Anatomically determined functional conduction delay in the posterior left atrium relationship to structural heart disease
This study sought to characterize the conduction properties of the posterior left atrium (PLA) in patients with different forms of structural heart disease undergoing cardiac surgery. The PLA plays an important role in the initiation and maintenance of atrial fibrillation. This study included 34 pat...
Gespeichert in:
Veröffentlicht in: | Journal of the American College of Cardiology 2008-02, Vol.51 (8), p.856-862 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 862 |
---|---|
container_issue | 8 |
container_start_page | 856 |
container_title | Journal of the American College of Cardiology |
container_volume | 51 |
creator | Roberts-Thomson, Kurt C Stevenson, Irene H Kistler, Peter M Haqqani, Haris M Goldblatt, John C Sanders, Prashanthan Kalman, Jonathan M |
description | This study sought to characterize the conduction properties of the posterior left atrium (PLA) in patients with different forms of structural heart disease undergoing cardiac surgery.
The PLA plays an important role in the initiation and maintenance of atrial fibrillation.
This study included 34 patients having elective cardiac surgery. There were 4 groups of patients: normal left ventricular (LV) function (coronary artery bypass grafting [CABG]); severe LV dysfunction (LVF/CABG); severe mitral regurgitation (MR); severe aortic stenosis (AS). Epicardial mapping of the PLA was performed in sinus rhythm and during differential pacing. Activation patterns, regional conduction velocity (CV), conduction heterogeneity, anisotropy, and total plaque activation time (TAT) were assessed.
Left atrial size in patients with LVF/CABG (47 +/- 7 mm) and MR (54 +/- 6 mm) was larger than patients with CABG (39 +/- 7 mm) and AS (42 +/- 6 mm; p < 0.05). During pacing, all patients developed a vertical line of conduction delay running between the pulmonary veins. The extent of this conduction delay was greater in patients with LVF/CABG and MR than patients with AS and CABG (p < 0.05). Conduction heterogeneity, anisotropy, and TAT were greater in patients with LVF/CABG and MR than patients with CABG (p < 0.05). These changes resulted in circuitous wave front propagation.
There is a line of functional conduction delay in a consistent anatomical location in the PLA in patients with structural heart disease. This is most marked in conditions associated with significant chronic atrial enlargement and leads to circuitous wave front propagation, suggesting a potential role in arrhythmogenesis. |
doi_str_mv | 10.1016/j.jacc.2007.11.037 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_70326884</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>70326884</sourcerecordid><originalsourceid>FETCH-LOGICAL-h271t-f5289284fbef2a7dcf05b0858253e116b6893ff0245a917960bcdc6ca6fa89fc3</originalsourceid><addsrcrecordid>eNpd0EtLxDAUBeAgijOO_gEXEhDctd6kk9dyEF8w4EbXJU0TmqFtxiRdzL-36rhxdbnwnbM4CF0TKAkQfr8rd9qYkgKIkpASKnGCloQxWVRMiVO0BFGxgoASC3SR0g4AuCTqHC2IpGrNBF2iw2bUOQze6L4_4NZmGwc_2ha7aTTZh1H32ISxnX6eGfT6gP2Ic2fxPqSZ-xBxb13GOkc_DTjO5Numzu9xDjjlOIenOBd1VseMW5-sTvYSnTndJ3t1vCv08fT4_vBSbN-eXx8226KjguTCMSoVlWvXWEe1aI0D1oBkkrLKEsIbLlXlHNA104oIxaExreFGc6elcqZaobvf3n0Mn5NNuR58Mrbv9WjDlGoBFeVSrmd4-w_uwhTnAVJNGHCiBAc5q5ujmprBtvU--kHHQ_03afUFHH58Yg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1506197608</pqid></control><display><type>article</type><title>Anatomically determined functional conduction delay in the posterior left atrium relationship to structural heart disease</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Roberts-Thomson, Kurt C ; Stevenson, Irene H ; Kistler, Peter M ; Haqqani, Haris M ; Goldblatt, John C ; Sanders, Prashanthan ; Kalman, Jonathan M</creator><creatorcontrib>Roberts-Thomson, Kurt C ; Stevenson, Irene H ; Kistler, Peter M ; Haqqani, Haris M ; Goldblatt, John C ; Sanders, Prashanthan ; Kalman, Jonathan M</creatorcontrib><description>This study sought to characterize the conduction properties of the posterior left atrium (PLA) in patients with different forms of structural heart disease undergoing cardiac surgery.
