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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">EHRA/HRS/APHRS/SOLAECE expert consensus on Atrial cardiomyopathies: Definition, characterisation, and clinical implication<sup><xref ref-type="fn" rid="d32e905">☆</xref></sup><sup><xref ref-type="fn" rid="d32e910">☆☆</xref></sup></title><author><name sortKey="Goette, Andreas" sort="Goette, Andreas" uniqKey="Goette A" first="Andreas" last="Goette">Andreas Goette</name><affiliation><nlm:aff id="aff0005">Departement of Cardiology and Intensive Care Medicine, St. Vincenz-Hospital Paderborn, Working Group: Molecular Electrophysiology, University Hospital Magdeburg, Germany</nlm:aff></affiliation></author><author><name sortKey="Kalman, Jonathan M" sort="Kalman, Jonathan M" uniqKey="Kalman J" first="Jonathan M." last="Kalman">Jonathan M. Kalman</name><affiliation><nlm:aff id="aff0010">University of Melbourne, Royal Melbourne Hospital, Melbourne, VIC, Australia</nlm:aff></affiliation></author><author><name sortKey="Aguinaga, Luis" sort="Aguinaga, Luis" uniqKey="Aguinaga L" first="Luis" last="Aguinaga">Luis Aguinaga</name><affiliation><nlm:aff id="aff0015">Centro Privado de Cardiología, Tucumán, Argentina</nlm:aff></affiliation></author><author><name sortKey="Akar, Joseph" sort="Akar, Joseph" uniqKey="Akar J" first="Joseph" last="Akar">Joseph Akar</name><affiliation><nlm:aff id="aff0020">Yale University, New Haven, CT, USA</nlm:aff></affiliation></author><author><name sortKey="Cabrera, Jose Angel" sort="Cabrera, Jose Angel" uniqKey="Cabrera J" first="Jose Angel" last="Cabrera">Jose Angel Cabrera</name><affiliation><nlm:aff id="aff0025">European University Quiron-Madrid, Madrid, Spain</nlm:aff></affiliation></author><author><name sortKey="Chen, Shih Ann" sort="Chen, Shih Ann" uniqKey="Chen S" first="Shih Ann" last="Chen">Shih Ann Chen</name><affiliation><nlm:aff id="aff0030">Veterans General Hospital, Taipei, Taiwan</nlm:aff></affiliation></author><author><name sortKey="Chugh, Sumeet S" sort="Chugh, Sumeet S" uniqKey="Chugh S" first="Sumeet S." last="Chugh">Sumeet S. Chugh</name><affiliation><nlm:aff id="aff0035">The Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Corradi, Domenico" sort="Corradi, Domenico" uniqKey="Corradi D" first="Domenico" last="Corradi">Domenico Corradi</name><affiliation><nlm:aff id="aff0040">University of Parma, Parma, Italy</nlm:aff></affiliation></author><author><name sortKey="D Avila, Andre" sort="D Avila, Andre" uniqKey="D Avila A" first="Andre" last="D Avila">Andre D Avila</name><affiliation><nlm:aff id="aff0045">Mount Sinai School of Medicine, New York, NY, USA</nlm:aff></affiliation></author><author><name sortKey="Dobrev, Dobromir" sort="Dobrev, Dobromir" uniqKey="Dobrev D" first="Dobromir" last="Dobrev">Dobromir Dobrev</name><affiliation><nlm:aff id="aff0050">Institute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen, Essen, Germany</nlm:aff></affiliation></author><author><name sortKey="Fenelon, Guilherme" sort="Fenelon, Guilherme" uniqKey="Fenelon G" first="Guilherme" last="Fenelon">Guilherme Fenelon</name><affiliation><nlm:aff id="aff0055">Federal University of Sao Paulo, San Paulo, Brazil</nlm:aff></affiliation></author><author><name sortKey="Gonzalez, Mario" sort="Gonzalez, Mario" uniqKey="Gonzalez M" first="Mario" last="Gonzalez">Mario Gonzalez</name><affiliation><nlm:aff id="aff0060">Penn State Heart and Vascular Institute, Penn State University, Hershey, PA, USA</nlm:aff></affiliation></author><author><name sortKey="Hatem, Stephane N" sort="Hatem, Stephane N" uniqKey="Hatem S" first="Stephane N." last="Hatem">Stephane N. Hatem</name><affiliation><nlm:aff id="aff0065">Department of Cardiology, Assistance Publique – Hô pitaux de Paris, Pitié-Salpêtrière Hospital, Sorbonne University, INSERM UMR_S1166, Institute of Cardiometabolism and Nutrition-ICAN, Paris, France</nlm:aff></affiliation></author><author><name sortKey="Helm, Robert" sort="Helm, Robert" uniqKey="Helm R" first="Robert" last="Helm">Robert Helm</name><affiliation><nlm:aff id="aff0070">Boston University School of Medicine, Boston Medical Center, Boston, MA, USA</nlm:aff></affiliation></author><author><name sortKey="Hindricks, Gerhard" sort="Hindricks, Gerhard" uniqKey="Hindricks G" first="Gerhard" last="Hindricks">Gerhard Hindricks</name><affiliation><nlm:aff id="aff0075">University of Leipzig Heart Center, Leipzig, Germany</nlm:aff></affiliation></author><author><name sortKey="Ho, Siew Yen" sort="Ho, Siew Yen" uniqKey="Ho S" first="Siew Yen" last="Ho">Siew Yen Ho</name><affiliation><nlm:aff id="aff0080">Royal Brompton Hospital and Imperial College London, London, UK</nlm:aff></affiliation></author><author><name sortKey="Hoit, Brian" sort="Hoit, Brian" uniqKey="Hoit B" first="Brian" last="Hoit">Brian Hoit</name><affiliation><nlm:aff id="aff0085">UH Case Medical Center, Cleveland, OH, USA</nlm:aff></affiliation></author><author><name sortKey="Jalife, Jose" sort="Jalife, Jose" uniqKey="Jalife J" first="Jose" last="Jalife">Jose Jalife</name><affiliation><nlm:aff id="aff0090">University of Michigan, Ann Arbor, MI, USA</nlm:aff></affiliation></author><author><name sortKey="Kim, Young Hoon" sort="Kim, Young Hoon" uniqKey="Kim Y" first="Young-Hoon" last="Kim">Young-Hoon Kim</name><affiliation><nlm:aff id="aff0095">Korea University Medical Center, Seoul, South Korea</nlm:aff></affiliation></author><author><name sortKey="Lip, Gregory Y H" sort="Lip, Gregory Y H" uniqKey="Lip G" first="Gregory Y. H." last="Lip">Gregory Y. H. Lip</name><affiliation><nlm:aff id="aff0100">University of Birmingham, Birmingham, UK</nlm:aff></affiliation></author><author><name sortKey="Ma, Chang Sheng" sort="Ma, Chang Sheng" uniqKey="Ma C" first="Chang-Sheng" last="Ma">Chang-Sheng Ma</name><affiliation><nlm:aff id="aff0105">Anzhen Hospital, Beijing, China</nlm:aff></affiliation></author><author><name sortKey="Marcus, Gregory M" sort="Marcus, Gregory M" uniqKey="Marcus G" first="Gregory M." last="Marcus">Gregory M. Marcus</name><affiliation><nlm:aff id="aff0110">University of California, San Francisco, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Murray, Katherine" sort="Murray, Katherine" uniqKey="Murray K" first="Katherine" last="Murray">Katherine Murray</name><affiliation><nlm:aff id="aff0115">Vanderbilt University, Nashville, TN, USA</nlm:aff></affiliation></author><author><name sortKey="Nogami, Akihiko" sort="Nogami, Akihiko" uniqKey="Nogami A" first="Akihiko" last="Nogami">Akihiko Nogami</name><affiliation><nlm:aff id="aff0120">University of Tsukuba, Ibaraki, Japan</nlm:aff></affiliation></author><author><name sortKey="Sanders, Prashanthan" sort="Sanders, Prashanthan" uniqKey="Sanders P" first="Prashanthan" last="Sanders">Prashanthan Sanders</name><affiliation><nlm:aff id="aff0125">Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia</nlm:aff></affiliation></author><author><name sortKey="Uribe, William" sort="Uribe, William" uniqKey="Uribe W" first="William" last="Uribe">William Uribe</name><affiliation><nlm:aff id="aff0130">Electrophysiology Deparment at Centros Especializados de San Vicente Fundació n and Clínica CES. Universidad CES, Universidad Pontificia Bolivariana (UPB), Medellin, Colombia</nlm:aff></affiliation></author><author><name sortKey="Van Wagoner, David R" sort="Van Wagoner, David R" uniqKey="Van Wagoner D" first="David R." last="Van Wagoner">David R. Van Wagoner</name><affiliation><nlm:aff id="aff0135">Department of Molecular Cardiology, Cleveland Clinic, Cleveland, OH, USA</nlm:aff></affiliation></author><author><name sortKey="Nattel, Stanley" sort="Nattel, Stanley" uniqKey="Nattel S" first="Stanley" last="Nattel">Stanley Nattel</name><affiliation><nlm:aff id="aff0140">Université de Montréal, Montreal Heart Institute Research Center and McGill University, Montreal, Quebec, Canada</nlm:aff></affiliation><affiliation><nlm:aff id="aff0145">Institute of Pharmacology, West German Heart and Vascular Center, Faculty of Medicine, University Duisburg-Essen, Essen, Germany</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">27588148</idno><idno type="pmc">4996910</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4996910</idno><idno type="RBID">PMC:4996910</idno><idno type="doi">10.1016/j.joa.2016.05.002</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">001345</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001345</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">EHRA/HRS/APHRS/SOLAECE expert consensus on Atrial cardiomyopathies: Definition, characterisation, and clinical implication<sup><xref ref-type="fn" rid="d32e905">☆</xref></sup><sup><xref