Cardiovascular research 2002-05, Vol.54 (2), p.204-216 |
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creator | Jalife, José Berenfeld, Omer Mansour, Moussa |
description | Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and the major cardiac cause of stroke. Recent studies in patients with paroxysmal AF have shown that the arrhythmia is triggered by focal sources localized usually in one of the cardiac veins. However, in chronic AF, the prevailing theory is that multiple random wavelets of activation coexist to create an unorganized atrial rhythm. Experiments in isolated hearts have demonstrated that stable, self-sustained rotors can exist in the atria and that high frequency activation by such rotors results in the complex patterns of activation that characterize AF. Studies in animals and patients support the view that at least some cases of paroxysmal and chronic AF are the result of the uninterrupted periodic activity of discrete reentrant sites. In this brief review article, we examine historical data and more recent experimental evidence behind the hypothesis that AF may be organized by one, or a small number of high-frequency reentrant sources localized in the left atrium. We then discuss the potential implications and evidence supporting such a hypothesis for human AF. Finally, we suggest future studies designed to unravel the detailed molecular, cellular and pathophysiological mechanisms responsible for AF initiation and maintenance. The work discussed may open potentially exciting new diagnostic and therapeutic possibilities. |
doi_str_mv | 10.1016/s0008-6363(02)00223-7 |
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Recent studies in patients with paroxysmal AF have shown that the arrhythmia is triggered by focal sources localized usually in one of the cardiac veins. However, in chronic AF, the prevailing theory is that multiple random wavelets of activation coexist to create an unorganized atrial rhythm. Experiments in isolated hearts have demonstrated that stable, self-sustained rotors can exist in the atria and that high frequency activation by such rotors results in the complex patterns of activation that characterize AF. Studies in animals and patients support the view that at least some cases of paroxysmal and chronic AF are the result of the uninterrupted periodic activity of discrete reentrant sites. In this brief review article, we examine historical data and more recent experimental evidence behind the hypothesis that AF may be organized by one, or a small number of high-frequency reentrant sources localized in the left atrium. We then discuss the potential implications and evidence supporting such a hypothesis for human AF. Finally, we suggest future studies designed to unravel the detailed molecular, cellular and pathophysiological mechanisms responsible for AF initiation and maintenance. 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Recent studies in patients with paroxysmal AF have shown that the arrhythmia is triggered by focal sources localized usually in one of the cardiac veins. However, in chronic AF, the prevailing theory is that multiple random wavelets of activation coexist to create an unorganized atrial rhythm. Experiments in isolated hearts have demonstrated that stable, self-sustained rotors can exist in the atria and that high frequency activation by such rotors results in the complex patterns of activation that characterize AF. Studies in animals and patients support the view that at least some cases of paroxysmal and chronic AF are the result of the uninterrupted periodic activity of discrete reentrant sites. In this brief review article, we examine historical data and more recent experimental evidence behind the hypothesis that AF may be organized by one, or a small number of high-frequency reentrant sources localized in the left atrium. We then discuss the potential implications and evidence supporting such a hypothesis for human AF. Finally, we suggest future studies designed to unravel the detailed molecular, cellular and pathophysiological mechanisms responsible for AF initiation and maintenance. The work discussed may open potentially exciting new diagnostic and therapeutic possibilities.