The PLA plays an important role in the initiation and maintenance of atrial fibrillation.
This study included 34 patients having elective cardiac surgery. There were 4 groups of patients: normal left ventricular (LV) function (coronary artery bypass grafting [CABG]); severe LV dysfunction (LVF/CABG); severe mitral regurgitation (MR); severe aortic stenosis (AS). Epicardial mapping of the PLA was performed in sinus rhythm and during differential pacing. Activation patterns, regional conduction velocity (CV), conduction heterogeneity, anisotropy, and total plaque activation time (TAT) were assessed.
Left atrial size in patients with LVF/CABG (47 +/- 7 mm) and MR (54 +/- 6 mm) was larger than patients with CABG (39 +/- 7 mm) and AS (42 +/- 6 mm; p < 0.05). During pacing, all patients developed a vertical line of conduction delay running between the pulmonary veins. The extent of this conduction delay was greater in patients with LVF/CABG and MR than patients with AS and CABG (p < 0.05). Conduction heterogeneity, anisotropy, and TAT were greater in patients with LVF/CABG and MR than patients with CABG (p < 0.05). These changes resulted in circuitous wave front propagation.
There is a line of functional conduction delay in a consistent anatomical location in the PLA in patients with structural heart disease. This is most marked in conditions associated with significant chronic atrial enlargement and leads to circuitous wave front propagation, suggesting a potential role in arrhythmogenesis.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2007.11.037</identifier><identifier>PMID: 18294572</identifier><language>eng</language><publisher>United States: Elsevier Limited</publisher><subject>Aged ; Atrial Fibrillation - etiology ; Cardiology ; Cardiovascular disease ; Coronary Artery Disease - complications ; Coronary Artery Disease - physiopathology ; Coronary Artery Disease - surgery ; Coronary vessels ; Electrophysiology ; Female ; Heart Atria - physiopathology ; Heart attacks ; Heart Conduction System - physiopathology ; Heart Valve Diseases - complications ; Heart Valve Diseases - physiopathology ; Heart Valve Diseases - surgery ; Humans ; Male ; Middle Aged ; Time Factors</subject><ispartof>Journal of the American College of Cardiology, 2008-02, Vol.51 (8), p.856-862</ispartof><rights>Copyright Elsevier Limited Feb 26, 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18294572$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Roberts-Thomson, Kurt C</creatorcontrib><creatorcontrib>Stevenson, Irene H</creatorcontrib><creatorcontrib>Kistler, Peter M</creatorcontrib><creatorcontrib>Haqqani, Haris M</creatorcontrib><creatorcontrib>Goldblatt, John C</creatorcontrib><creatorcontrib>Sanders, Prashanthan</creatorcontrib><creatorcontrib>Kalman, Jonathan M</creatorcontrib><title>Anatomically determined functional conduction delay in the posterior left atrium relationship to structural heart disease</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>This study sought to characterize the conduction properties of the posterior left atrium (PLA) in patients with different forms of structural heart disease undergoing cardiac surgery.
The PLA plays an important role in the initiation and maintenance of atrial fibrillation.
This study included 34 patients having elective cardiac surgery. There were 4 groups of patients: normal left ventricular (LV) function (coronary artery bypass grafting [CABG]); severe LV dysfunction (LVF/CABG); severe mitral regurgitation (MR); severe aortic stenosis (AS). Epicardial mapping of the PLA was performed in sinus rhythm and during differential pacing. Activation patterns, regional conduction velocity (CV), conduction heterogeneity, anisotropy, and total plaque activation time (TAT) were assessed.