ref-type="fn" rid="d32e910">☆☆</xref></sup></title><author><name sortKey="Goette, Andreas" sort="Goette, Andreas" uniqKey="Goette A" first="Andreas" last="Goette">Andreas Goette</name><affiliation><nlm:aff id="aff0005">Departement of Cardiology and Intensive Care Medicine, St. Vincenz-Hospital Paderborn, Working Group: Molecular Electrophysiology, University Hospital Magdeburg, Germany</nlm:aff></affiliation></author><author><name sortKey="Kalman, Jonathan M" sort="Kalman, Jonathan M" uniqKey="Kalman J" first="Jonathan M." last="Kalman">Jonathan M. Kalman</name><affiliation><nlm:aff id="aff0010">University of Melbourne, Royal Melbourne Hospital, Melbourne, VIC, Australia</nlm:aff></affiliation></author><author><name sortKey="Aguinaga, Luis" sort="Aguinaga, Luis" uniqKey="Aguinaga L" first="Luis" last="Aguinaga">Luis Aguinaga</name><affiliation><nlm:aff id="aff0015">Centro Privado de Cardiología, Tucumán, Argentina</nlm:aff></affiliation></author><author><name sortKey="Akar, Joseph" sort="Akar, Joseph" uniqKey="Akar J" first="Joseph" last="Akar">Joseph Akar</name><affiliation><nlm:aff id="aff0020">Yale University, New Haven, CT, USA</nlm:aff></affiliation></author><author><name sortKey="Cabrera, Jose Angel" sort="Cabrera, Jose Angel" uniqKey="Cabrera J" first="Jose Angel" last="Cabrera">Jose Angel Cabrera</name><affiliation><nlm:aff id="aff0025">European University Quiron-Madrid, Madrid, Spain</nlm:aff></affiliation></author><author><name sortKey="Chen, Shih Ann" sort="Chen, Shih Ann" uniqKey="Chen S" first="Shih Ann" last="Chen">Shih Ann Chen</name><affiliation><nlm:aff id="aff0030">Veterans General Hospital, Taipei, Taiwan</nlm:aff></affiliation></author><author><name sortKey="Chugh, Sumeet S" sort="Chugh, Sumeet S" uniqKey="Chugh S" first="Sumeet S." last="Chugh">Sumeet S. Chugh</name><affiliation><nlm:aff id="aff0035">The Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Corradi, Domenico" sort="Corradi, Domenico" uniqKey="Corradi D" first="Domenico" last="Corradi">Domenico Corradi</name><affiliation><nlm:aff id="aff0040">University of Parma, Parma, Italy</nlm:aff></affiliation></author><author><name sortKey="D Avila, Andre" sort="D Avila, Andre" uniqKey="D Avila A" first="Andre" last="D Avila">Andre D Avila</name><affiliation><nlm:aff id="aff0045">Mount Sinai School of Medicine, New York, NY, USA</nlm:aff></affiliation></author><author><name sortKey="Dobrev, Dobromir" sort="Dobrev, Dobromir" uniqKey="Dobrev D" first="Dobromir" last="Dobrev">Dobromir Dobrev</name><affiliation><nlm:aff id="aff0050">Institute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen, Essen, Germany</nlm:aff></affiliation></author><author><name sortKey="Fenelon, Guilherme" sort="Fenelon, Guilherme" uniqKey="Fenelon G" first="Guilherme" last="Fenelon">Guilherme Fenelon</name><affiliation><nlm:aff id="aff0055">Federal University of Sao Paulo, San Paulo, Brazil</nlm:aff></affiliation></author><author><name sortKey="Gonzalez, Mario" sort="Gonzalez, Mario" uniqKey="Gonzalez M" first="Mario" last="Gonzalez">Mario Gonzalez</name><affiliation><nlm:aff id="aff0060">Penn State Heart and Vascular Institute, Penn State University, Hershey, PA, USA</nlm:aff></affiliation></author><author><name sortKey="Hatem, Stephane N" sort="Hatem, Stephane N" uniqKey="Hatem S" first="Stephane N." last="Hatem">Stephane N. Hatem</name><affiliation><nlm:aff id="aff0065">Department of Cardiology, Assistance Publique – Hô pitaux de Paris, Pitié-Salpêtrière Hospital, Sorbonne University, INSERM UMR_S1166, Institute of Cardiometabolism and Nutrition-ICAN, Paris, France</nlm:aff></affiliation></author><author><name sortKey="Helm, Robert" sort="Helm, Robert" uniqKey="Helm R" first="Robert" last="Helm">Robert Helm</name><affiliation><nlm:aff id="aff0070">Boston University School of Medicine, Boston Medical Center, Boston, MA, USA</nlm:aff></affiliation></author><author><name sortKey="Hindricks, Gerhard" sort="Hindricks, Gerhard" uniqKey="Hindricks G" first="Gerhard" last="Hindricks">Gerhard Hindricks</name><affiliation><nlm:aff id="aff0075">University of Leipzig Heart Center, Leipzig, Germany</nlm:aff></affiliation></author><author><name sortKey="Ho, Siew Yen" sort="Ho, Siew Yen" uniqKey="Ho S" first="Siew Yen" last="Ho">Siew Yen Ho</name><affiliation><nlm:aff id="aff0080">Royal Brompton Hospital and Imperial College London, London, UK</nlm:aff></affiliation></author><author><name sortKey="Hoit, Brian" sort="Hoit, Brian" uniqKey="Hoit B" first="Brian" last="Hoit">Brian Hoit</name><affiliation><nlm:aff id="aff0085">UH Case Medical Center, Cleveland, OH, USA</nlm:aff></affiliation></author><author><name sortKey="Jalife, Jose" sort="Jalife, Jose" uniqKey="Jalife J" first="Jose" last="Jalife">Jose Jalife</name><affiliation><nlm:aff id="aff0090">University of Michigan, Ann Arbor, MI, USA</nlm:aff></affiliation></author><author><name sortKey="Kim, Young Hoon" sort="Kim, Young Hoon" uniqKey="Kim Y" first="Young-Hoon" last="Kim">Young-Hoon Kim</name><affiliation><nlm:aff id="aff0095">Korea University Medical Center, Seoul, South Korea</nlm:aff></affiliation></author><author><name sortKey="Lip, Gregory Y H" sort="Lip, Gregory Y H" uniqKey="Lip G" first="Gregory Y. H." last="Lip">Gregory Y. H. Lip</name><affiliation><nlm:aff id="aff0100">University of Birmingham, Birmingham, UK</nlm:aff></affiliation></author><author><name sortKey="Ma, Chang Sheng" sort="Ma, Chang Sheng" uniqKey="Ma C" first="Chang-Sheng" last="Ma">Chang-Sheng Ma</name><affiliation><nlm:aff id="aff0105">Anzhen Hospital, Beijing, China</nlm:aff></affiliation></author><author><name sortKey="Marcus, Gregory M" sort="Marcus, Gregory M" uniqKey="Marcus G" first="Gregory M." last="Marcus">Gregory M. Marcus</name><affiliation><nlm:aff id="aff0110">University of California, San Francisco, CA, USA</nlm:aff></affiliation></author><author><name sortKey="Murray, Katherine" sort="Murray, Katherine" uniqKey="Murray K" first="Katherine" last="Murray">Katherine Murray</name><affiliation><nlm:aff id="aff0115">Vanderbilt University, Nashville, TN, USA</nlm:aff></affiliation></author><author><name sortKey="Nogami, Akihiko" sort="Nogami, Akihiko" uniqKey="Nogami A" first="Akihiko" last="Nogami">Akihiko Nogami</name><affiliation><nlm:aff id="aff0120">University of Tsukuba, Ibaraki, Japan</nlm:aff></affiliation></author><author><name sortKey="Sanders, Prashanthan" sort="Sanders, Prashanthan" uniqKey="Sanders P" first="Prashanthan" last="Sanders">Prashanthan Sanders</name><affiliation><nlm:aff id="aff0125">Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia</nlm:aff></affiliation></author><author><name sortKey="Uribe, William" sort="Uribe, William" uniqKey="Uribe W" first="William" last="Uribe">William Uribe</name><affiliation><nlm:aff id="aff0130">Electrophysiology Deparment at Centros Especializados de San Vicente Fundació n and Clínica CES. Universidad CES, Universidad Pontificia Bolivariana (UPB), Medellin, Colombia</nlm:aff></affiliation></author><author><name sortKey="Van Wagoner, David R" sort="Van Wagoner, David R" uniqKey="Van Wagoner D" first="David R." last="Van Wagoner">David R. Van Wagoner</name><affiliation><nlm:aff id="aff0135">Department of Molecular Cardiology, Cleveland Clinic, Cleveland, OH, USA</nlm:aff></affiliation></author><author><name sortKey="Nattel, Stanley" sort="Nattel, Stanley" uniqKey="Nattel S" first="Stanley" last="Nattel">Stanley Nattel</name><affiliation><nlm:aff id="aff0140">Université de Montréal, Montreal Heart Institute Research Center and McGill University, Montreal, Quebec, Canada</nlm:aff></affiliation><affiliation><nlm:aff id="aff0145">Institute of Pharmacology, West German Heart and Vascular Center, Faculty of Medicine, University Duisburg-Essen, Essen, Germany</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Arrhythmia</title><idno type="ISSN">1880-4276</idno><idno type="eISSN">1883-2148</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Hoit, B D" uniqKey="Hoit B">B.D. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Arrhythm</journal-id><journal-id journal-id-type="iso-abbrev">J Arrhythm</journal-id><journal-title-group><journal-title>Journal of Arrhythmia</journal-title></journal-title-group><issn pub-type="ppub">1880-4276</issn><issn pub-type="epub">1883-2148</issn><publisher><publisher-name>Elsevier</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">27588148</article-id><article-id pub-id-type="pmc">4996910</article-id><article-id pub-id-type="publisher-id">S1880-4276(16)30042-4</article-id><article-id pub-id-type="doi">10.1016/j.joa.2016.05.002</article-id><article-categories><subj-group subj-group-type="heading"><subject>Guideline</subject></subj-group></article-categories><title-group><article-title>EHRA/HRS/APHRS/SOLAECE expert consensus on Atrial cardiomyopathies: Definition, characterisation, and clinical implication<sup><xref ref-type="fn" rid="d32e905">☆</xref></sup><sup><xref ref-type="fn" rid="d32e910">☆☆</xref></sup></article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Goette</surname><given-names>Andreas</given-names></name><role>(EHRA chair)</role><email>andreas.goette@vincenz.de</email><xref rid="aff0005" ref-type="aff">a</xref><xref rid="cor1" ref-type="corresp">⁎</xref></contrib><contrib contrib-type="author"><name><surname>Kalman</surname><given-names>Jonathan M.