</description><subject>Acetylcholine</subject><subject>Animals</subject><subject>Atrial Fibrillation - etiology</subject><subject>Atrial Fibrillation - pathology</subject><subject>Atrial Fibrillation - physiopathology</subject><subject>Atrial Flutter - physiopathology</subject><subject>Atrial Function, Left</subject><subject>Chronic Disease</subject><subject>Dogs</subject><subject>Electric Stimulation</subject><subject>Electrocardiography</subject><subject>Evoked Potentials, Motor</subject><subject>Heart Atria - pathology</subject><subject>Humans</subject><subject>Perfusion</subject><subject>Pulmonary Veins</subject><subject>Research Design</subject><subject>Vagus Nerve</subject><issn>0008-6363</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkM1OwzAQhH0A0VJ4BJBPCA4Br53ECTdU8Se14gCcrY2zUYOSuNjJoW9PQis4rXY0szv6GLsAcQsC0rsghMiiVKXqWsgbIaRUkT5i8z95xk5D-BrXJNHxCZuBFKlUUs_Zeu36DXnuXe984NiVvKoLXzcNjsKOW9eVg-1r191z5C3ZDXZ1aLmrOPa-xubfPnrO2HGFTaDzw1ywz6fHj-VLtHp7fl0-rCIba9FHBSiBOWEel6RyDaCUBBJk9dgLUZLIMokSAOK4AgRNZDFByFJRUBlXasGu9ne33n0PFHrT1sHS2KIjNwSjIRvB5Ho0Jnuj9S4ET5XZ-rpFvzMgzMTOvE-QzATJCGl-2Zkpd3l4MBQtlf-pAzj1AwqQbIc</recordid><startdate>20020501</startdate><enddate>20020501</enddate><creator>Jalife, José</creator><creator>Berenfeld, Omer</creator><creator>Mansour, Moussa</creator><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>20020501</creationdate><title>Mother rotors and fibrillatory conduction: a mechanism of atrial fibrillation</title><author>Jalife, José ; Berenfeld, Omer ; Mansour, Moussa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-b130a9ea94de397113321e0ec7206aa2e0882a211144f1a17eeca5a1860bed4f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Acetylcholine</topic><topic>Animals</topic><topic>Atrial Fibrillation - etiology</topic><topic>Atrial Fibrillation - pathology</topic><topic>Atrial Fibrillation - physiopathology</topic><topic>Atrial Flutter - physiopathology</topic><topic>Atrial Function, Left</topic><topic>Chronic Disease</topic><topic>Dogs</topic><topic>Electric Stimulation</topic><topic>Electrocardiography</topic><topic>Evoked Potentials, Motor</topic><topic>Heart Atria - pathology</topic><topic>Humans</topic><topic>Perfusion</topic><topic>Pulmonary Veins</topic><topic>Research Design</topic><topic>Vagus Nerve</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jalife, José</creatorcontrib><creatorcontrib>Berenfeld, Omer</creatorcontrib><creatorcontrib>Mansour, Moussa</creatorcontrib><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>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jalife, José</au><au>Berenfeld, Omer</au><au>Mansour, Moussa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mother rotors and fibrillatory conduction: a mechanism of atrial fibrillation</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2002-05-01</date><risdate>2002</risdate><volume>54</volume><issue>2</issue><spage>204</spage><epage>216</epage><pages>204-216</pages><issn>0008-6363</issn><abstract>Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and the major cardiac cause of stroke. Recent studies in patients with paroxysmal AF have shown that the arrhythmia is triggered by focal sources localized usually in one of the cardiac veins. However, in chronic AF, the prevailing theory is that multiple random wavelets of activation coexist to create an unorganized atrial rhythm. Experiments in isolated hearts have demonstrated that stable, self-sustained rotors can exist in the atria and that high frequency activation by such rotors results in the complex patterns of activation that characterize AF. Studies in animals and patients support the view that at least some cases of paroxysmal and chronic AF are the result of the uninterrupted periodic activity of discrete reentrant sites. In this brief review article, we examine historical data and more recent experimental evidence behind the hypothesis that AF may be organized by one, or a small number of high-frequency reentrant sources localized in the left atrium. 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source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Acetylcholine Animals Atrial Fibrillation - etiology Atrial Fibrillation - pathology Atrial Fibrillation - physiopathology Atrial Flutter - physiopathology Atrial Function, Left Chronic Disease Dogs Electric Stimulation Electrocardiography Evoked Potentials, Motor Heart Atria - pathology Humans Perfusion Pulmonary Veins Research Design Vagus Nerve |
title | Mother rotors and fibrillatory conduction: a mechanism of atrial fibrillation |
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