Left atrial size in patients with LVF/CABG (47 +/- 7 mm) and MR (54 +/- 6 mm) was larger than patients with CABG (39 +/- 7 mm) and AS (42 +/- 6 mm; p < 0.05). During pacing, all patients developed a vertical line of conduction delay running between the pulmonary veins. The extent of this conduction delay was greater in patients with LVF/CABG and MR than patients with AS and CABG (p < 0.05). Conduction heterogeneity, anisotropy, and TAT were greater in patients with LVF/CABG and MR than patients with CABG (p < 0.05). These changes resulted in circuitous wave front propagation.
There is a line of functional conduction delay in a consistent anatomical location in the PLA in patients with structural heart disease. This is most marked in conditions associated with significant chronic atrial enlargement and leads to circuitous wave front propagation, suggesting a potential role in arrhythmogenesis.</description><subject>Aged</subject><subject>Atrial Fibrillation - etiology</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Coronary Artery Disease - complications</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Coronary Artery Disease - surgery</subject><subject>Coronary vessels</subject><subject>Electrophysiology</subject><subject>Female</subject><subject>Heart Atria - physiopathology</subject><subject>Heart attacks</subject><subject>Heart Conduction System - physiopathology</subject><subject>Heart Valve Diseases - complications</subject><subject>Heart Valve Diseases - physiopathology</subject><subject>Heart Valve Diseases - surgery</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Time Factors</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0EtLxDAUBeAgijOO_gEXEhDctd6kk9dyEF8w4EbXJU0TmqFtxiRdzL-36rhxdbnwnbM4CF0TKAkQfr8rd9qYkgKIkpASKnGCloQxWVRMiVO0BFGxgoASC3SR0g4AuCTqHC2IpGrNBF2iw2bUOQze6L4_4NZmGwc_2ha7aTTZh1H32ISxnX6eGfT6gP2Ic2fxPqSZ-xBxb13GOkc_DTjO5Numzu9xDjjlOIenOBd1VseMW5-sTvYSnTndJ3t1vCv08fT4_vBSbN-eXx8226KjguTCMSoVlWvXWEe1aI0D1oBkkrLKEsIbLlXlHNA104oIxaExreFGc6elcqZaobvf3n0Mn5NNuR58Mrbv9WjDlGoBFeVSrmd4-w_uwhTnAVJNGHCiBAc5q5ujmprBtvU--kHHQ_03afUFHH58Yg</recordid><startdate>20080226</startdate><enddate>20080226</enddate><creator>Roberts-Thomson, Kurt C</creator><creator>Stevenson, Irene H</creator><creator>Kistler, Peter M</creator><creator>Haqqani, Haris M</creator><creator>Goldblatt, John C</creator><creator>Sanders, Prashanthan</creator><creator>Kalman, Jonathan M</creator><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20080226</creationdate><title>Anatomically determined functional conduction delay in the posterior left atrium relationship to structural heart disease</title><author>Roberts-Thomson, Kurt C ; Stevenson, Irene H ; Kistler, Peter M ; Haqqani, Haris M ; Goldblatt, John C ; Sanders, Prashanthan ; Kalman, Jonathan M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h271t-f5289284fbef2a7dcf05b0858253e116b6893ff0245a917960bcdc6ca6fa89fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Aged</topic><topic>Atrial Fibrillation - etiology</topic><topic>Cardiology</topic><topic>Cardiovascular disease</topic><topic>Coronary Artery Disease - complications</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Coronary Artery Disease - surgery</topic><topic>Coronary vessels</topic><topic>Electrophysiology</topic><topic>Female</topic><topic>Heart Atria - physiopathology</topic><topic>Heart attacks</topic><topic>Heart Conduction System - physiopathology</topic><topic>Heart Valve Diseases - complications</topic><topic>Heart Valve Diseases - physiopathology</topic><topic>Heart Valve Diseases - surgery</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Roberts-Thomson, Kurt C</creatorcontrib><creatorcontrib>Stevenson, Irene H</creatorcontrib><creatorcontrib>Kistler, Peter M</creatorcontrib><creatorcontrib>Haqqani, Haris M</creatorcontrib><creatorcontrib>Goldblatt, John C</creatorcontrib><creatorcontrib>Sanders, Prashanthan</creatorcontrib><creatorcontrib>Kalman, Jonathan M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Roberts-Thomson, Kurt C</au><au>Stevenson, Irene H</au><au>Kistler, Peter M</au><au>Haqqani, Haris M</au><au>Goldblatt, John C</au><au>Sanders, Prashanthan</au><au>Kalman, Jonathan M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anatomically determined functional conduction delay in the posterior left atrium relationship to structural heart disease</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2008-02-26</date><risdate>2008</risdate><volume>51</volume><issue>8</issue><spage>856</spage><epage>862</epage><pages>856-862</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><abstract>This study sought to characterize the conduction properties of the posterior left atrium (PLA) in patients with different forms of structural heart disease undergoing cardiac surgery.