</given-names></name><role>(APHRS co-chair)</role><email>jon.kalman@mh.org.au</email><xref rid="aff0010" ref-type="aff">b</xref><xref rid="cor2" ref-type="corresp">⁎⁎</xref></contrib><contrib contrib-type="author"><name><surname>Aguinaga</surname><given-names>Luis</given-names></name><role>(SOLAECE co-chair)</role><email>lsaguinaga@gmail.com</email><xref rid="aff0015" ref-type="aff">c</xref><xref rid="cor3" ref-type="corresp">⁎⁎⁎</xref><xref rid="fn1" ref-type="fn">1</xref></contrib><contrib contrib-type="author"><name><surname>Akar</surname><given-names>Joseph</given-names></name><xref rid="aff0020" ref-type="aff">d</xref></contrib><contrib contrib-type="author"><name><surname>Cabrera</surname><given-names>Jose Angel</given-names></name><xref rid="aff0025" ref-type="aff">e</xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>Shih Ann</given-names></name><xref rid="aff0030" ref-type="aff">f</xref></contrib><contrib contrib-type="author"><name><surname>Chugh</surname><given-names>Sumeet S.</given-names></name><xref rid="aff0035" ref-type="aff">g</xref></contrib><contrib contrib-type="author"><name><surname>Corradi</surname><given-names>Domenico</given-names></name><xref rid="aff0040" ref-type="aff">h</xref></contrib><contrib contrib-type="author"><name><surname>D׳Avila</surname><given-names>Andre</given-names></name><xref rid="aff0045" ref-type="aff">i</xref></contrib><contrib contrib-type="author"><name><surname>Dobrev</surname><given-names>Dobromir</given-names></name><xref rid="aff0050" ref-type="aff">j</xref></contrib><contrib contrib-type="author"><name><surname>Fenelon</surname><given-names>Guilherme</given-names></name><xref rid="aff0055" ref-type="aff">k</xref></contrib><contrib contrib-type="author"><name><surname>Gonzalez</surname><given-names>Mario</given-names></name><xref rid="aff0060" ref-type="aff">l</xref></contrib><contrib contrib-type="author"><name><surname>Hatem</surname><given-names>Stephane N.</given-names></name><xref rid="aff0065" ref-type="aff">m</xref></contrib><contrib contrib-type="author"><name><surname>Helm</surname><given-names>Robert</given-names></name><xref rid="aff0070" ref-type="aff">n</xref></contrib><contrib contrib-type="author"><name><surname>Hindricks</surname><given-names>Gerhard</given-names></name><xref rid="aff0075" ref-type="aff">o</xref></contrib><contrib contrib-type="author"><name><surname>Ho</surname><given-names>Siew Yen</given-names></name><xref rid="aff0080" ref-type="aff">p</xref></contrib><contrib contrib-type="author"><name><surname>Hoit</surname><given-names>Brian</given-names></name><xref rid="aff0085" ref-type="aff">q</xref></contrib><contrib contrib-type="author"><name><surname>Jalife</surname><given-names>Jose</given-names></name><xref rid="aff0090" ref-type="aff">r</xref></contrib><contrib contrib-type="author"><name><surname>Kim</surname><given-names>Young-Hoon</given-names></name><xref rid="aff0095" ref-type="aff">s</xref></contrib><contrib contrib-type="author"><name><surname>Lip</surname><given-names>Gregory Y.H.</given-names></name><xref rid="aff0100" ref-type="aff">t</xref></contrib><contrib contrib-type="author"><name><surname>Ma</surname><given-names>Chang-Sheng</given-names></name><xref rid="aff0105" ref-type="aff">u</xref></contrib><contrib contrib-type="author"><name><surname>Marcus</surname><given-names>Gregory M.</given-names></name><xref rid="aff0110" ref-type="aff">v</xref></contrib><contrib contrib-type="author"><name><surname>Murray</surname><given-names>Katherine</given-names></name><xref rid="aff0115" ref-type="aff">w</xref></contrib><contrib contrib-type="author"><name><surname>Nogami</surname><given-names>Akihiko</given-names></name><xref rid="aff0120" ref-type="aff">x</xref></contrib><contrib contrib-type="author"><name><surname>Sanders</surname><given-names>Prashanthan</given-names></name><xref rid="aff0125" ref-type="aff">y</xref></contrib><contrib contrib-type="author"><name><surname>Uribe</surname><given-names>William</given-names></name><xref rid="aff0130" ref-type="aff">z</xref></contrib><contrib contrib-type="author"><name><surname>Van Wagoner</surname><given-names>David R.</given-names></name><xref rid="aff0135" ref-type="aff">aa</xref></contrib><contrib contrib-type="author"><name><surname>Nattel</surname><given-names>Stanley</given-names></name><role>(HRS co-chair)</role><email>stanley.nattel@icm-mhi.org</email><xref rid="aff0140" ref-type="aff">ab</xref><xref rid="aff0145" ref-type="aff">ac</xref><xref rid="cor4" ref-type="corresp">⁎⁎⁎⁎</xref></contrib><contrib contrib-type="author"><collab>Document Reviewers: Osmar A. Centurion (Paraguay), Karl-Heinz Kuck (Germany), Kristen K. Patton (USA), John L. Sapp (Canada), Martin Stiles (New Zealand), Jesper Hastrup Svendsen (Denmark), and Gaurav A. Upadhyay (USA)</collab></contrib><contrib contrib-type="author"><collab>Review coordinator: Alena Shantsila (UK)</collab></contrib></contrib-group><aff id="aff0005"><label>a</label>Departement of Cardiology and Intensive Care Medicine, St. Vincenz-Hospital Paderborn, Working Group: Molecular Electrophysiology, University Hospital Magdeburg, Germany</aff><aff id="aff0010"><label>b</label>University of Melbourne, Royal Melbourne Hospital, Melbourne, VIC, Australia</aff><aff id="aff0015"><label>c</label>Centro Privado de Cardiología, Tucumán, Argentina</aff><aff id="aff0020"><label>d</label>Yale University, New Haven, CT, USA</aff><aff id="aff0025"><label>e</label>European University Quiron-Madrid, Madrid, Spain</aff><aff id="aff0030"><label>f</label>Veterans General Hospital, Taipei, Taiwan</aff><aff id="aff0035"><label>g</label>The Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA</aff><aff id="aff0040"><label>h</label>University of Parma, Parma, Italy</aff><aff id="aff0045"><label>i</label>Mount Sinai School of Medicine, New York, NY, USA</aff><aff id="aff0050"><label>j</label>Institute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen, Essen, Germany</aff><aff id="aff0055"><label>k</label>Federal University of Sao Paulo, San Paulo, Brazil</aff><aff id="aff0060"><label>l</label>Penn State Heart and Vascular Institute, Penn State University, Hershey, PA, USA</aff><aff id="aff0065"><label>m</label>Department of Cardiology, Assistance Publique – Hô pitaux de Paris, Pitié-Salpêtrière Hospital, Sorbonne University, INSERM UMR_S1166, Institute of Cardiometabolism and Nutrition-ICAN, Paris, France</aff><aff id="aff0070"><label>n</label>Boston University School of Medicine, Boston Medical Center, Boston, MA, USA</aff><aff id="aff0075"><label>o</label>University of Leipzig Heart Center, Leipzig, Germany</aff><aff id="aff0080"><label>p</label>Royal Brompton Hospital and Imperial College London, London, UK</aff><aff id="aff0085"><label>q</label>UH Case Medical Center, Cleveland, OH, USA</aff><aff id="aff0090"><label>r</label>University of Michigan, Ann Arbor, MI, USA</aff><aff id="aff0095"><label>s</label>Korea University Medical Center, Seoul, South Korea</aff><aff id="aff0100"><label>t</label>University of Birmingham, Birmingham, UK</aff><aff id="aff0105"><label>u</label>Anzhen Hospital, Beijing, China</aff><aff id="aff0110"><label>v</label>University of California, San Francisco, CA, USA</aff><aff id="aff0115"><label>w</label>Vanderbilt University, Nashville, TN, USA</aff><aff id="aff0120"><label>x</label>University of Tsukuba, Ibaraki, Japan</aff><aff id="aff0125"><label>y</label>Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia</aff><aff id="aff0130"><label>z</label>Electrophysiology Deparment at Centros Especializados de San Vicente Fundació n and Clínica CES. Universidad CES, Universidad Pontificia Bolivariana (UPB), Medellin, Colombia</aff><aff id="aff0135"><label>aa</label>Department of Molecular Cardiology, Cleveland Clinic, Cleveland, OH, USA</aff><aff id="aff0140"><label>ab</label>Université de Montréal, Montreal Heart Institute Research Center and McGill University, Montreal, Quebec, Canada</aff><aff id="aff0145"><label>ac</label>Institute of Pharmacology, West German Heart and Vascular Center, Faculty of Medicine, University Duisburg-Essen, Essen, Germany</aff><author-notes><corresp id="cor1"><label>⁎</label>Correspondence to: Chefarzt Medizinische Klinik II, St. Vincenz-Krankenhaus, Am Busdorf 2, 33098 Paderborn, Germany. Fax: 05251/861652.Chefarzt Medizinische Klinik II, St. Vincenz-KrankenhausAm Busdorf 2Paderborn33098Germany <email>andreas.goette@vincenz.de</email></corresp><corresp id="cor2"><label>⁎⁎</label>Correspondence to: University of Melbourne, Royal Melbourne Hospital, Melbourne, VIC 3050, Australia. Fax: +61 3 9349 5411. <email>jon.kalman@mh.org.au</email></corresp><corresp id="cor3"><label>⁎⁎⁎</label>Corresponding author. <email>lsaguinaga@gmail.com</email></corresp><corresp id="cor4"><label>⁎⁎⁎⁎</label>Corresponding author at: University of Montreal, Montreal Heart Institute Research Center, 5000 Belanger St. E., Montreal, QC, Canada H1T 1C8. Fax: +1 514 593 2493University of Montreal, Montreal Heart Institute Research Center5000 Belanger St. E.MontrealQCH1T 1C8Canada <email>stanley.nattel@icm-mhi.org</email></corresp><fn id="fn1"><label>1</label><p id="ntp0020">Presidente Sociedad de Cardiología de Tucumàn, Ex-PRESIDENTE DE SOLAECE, Sociedad Latinoamericana de Estimulació nCardíaca y Electrofisiología. Tel.: +54 381 4217676.</p></fn></author-notes><pub-date pub-type="pmc-release"><day>11</day><month>7</month><year>2016</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>8</month><year>2016</year></pub-date><pub-date pub-type="epub"><day>11</day><month>7</month><year>2016</year></pub-date><volume>32</volume><issue>4</issue><fpage>247</fpage><lpage>278</lpage><permissions><copyright-statement>© 2016 The article has been co-published with permission in EP-Europace, HeartRhythm and Journal of Arrythmia. All rights reserved in respect of HeartRhythm and Journal of Arrythmia. © The Authors 2016. For EP-Europace, © The Author 2016</copyright-statement><copyright-year>2016</copyright-year><license license-type="CC BY-NC-ND" xlink:href="http://creativecommons.org/licenses/by-nc-nd/4.0/"><license-p>This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).</license-p></license></permissions></article-meta></front><body><sec id="s0005"><label>1</label><title>Introduction and definition of atrial cardiomyopathy</title><p>The atria provide an important contribution to cardiac function <xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib2" ref-type="bibr">[2]</xref>. Besides their impact on ventricular filling, they serve as a volume reservoir, host pacemaker cells and important parts of the cardiac conduction system (e.g. sinus node, AV node), and secrete natriuretic peptides like atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that regulate fluid homoeostasis. Atrial myocardium is affected by many cardiac and non-cardiac conditions <xref rid="bib3" ref-type="bibr">[3]</xref> and is, in some respects, more sensitive than ventricular <xref rid="bib4" ref-type="bibr">[4]</xref>. The atria are activated, besides the three specialised intermodal tracts <xref rid="bib5" ref-type="bibr">[5]</xref>, <xref rid="bib6" ref-type="bibr">[6]</xref>, through working cardiomyocytes, so that any architectural or structural change in the atrial myocardium may cause significant electrophysiological disturbances. In addition, atrial cells (both cardiomyocytes and non-cardiomyocyte elements like fibroblasts, endothelial cells, and neurons) react briskly and extensively to pathological stimuli <xref rid="bib3" ref-type="bibr">[3]</xref> and are susceptible to a range of genetic influences <xref rid="bib7" ref-type="bibr">[7]</xref>. Responses include atrial cardiomyocyte hypertrophy and contractile dysfunction, arrhythmogenic changes in cardiomyocyte ion-channel and transporter function, atrial fibroblast proliferation, hyperinnervation, and thrombogenic changes <xref rid="bib2" ref-type="bibr">[2]</xref>. Thus, atrial pathologies have a substantial impact on cardiac performance, arrhythmia occurrence, and stroke risk <xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib8" ref-type="bibr">[8]</xref>.</p><p>Ventricular cardiomyopathies have been well classified; however, a definition and detailed analysis of ‘atrial cardiomyopathy’ is lacking from the literature. The purpose of the present consensus report, prepared by a working group with representation from the European Heart Rhythm Association (EHRA), the Heart Rhythm Society (HRS), the Asian Pacific Heart Rhythm Society (APHRS), and Sociedad Latino Americana de Estimulacion Cardiaca y Electrofisiologia (SOLAECE), was to define atrial cardiomyopathy, to review the relevant literature, and to consider the impact of atrial cardiomyopathies on arrhythmia management and stroke.</p><sec id="s0010"><label>1.1</label><title>Definition of atrial cardiomyopathy</title><p>The working group proposes the following working definition of atrial cardiomyopathy: ‘Any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations’ (<xref rid="t0005" ref-type="table">Table 1</xref>).</p><p>Many diseases (like hypertension, heart failure, diabetes, and myocarditis) or conditions (like ageing and endocrine abnormalities) are known to induce or contribute to an atrial cardiomyopathy. However, the induced changes are not necessarily disease-specific and pathological changes often share many similarities <xref rid="bib9" ref-type="bibr">[9]</xref>, <xref rid="bib10" ref-type="bibr">[10]</xref>. The extent of pathological changes may vary over time and atrial location, causing substantial intraindividual and interindividual differences. In addition, while some pathological processes may affect the atria very selectively (e.g. atrial fibrillation-induced remodelling), most cardiomyopathies that affect the atria also involve the ventricles to a greater or lesser extent. There is no presently accepted histopathological classification of atrial pathologies. Therefore, we have proposed here a working histological/ pathopysiological classification scheme for atrial cardiomyopathies (<xref rid="t0005" ref-type="table">Table 1</xref>; <xref rid="f0005" ref-type="fig">Fig. 1</xref>). We use the acronym EHRAS (for <underline>E</underline>HRA/<underline>HR</underline>S/ <underline>A</underline>PHRS/<underline>S</underline>OLAECE), defining four classes: (I) principal cardiomyocyte changes <xref rid="bib11" ref-type="bibr">[11]</xref>, <xref rid="bib12" ref-type="bibr">[12]</xref>, <xref rid="bib13" ref-type="bibr">[13]</xref>, <xref rid="bib14" ref-type="bibr">[14]</xref>, <xref rid="bib15" ref-type="bibr">[15]</xref>; (II) principally fibrotic changes <xref rid="bib10" ref-type="bibr">[10]</xref>, <xref rid="bib14" ref-type="bibr">[14]</xref>, <xref rid="bib16" ref-type="bibr">[16]</xref>; (III) combined cardiomyocyte-pathology/fibrosis <xref rid="bib9" ref-type="bibr">[9]</xref>, <xref rid="bib11" ref-type="bibr">[11]</xref>, <xref rid="bib12" ref-type="bibr">[12]</xref>; (IV) primarily non-collagen infiltration (with or without cardiomyocyte changes) <xref rid="bib17" ref-type="bibr">[17]</xref>, <xref rid="bib18" ref-type="bibr">[18]</xref>, <xref rid="bib19" ref-type="bibr">[19]</xref>. This simple classification may help to convey the primary underlying pathology in various clinical conditions. The EHRAS class may vary over time and may differ at atrial sites in certain patients. Thus, this classification is purely descriptive and in contrast to other classifications (NYHA class, CCS class etc.), there is no progression in severity from EHRAS class I to EHRAS IV (<xref rid="t0010" ref-type="table">Table 2</xref>). The classification may be useful to describe pathological changes in biopsies and to correlate pathologies with results obtained from imaging technologies etc. In the future, this may help to define a tailored therapeutic approach in atrial fibrillation (AF) (<xref rid="f0005" ref-type="fig">Fig. 1</xref>, <xref rid="f0010" ref-type="fig">Fig. 2</xref>, <xref rid="f0015" ref-type="fig">Fig. 3</xref>).</p></sec></sec><sec id="s0015"><label>2</label><title>Anatomical considerations and atrial muscular architecture</title><sec id="s0020"><label>2.1</label><title>Normal atrial structures</title><sec id="s0025"><label>2.1.1</label><title>Gross morphology</title><p>Each atrium has a morphologically characteristic atrial body and appendage (<xref rid="f0020" ref-type="fig">Fig. 4</xref>). In the body, there is a venous component with the orifices of the systemic or pulmonary veins (PVs) and a vestibular component that surrounds the atrial outlet <xref rid="bib20" ref-type="bibr">[20]</xref>. The interatrial septum (IAS) separates the atrial bodies. The venous component of the left atrium (LA) is located posterosuperiorly and receives the PVs at the four corners, forming a prominent atrial dome. The LA is situated more posteriorly and superiorly than the right atrium separated by the obliquity of the plane of the IAS <xref rid="bib21" ref-type="bibr">[21]</xref>.