The PLA plays an important role in the initiation and maintenance of atrial fibrillation.
This study included 34 patients having elective cardiac surgery. There were 4 groups of patients: normal left ventricular (LV) function (coronary artery bypass grafting [CABG]); severe LV dysfunction (LVF/CABG); severe mitral regurgitation (MR); severe aortic stenosis (AS). Epicardial mapping of the PLA was performed in sinus rhythm and during differential pacing. Activation patterns, regional conduction velocity (CV), conduction heterogeneity, anisotropy, and total plaque activation time (TAT) were assessed.
Left atrial size in patients with LVF/CABG (47 +/- 7 mm) and MR (54 +/- 6 mm) was larger than patients with CABG (39 +/- 7 mm) and AS (42 +/- 6 mm; p < 0.05). During pacing, all patients developed a vertical line of conduction delay running between the pulmonary veins. The extent of this conduction delay was greater in patients with LVF/CABG and MR than patients with AS and CABG (p < 0.05). Conduction heterogeneity, anisotropy, and TAT were greater in patients with LVF/CABG and MR than patients with CABG (p < 0.05). These changes resulted in circuitous wave front propagation.
There is a line of functional conduction delay in a consistent anatomical location in the PLA in patients with structural heart disease. This is most marked in conditions associated with significant chronic atrial enlargement and leads to circuitous wave front propagation, suggesting a potential role in arrhythmogenesis.</abstract><cop>United States</cop><pub>Elsevier Limited</pub><pmid>18294572</pmid><doi>10.1016/j.jacc.2007.11.037</doi><tpages>7</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0735-1097 |
ispartof | Journal of the American College of Cardiology, 2008-02, Vol.51 (8), p.856-862 |
issn | 0735-1097 1558-3597 |
language | eng |
recordid | cdi_proquest_miscellaneous_70326884 |
source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Aged Atrial Fibrillation - etiology Cardiology Cardiovascular disease Coronary Artery Disease - complications Coronary Artery Disease - physiopathology Coronary Artery Disease - surgery Coronary vessels Electrophysiology Female Heart Atria - physiopathology Heart attacks Heart Conduction System - physiopathology Heart Valve Diseases - complications Heart Valve Diseases - physiopathology Heart Valve Diseases - surgery Humans Male Middle Aged Time Factors |
title | Anatomically determined functional conduction delay in the posterior left atrium relationship to structural heart disease |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-18T12%3A16%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Anatomically%20determined%20functional%20conduction%20delay%20in%20the%20posterior%20left%20atrium%20relationship%20to%20structural%20heart%20disease&rft.jtitle=Journal%20of%20the%20American%20College%20of%20Cardiology&rft.au=Roberts-Thomson,%20Kurt%20C&rft.date=2008-02-26&rft.volume=51&rft.issue=8&rft.spage=856&rft.epage=862&rft.pages=856-862&rft.issn=0735-1097&rft.eissn=1558-3597&rft_id=info:doi/10.1016/j.jacc.2007.11.037&rft_dat=%3Cproquest_pubme%3E70326884%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1506197608&rft_id=info:pmid/18294572&rfr_iscdi=true |