</p><p>The LA appendage (LAA) is smaller than the right atrium appendage (RAA). Narrower and with different shapes has a distinct opening to the atrial body and overlies the left circumflex coronary artery. Its endocardial aspect is lined by a complex network of muscular ridges and mem-branes <xref rid="bib22" ref-type="bibr">[22]</xref>, <xref rid="bib23" ref-type="bibr">[23]</xref>. Different LAA morphologies have been described, and it appears that LAA morphology correlates with the risk of thrombogenesis <xref rid="bib24" ref-type="bibr">[24]</xref>.</p><p>Bachmann׳s bundle is a broad epicardial muscular band running along the anterior wall of both atria (<xref rid="f0020" ref-type="fig">Fig. 4</xref>). The rightward arms extend superiorly towards the sinus node and inferiorly towards the right atrioventricular groove, while the leftward arms blend with deeper myofibres to pass around the neck of the LAA and reunite posteriorly to join the circumferential vestibule of the LA. The walls of LA are non-uniform in thickness (1–15 mm) and thicker than the right atrium <xref rid="bib25" ref-type="bibr">[25]</xref>.</p></sec></sec><sec id="s0030"><label>2.2</label><title>Normal atrial myocardium</title><sec id="s0035"><label>2.2.1</label><title>Atrial cardiomyocytes</title><p>Atrial cardiomyocytes are geometrically complex cylinders that sometimes bifurcate at their ends where they connect with adjacent fibres via band-like ‘intercalated discs’. This contractile syncytium is organised in well-defined bands that establish non-uniform anisotropic propagation of the atrial impulse <xref rid="bib9" ref-type="bibr">[9]</xref>, <xref rid="bib11" ref-type="bibr">[11]</xref>, <xref rid="bib26" ref-type="bibr">[26]</xref>. The only clear light-microscopic morphological difference between atrial and ventricular cardiomyocytes is in size <xref rid="bib27" ref-type="bibr">[27]</xref>. In paraffin-embedded human specimens, the cardiomyocyte transverse diameter is ×12 mm in the LAs vs. 20–22 mm in the ventricles <xref rid="bib11" ref-type="bibr">[11]</xref>, <xref rid="bib28" ref-type="bibr">[28]</xref>. Atrial cardiomyocytes are mainly mononucleated; a minor fraction possess two or more nuclei. The nucleus is usually centrally located, with granular and/or condensed chromatin. The nuclear shape is influenced by fibre contraction, becoming more fusiform with longitudinal cell stretch <xref rid="bib29" ref-type="bibr">[29]</xref>. Biochemically, atrial cardiomyocytes have greater lipid content than ventricular muscle cells <xref rid="bib30" ref-type="bibr">[30]</xref>.</p><p>Atrial cardiomyocytes share many characteristics with ventricular in terms of nucleus, contractile apparatus, cytoskeleton, and organelles <xref rid="bib27" ref-type="bibr">[27]</xref>, <xref rid="bib29" ref-type="bibr">[29]</xref>, <xref rid="bib31" ref-type="bibr">[31]</xref>, <xref rid="bib32" ref-type="bibr">[32]</xref>. Unlike ventricular cardiomyocytes, atrial cardiomyocytes do not possess an extensive T-tubule network but they do have prominent sarcoplasmic reticulum (SR) elements known as Z-tubules <xref rid="bib33" ref-type="bibr">[33]</xref>. Therefore, the atrial sarcolemma does not protrude into the cell, and voltage-operated Ca<sup>2+</sup> channels mainly function at the cell periphery <xref rid="bib34" ref-type="bibr">[34]</xref>. Atrial cardiomyocytes display specific granules (100–400 nm) situated mainly in the paranuclear area adjacent to the Golgi apparatus, which contain ANP, the BNP, and related peptides <xref rid="bib23" ref-type="bibr">[23]</xref>, <xref rid="bib24" ref-type="bibr">[24]</xref>.</p></sec><sec id="s0040"><label>2.2.2</label><title>Atrial interstitium</title><p>Atrial interstitium consists of cellular and extracellular components (see <xref rid="f0010" ref-type="fig">Fig. 2</xref>, <xref rid="f0015" ref-type="fig">Fig. 3</xref>, <xref rid="f0020" ref-type="fig">Fig. 4</xref>, <xref rid="f0025" ref-type="fig">Fig. 5</xref>). The cellular elements include fibroblast/myofibroblasts, adipocytes, undifferentiated mesenchymal cells, and isolated inflammatory cells. The atrial wall has a significant number of medium-sized blood vessels, especially in the sub-epicardium. Mature adipose tissue is frequently found in atrial myocardium, especially the epicardium, and often permeates the layers around intramural coronary branches. The number of adipocytes is highly variable and increases with age <xref rid="bib27" ref-type="bibr">[27]</xref>. The extracellular components consist of collagen fibres, which form most of the myocardial skeleton, proteoglycan particles, lipidic debris, spherical micro-particles, and matrix vesicles <xref rid="bib27" ref-type="bibr">[27]</xref>.</p><p>Collagen fibres, mainly type I, are both normal and essential components (<xref rid="f0005" ref-type="fig">Fig. 1</xref>, <xref rid="f0010" ref-type="fig">Fig. 2</xref>, <xref rid="f0015" ref-type="fig">Fig. 3</xref>, <xref rid="f0020" ref-type="fig">Fig. 4</xref>, <xref rid="f0025" ref-type="fig">Fig. 5</xref>). Atrial fibrous tissue may be sub-divided into pure interstitial and perivascular (or adventitial). Interstitial collagen fibres represent ×5% of the atrial wall volume. The atrial myocardium is also the site of sparse postganglionic nerve endings (from the ‘intrinsic cardiac nervous system’), mostly within discrete fat pads but also among cardiomyocytes <xref rid="bib35" ref-type="bibr">[35]</xref>.</p></sec></sec></sec><sec id="s0045"><label>3</label><title>Atrial-specific physiological and functional considerations</title><sec id="s0050"><label>3.1</label><title>Atrial-selective electrophysiological properties</title><p>The atria have a number of electrophysiological features that distinguish them from the ventricles and govern their arrhythmia susceptibility.</p></sec><sec id="s0055"><label>3.2</label><title>Action potential/ion-channel properties</title><p>Atrial cardiomyocytes have distinct action potential (AP) properties from ventricular cardiomyocytes, resulting in a large part from distinct ion-channel properties and distribution (<xref rid="f0030" ref-type="fig">Fig. 6</xref>A) <xref rid="bib36" ref-type="bibr">[36]</xref>, <xref rid="bib37" ref-type="bibr">[37]</xref>. Atrial background inward-rectifier K<sup>+</sup> current (I<sub>K1</sub>) is smaller than that of ventricular K<sup>+</sup> current, resulting in a less negative resting potential and more gradual slope of phase-3 repolarization. Atrial cells also have two K<sup>+</sup>-currents that are absent in ventricle cells: the ultrarapid delayed rectifier current (<italic>I</italic><sub>Kur</sub>) and the acetylcholine-regulated K<sup>+</sup>-current (<italic>I</italic><sub>KACh</sub>). In addition, there is evidence that atrial Na<sup>+</sup>-current has different properties compared with ventricular current <xref rid="bib38" ref-type="bibr">[38]</xref>. As well as distinctions between atrial and ventricular APs, different atrial regions may have discrete AP and ion-channel properties <xref rid="bib37" ref-type="bibr">[37]</xref>, <xref rid="bib39" ref-type="bibr">[39]</xref>. These cellular electrophysiological characteristics have implications for antiarrhythmic drug action and design, and may also affect the responses to atrial arrhythmias and disease <xref rid="bib36" ref-type="bibr">[36]</xref>, <xref rid="bib37" ref-type="bibr">[37]</xref>.</p></sec><sec id="s0060"><label>3.3</label><title>Intercellular coupling properties</title><p>The atria have a different pattern of cell-to-cell coupling protein (connexin) distribution compared with ventricular myocardium <xref rid="bib36" ref-type="bibr">[36]</xref>. Whereas working ventricular cardiomyocytes express connexin-43 exclusively, atrial cardiomyocytes have significant expression of connexin-40 (<xref rid="f0030" ref-type="fig">Fig. 6</xref>B) <xref rid="bib36" ref-type="bibr">[36]</xref>. Heterogeneities in connexin-40 distribution are common in paroxysmal AF and may play a pathophysiological role <xref rid="bib40" ref-type="bibr">[40]</xref>, and gene variants affecting connexin-40 sequence and/or transcription predispose to AF occurrence <xref rid="bib41" ref-type="bibr">[41]</xref>.</p></sec><sec id="s0065"><label>3.4</label><title>Atrial structural properties</title><p>The atria have a very complex 3D structure (<xref rid="f0030" ref-type="fig">Fig. 6</xref>C) not found in the ventricles. These include interatrial connections limited to Bachmann׳s bundle, the septum, and the CS; pectinate muscles, the crista terminalis, and fibres surrounding the coronary sinus in the right atrium; and the PVs with complex fibre orientation around them in the LA. These structural complexities have important potential implications for atrial patho-physiology and management of atrial arrhythmias <xref rid="bib42" ref-type="bibr">[42]</xref>. Extensive recent work has gone into the realistic mathematical reconstruction of such geometric complexities <xref rid="bib43" ref-type="bibr">[43]</xref>, and they have been incorporated into analytical approaches designed to implement patient-specific arrhythmia therapies <xref rid="bib44" ref-type="bibr">[44]</xref>. Cable-like strands of atrial tissue like the pectinate muscles and crista terminalis are organised such that conduction within them is primarily longitudinal, with an ‘anisotropy ratio’ (longitudinal/transverse conduction velocities) as great as 10, whereas in working ventricular muscle the ratio is typically more between 2 and 4 <xref rid="bib45" ref-type="bibr">[45]</xref>.</p></sec><sec id="s0070"><label>3.5</label><title>Autonomic ganglia</title><p>There are autonomic ganglia on the surface of the heart that are important way-stations for cardiac autonomic control <xref rid="bib46" ref-type="bibr">[46]</xref>. Moreover, alterations in local cardiac innervation and intracardiac autonomic reflexes play an important role in physiology and arrhythmia control. Most of the cardiac autonomic ganglia are located on the atria, and in particular in the region of the PV ostia. Thus, they are well positioned to affect atrial electrical activity in regions particularly important in AF, and their alteration by therapeutic manoeuvers like PV ablation may contribute to antiarrhythmic efficacy <xref rid="bib42" ref-type="bibr">[42]</xref>, <xref rid="bib46" ref-type="bibr">[46]</xref>, <xref rid="bib47" ref-type="bibr">[47]</xref>.</p></sec><sec id="s0075"><label>3.6</label><title>Left atrium mechanics</title><p>The left atrial contribution to overall cardiovascular performance is determined by unique factors. First, left atrial function critically determines left ventricular (LV) filling. Second, chamber-specific structural, electrical and ion remodelling alter left atrial function and arrhythmia susceptibility. Third, atrial function is highly relevant for the therapeutic responses of AF. Fourth, LA volume is an important biomarker that integrates the magnitude and duration of LV diastolic dysfunction. The development of sophisticated, non-invasive indices of LA size, and function might help to clinically exploit the importance of LA function in prognosis and risk stratification <xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib48" ref-type="bibr">[48]</xref>.</p><p>Fibre orientation of the two thin muscular layers (the fascicles of which both originate and terminate at the atrioventricular ring) introduce a complexity that challenges functional analysis. Ultrastructurally, atrial cardiomyocytes are smaller in diameter, have fewer T-tubules, and more abundant Golgi apparatus than ventricular. In addition, rates of contraction and relaxation, conduction velocity, and anisotropy differ, as does the myosin isoform composition and the expression of ion transporters, channels, and gap junctional proteins (see relevant sections).</p></sec><sec id="s0080"><label>3.7</label><title>Functions of the left atrium</title><p>The principal role of the LA is to modulate LV filling and cardiovascular performance by operating as a reservoir for PV return during LV systole, a conduit for PV return during early LV diastole, and as a booster pump that augments LV filling during LV diastole. There is a critical interplay between these atrial functions and ventricular systolic and diastolic performance. Thus, while LA compliance (or its inverse, stiffness), and, to a lesser extent, LA contractility and relaxation are the major determinants of reservoir function during LV systole, LV end-systolic volume and descent of the LV base during systole are important contributors. Conduit function is also governed by LA compliance and is reciprocally related to reservoir function, but because the mitral valve is open in diastole, conduit function is also closely related to LV compliance (of which relaxation is a major determinant). Atrial booster-pump function reflects the magnitude and timing of atrial contractility, but also depends on venous return (atrial preload), LV end-diastolic pressures (atrial afterload), and LV systolic reserve.</p><sec id="s0085"><label>3.7.1</label><title>Left atrium booster-pump function</title><p>Left atrium booster-pump function represents the augmented LV-filling resulting from active atrial contraction (minus retrograde blood-ejection into the PVs) and has been estimated by measurements of (i) cardiac output with and without effective atrial systole, (ii) relative LV-filling using spectral Doppler of transmitral, PV, and LA-appendage flow, (iii) LA-shortening and volumetric analysis, and (iv) tissue Doppler and deformation analysis (strain and strain-rate imaging) of the LA-body <xref rid="bib1" ref-type="bibr">[1]</xref>. Booster-pump function can also be evaluated echocardiographically by estimating the kinetic energy and force generated by LA contraction. The relative importance of the LA contribution to LV filling and cardiac output remain controversial. A load-independent index of LA contraction based on the analysis of instantaneous relation between LA pressure and volume, analogous to LV end-systolic elastance measurements, has been used as a load-independent measure of LA pump function, validated ex vivo and in the intact dog (<xref rid="f0035" ref-type="fig">Fig. 7</xref>) <xref rid="bib49" ref-type="bibr">[49]</xref>. While LA pressure–volume loops can be generated with invasive and semi-invasive means in humans <xref rid="bib50" ref-type="bibr">[50]</xref>, these methods are cumbersome, time-consuming, and difficult to apply. Measurement of myocardial strain and strain rate, which represent the magnitude and rate of myocardial deformation, assessed using either tissue Doppler velocities (tissue Doppler imaging, TDI) or by 2D echocardiographic (2D speckle-tracking or STE) techniques (<xref rid="f0040" ref-type="fig">Fig. 8</xref>) provide objective, non-invasive measurements of LA myocardial performance and contractility that overcome these limitations <xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib51" ref-type="bibr">[51]</xref>.</p></sec><sec id="s0090"><label>3.7.2</label><title>Left atrium reservoir function</title><p>Nearly half of the LV stroke volume and its associated energy are stored in the LA during LV systole. This energy is subsequently expended during the LV diastole. Reservoir function is governed largely by atrial compliance during ventricular systole, which is measured most rigorously by fitting atrial pressures and dimensions, taken either at the time of mitral valve opening/closure over a range of atrial pressures and volumes or during ventricular diastole, to an exponential equation <xref rid="bib52" ref-type="bibr">[52]</xref>. Although this method requires atrial dimensions and pressures, the relative reservoir function can be estimated simply with PV Doppler: the proportion of LA inflow during ventricular systole provides an index of the reservoir capacity of the atrium. Reservoir function can also be estimated from LA time–volume relations as either the total ejection fraction or distensibility fraction, calculated as the maximum minus minimum LA volume, normalised to maximal or minimal LA volume, respectively.</p><p>Although largely neglected, the LA–appendage is more compliant than the LA–body <xref rid="bib52" ref-type="bibr">[52]</xref>, so the contribution of the appendage to overall LA compliance is substantial with potential negative implications for routine atrial appendectomy/ligation during mitral valve surgery.</p><p>Left atrium strain and strain rates during LV systole predict successful sinus rhythm restoration following DC cardioversion or AF ablation, and are surrogates of atrial fibrosis and structural remodelling; coupled with an estimate of atrial pressure (e.g. transmitral E/E′), strain has the potential to estimate atrial distensibility non-invasively <xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib53" ref-type="bibr">[53]</xref>.</p></sec><sec id="s0095"><label>3.7.3</label><title>Left atrium conduit function</title><p>Left atrium conduit function occurs primarily during ventricular diastole and represents the trasport of blood volume that cannot be attributed to either reservoir or booster-pump functions, accounting for approximately one-third of atrial flow <xref rid="bib54" ref-type="bibr">[54]</xref>. A reciprocal relation exists between LA conduit and reservoir functions; a redistribution between these functions is an important compensatory mechanism that facilitates LV filling with myocardial ischaemia, hypertensive heart disease, and mitral stenosis (MS). Conduit function is estimated by the early diastolic transmitral flow, diastolic PV-flow, and LA strain and strain rate during early diastole.</p></sec></sec><sec id="s0100"><label>3.8</label><title>Atrial-selective Ca <xref rid="bib21" ref-type="bibr">[21]</xref> handling</title><p>There are major differences in the expression and function of Ca<sup>2+</sup>-handling proteins between atria and ventricles (<xref rid="f0045" ref-type="fig">Fig. 9</xref>) <xref rid="bib55" ref-type="bibr">[55]</xref>. The atria have reduced cardiomyocyte contraction and relaxation times and shorter Ca<sup>2+</sup>-transient duration <xref rid="bib56" ref-type="bibr">[56]</xref>, <xref rid="bib57" ref-type="bibr">[57]</xref>, <xref rid="bib58" ref-type="bibr">[58]</xref>. In atria, protein levels <xref rid="bib57" ref-type="bibr">[57]</xref>, <xref rid="bib59" ref-type="bibr">[59]</xref> and activity <xref rid="bib57" ref-type="bibr">[57]</xref>, <xref rid="bib59" ref-type="bibr">[59]</xref> of the SR Ca<sup>2+</sup>-ATPase2a (Serca2a) are two-fold higher, whereas the Serca2a-inhibitor phospholamban (PLB) is less abundant, vs. ventricles <xref rid="bib57" ref-type="bibr">[57]</xref>, <xref rid="bib59" ref-type="bibr">[59]</xref>. Atrial, but not ventricular, Serca2a is also regulated by sarcolipin (SLN) and SLN ablation increases atrial SR Ca<sup>2+</sup>-uptake and contractility <xref rid="bib60" ref-type="bibr">[60]</xref>. <sc>L</sc>-type Ca<sup>2+</sup>-current <xref rid="bib61" ref-type="bibr">[61]</xref> is similar in both chambers, whereas protein levels of ryanodine receptor type-2, calsequestrin, triadin, junction and Na<sup>2+</sup> –Ca<sup>2+</sup> exchanger are lower in atria than in ventricles <xref rid="bib59" ref-type="bibr">[59]</xref>, <xref rid="bib62" ref-type="bibr">[62]</xref>, <xref rid="bib63" ref-type="bibr">[63]</xref>. In contrast to ventricular myocardium, T-tubules are less abundant in atrial cardiomyocytes <xref rid="bib64" ref-type="bibr">[64]</xref>. In addition, atrial cardiomyocytes possess much more Ca<sup>2+</sup>-buffering mitochondria than ventricular cardiomyocytes <xref rid="bib56" ref-type="bibr">[56]</xref>. As a consequence, the atrial Ca<sup>2+</sup> wave starts in the myocyte periphery and then propagates to the centre of the myocyte, activating additional Ca<sup>2+</sup>-releasing sites in the SR <xref rid="bib55" ref-type="bibr">[55]</xref>.</p></sec></sec><sec id="s0105"><label>4</label><title>Pathology of atrial cardiomyopathies</title><sec id="s0110"><label>4.1</label><title>Lone atrial fibrillation (atrial fibrillation without concomitant conditions)</title><p>‘Lone’ atrial fibrillation (LAF) is diagnosed when no apparent explanation or underlying comorbidity can be identified <xref rid="bib65" ref-type="bibr">[65]</xref>, <xref rid="bib66" ref-type="bibr">[66]</xref>. Over the last few years, new epidemiological associations with AF have emerged and the number of true LAF cases has progressively decreased <xref rid="bib67" ref-type="bibr">[67]</xref>. Like AF associated with comorbidities, LAF occurs more frequently in males than in females with a ratio of 3–4:1 <xref rid="bib68" ref-type="bibr">[68]</xref>. Recent studies have shown that true cases of LAF can be diagnosed even in subjects older than 60 years, so that this age limit seems inappropriately conservative <xref rid="bib69" ref-type="bibr">[69]</xref>. At the same time, it is unclear whether cases with left atrial enlargement should be excluded from the LAF category. In fact, LA enlargement might even be the consequence of the arrhythmia <xref rid="bib70" ref-type="bibr">[70]</xref>.</p><p>‘Lone’ atrial fibrillation is at the lower end of the thromboembolic risk spectrum, with only a 1–2% cumulative 15-year risk of stroke <xref rid="bib66" ref-type="bibr">[66]</xref>. How-ever, with ageing and/or the occurrence of cardiovascular comorbidities, the risk of AF-related complications (including thromboembolic events) increases <xref rid="bib71" ref-type="bibr">[71]</xref>. Patients originally diagnosed with LAF may follow different clinical courses based on their left atrial volume: individuals who retain normal LA size throughout long-term follow-up show a relatively benign course, while those with LA enlargement experience adverse events like stroke, myocardial infarction, and heart failure <xref rid="bib72" ref-type="bibr">[72]</xref>. The majority of LAF patients first present with paroxysmal episodes and show low progression rates into permanent AF <xref rid="bib71" ref-type="bibr">[71]</xref>, <xref rid="bib73" ref-type="bibr">[73]</xref>.</p><p>Atrial fibrillation has clear genetic determinants <xref rid="bib7" ref-type="bibr">[7]</xref>. These include common gene variants with low predictive strength and rare gene mutations that have much greater penetrance <xref rid="bib7" ref-type="bibr">[7]</xref>.</p><p>Frustaci et al <xref rid="bib14" ref-type="bibr">[14]</xref>. explored the histological morphology of right atrial septal biopsies from patients with lone paroxysmal AF, finding chronic inflammatory infiltrates, foci of myocyte necrosis, focal replacement fibrosis, and myocyte cytoplasmic vacuoles consistent with myolysis. Of their 12 patients, 10 showed EHRAS class III changes and 2 showed EHRAS class II. Stiles et al <xref rid="bib74" ref-type="bibr">[74]</xref>. found bi-atrial structural change, conduction abnormalities, and sinus node dysfunction in paroxysmal LAF patients. Skalidis et al <xref rid="bib75" ref-type="bibr">[75]</xref>. demonstrated atrial perfusion abnormalities and coronary flow reserve impairment. Much more recently, morphometric assessment of atrial biopsies from the LA posterior wall of persistent or long-lasting persistent LAF patients demonstrated cardiomyocyte hypertrophy, myolytic damage, interstitial fibrosis, and reduced connexin-43 expression vs. controls <xref rid="bib76" ref-type="bibr">[76]</xref>.</p></sec><sec id="s0115"><label>4.2</label><title>Isolated atrial amyloidosis</title><p>The accumulation of insoluble, misfolded proteins is linked to an increasing number of age-related degenerative diseases <xref rid="bib77" ref-type="bibr">[77]</xref>. Amyloidosis represent the deposition of insoluble, fibrillar proteins in a cross b-sheet structure that characteristically binds dyes such as Congo red. The most common form of age-related or senile amyloidosis is limited to the atrium, a condition known as isolated atrial amyloidosis (IAA) <xref rid="bib17" ref-type="bibr">[17]</xref>, <xref rid="bib78" ref-type="bibr">[78]</xref>. The incidence of atrial amyloidosis increases with age, exceeding 90% in the ninth decade <xref rid="bib79" ref-type="bibr">[79]</xref>. Isolated atrial amyloidosis is also linked to structural heart disease. In atrial biopsies from 167 patients undergoing cardiac surgery, 23 of 26 amyloid-positive specimens were from patients with rheumatic heart disease (RHD), while the remaining 3 came from patients with atrial septal defects <xref rid="bib80" ref-type="bibr">[80]</xref>. The overall incidence of 16% was greater than that was seen in control atrial autopsy specimens from trauma victims (3%). Histologically, IAA is classified as EHRAS IVa (<xref rid="f0015" ref-type="fig">Fig. 3</xref>; <xref rid="t0010" ref-type="table">Table 2</xref>). Atrial natriuretic peptide is a fibrillogenic protein that forms IAA <xref rid="bib81" ref-type="bibr">[81]</xref>. Amyloid deposits are immunoreactive for ANP in most patients <xref rid="bib17" ref-type="bibr">[17]</xref>, while transthyretin, a transport protein implicated in systemic senile amyloidosis, was also identified in 10% <xref rid="bib4" ref-type="bibr">[4]</xref> (NT-pro-ANP has been identified in other studies <xref rid="bib82" ref-type="bibr">[82]</xref>). As with fibrosis, amyloidosis can cause local conduction block and P-wave duration is increased in IAA. Atrial amyloid is found more commonly in patients with AF vs. sinus rhythm (<xref rid="f0015" ref-type="fig">Fig. 3</xref>). Both AF and IAA increased with advancing age and female sex, but the relationship between the two is independent of age and gender <xref rid="bib83" ref-type="bibr">[83]</xref>, <xref rid="bib84" ref-type="bibr">[84]</xref>. Isolated atrial amyloidosis is detected in 80% of PV sleeves of elderly patients <xref rid="bib84" ref-type="bibr">[84]</xref>. For organ-specific amyloidosis such as Alzheimer׳s disease, there is no detectable correlation between quantity of fibrillar deposits and disease advancement <xref rid="bib85" ref-type="bibr">[85]</xref>. Rather, disease phenotype correlates most closely with accumulation of soluble, prefibrillar protein aggregates <xref rid="bib86" ref-type="bibr">[86]</xref>. Preamyloid oligomers (PAOs) are cytotoxic to cardiomyocytes <xref rid="bib87" ref-type="bibr">[87]</xref>. They do not bind Congo red and thus are not visible by standard amyloid staining methods. Using a conformation-specific antibody, PAOs often co-localising with ANP were detected in atrial samples of 74 of 92 patients without AF undergoing cardiac surgery <xref rid="bib88" ref-type="bibr">[88]</xref>. The preamyloid oligomer content was independently associated with hypertension. Additional studies are needed to further confirm this association and whether PAOs are increased in AF.</p></sec><sec id="s0120"><label>4.3</label><title>NPPA mutations</title><p>Atrial natriuretic peptide is released from the atria in response to atrial stretch or volume expansion, and produces natriuresis, diuresis, and vasodilation <xref rid="bib89" ref-type="bibr">[89]</xref>. It also interacts with other endogenous systems, inhibiting the renin–angiotensin-II–aldosterone and sympathetic nervous systems, and regulates ion currents <xref rid="bib90" ref-type="bibr">[90]</xref>, <xref rid="bib91" ref-type="bibr">[91]</xref>. Atrial natriuretic peptide-knockout mice develop cardiac hypertrophy and exaggerated responses to hypertrophic stress <xref rid="bib92" ref-type="bibr">[92]</xref>. The gene encoding the precursor protein for ANP, NPPA, encodes prepro-ANP, a 151 amino acid protein that includes a signal peptide cleaved off to form pro-ANP <xref rid="bib93" ref-type="bibr">[93]</xref>, which is stored in dense granules in the atria. Released pro-ANP undergoes proteolytic processing to generate N-terminal pro-ANP and ANP, 98 and 28 amino acids in length, respectively. N-terminal pro-ANP is cleaved into three hormones with biological activity similar to ANP: long-acting natriuretic hormone (LANH), vessel dilator peptide, and kaliuretic hormone.</p><p>Genetic studies have linked abnormal ANP production to familial atrial tachyrrhythmias and atrial cardiomyopathy. In a large family with Holt–Oram syndrome, a missense mutation in T-box transcription factor 5 (TBx5) resulted in an atypical phenotype with early-onset AF and the overexpression of multiple genes, including NPPA <xref rid="bib94" ref-type="bibr">[94]</xref>. In a large family with multiple members having early-onset LAF, a 2-bp deletion was identified that abolishes the ANP stop codon, producing a mature protein containing the usual 28 amino acids plus an anomalous C-terminus of 12 additional residues <xref rid="bib95" ref-type="bibr">[95]</xref>. The mutant ANP peptide is present in affected family members at plasma concentrations 5–10 times higher than wild-type ANP. Studies of the electrophysiological effects of ANP have been inconsistent <xref rid="bib96" ref-type="bibr">[96]</xref>.</p><p>Additional NPPA variants (S64R and A117V) have also been linked to AF <xref rid="bib97" ref-type="bibr">[97]</xref>, <xref rid="bib98" ref-type="bibr">[98]</xref>. The S64R variant occurs in vessel dilator peptide rather than ANP. A truncated peptide containing this mutation increased I<sub>Ks</sub> several fold, an effect predicted to shorten action potential duration (APD) <xref rid="bib97" ref-type="bibr">[97]</xref>, but the variant has also been identified in unaffected elderly individuals without AF <xref rid="bib96" ref-type="bibr">[96]</xref>, and its functional pathological significance remains uncertain.</p><p>More recently, an autosomal-recessive atrial cardiomyopathy was described in patients harbouring an NPPA mutation (Arg150Gln) predicted to be damaging to protein structure <xref rid="bib99" ref-type="bibr">[99]</xref>. The phenotype is characterised by biatrial enlargement, initially associated with atrial tachyarrhythmias such as AF and atrial flutter <xref rid="bib100" ref-type="bibr">[100]</xref>. Biatrial enlargement progresses to partial and ultimately severe atrial standstill, associated with progressive decreases in atrial voltage and extensive atrial scarring. Whether atrial structural changes are primary, or secondary to atrial enlargement, is unknown. Loss of the antihypertrophic effects of ANP may cause the massive atrial enlargement seen in these patients.</p></sec><sec id="s0125"><label>4.4</label><title>Hereditary muscular dystrophies</title><p>A common finding in many inherited muscular dystrophies is cardiac involvement, related to myocyte degeneration with fatty or fibrotic replacement (<xref rid="t0015" ref-type="table">Table 3</xref>) <xref rid="bib101" ref-type="bibr">[101]</xref>, <xref rid="bib102" ref-type="bibr">[102]</xref>, <xref rid="bib103" ref-type="bibr">[103]</xref>. In some cases, this can be the presenting or predominant clinical manifestation. Multiple complexes and pathways are involved in the maintenance of myocyte integrity, and a defective or absent protein component can lead to progressive cell death. The large dystrophin–glycoprotein complex links the myocyte cytoskeleton to the extracellular basement membrane. For diseases of dystrophin, sarcoglycans, and other complex-related proteins, the most prominent manifestation is a dilated cardiomyopathy due to diffuse myocyte involvement, with arrhythmias and conduction abnormalities secondary to LV dysfunction <xref rid="bib101" ref-type="bibr">[101]</xref>, <xref rid="bib102" ref-type="bibr">[102]</xref>, <xref rid="bib103" ref-type="bibr">[103]</xref>, <xref rid="bib104" ref-type="bibr">[104]</xref>, <xref rid="bib105" ref-type="bibr">[105]</xref>. Specific atrial involvement can lead to sinus node disease and/or atrial arrhythmias with associated thromboembolic events <xref rid="bib106" ref-type="bibr">[106]</xref>, <xref rid="bib107" ref-type="bibr">[107]</xref>. Myotonic dystrophy type I is the most common muscular dystrophy presenting in adults <xref rid="bib108" ref-type="bibr">[108]</xref>. Up to 15% develop atrial arrhythmias during a 10-year follow-up <xref rid="bib109" ref-type="bibr">[109]</xref>. The presence of conduction defects and atrial arrhythmias are independent risk factors for sudden death <xref rid="bib103" ref-type="bibr">[103]</xref>, <xref rid="bib110" ref-type="bibr">[110]</xref>. In Emery-Dreifuss and Limb-Girdle type IB disease, widespread atrial fibrosis can lead to atrial standstill <xref rid="bib101" ref-type="bibr">[101]</xref>. In Emery-Dreifuss, AF and atrial flutter with slow ventricular responses and asystolic pauses can be observed, coupled with the occurrence of thromboembolism and stroke <xref rid="bib111" ref-type="bibr">[111]</xref>. In facioscapulohumeral muscular dystrophy, arrhythmias are rare, with the most common being supraventricular tachycardia <xref rid="bib112" ref-type="bibr">[112]</xref>. Histologically, the tissue composition may vary substantially, including all EHRAS classes (see <xref rid="t0010" ref-type="table">Table 2</xref>).</p></sec><sec id="s0130"><label>4.5</label><title>Atrial cardiomyopathy due to congestive heart failure</title><p>Congestive heart failure (CHF) is a common cause (contributing condition) of AF <xref rid="bib3" ref-type="bibr">[3]</xref>. The CHF-induced atrial phenotype is complex. A particularly important component is atrial fibrosis, which in experimental models occurs earlier in the course of CHF, and to a much greater extent, than in the ventricles, at least in part because of atrial-ventricular fibroblast–phenotype differences <xref rid="bib4" ref-type="bibr">[4]</xref>. Congestive heart failure-related fibrosis slowly, if at all, and the AF-promoting substrate predominantly tracks fibrosis rather than other components of atrial remodelling like ion-current or connexin changes. Unlike the case for AF-induced remodelling, the atrial ion-current changes in CHF do not abbreviate APD or cause overall conduction slowing <xref rid="bib113" ref-type="bibr">[113]</xref>, <xref rid="bib114" ref-type="bibr">[114]</xref>, so they do not contribute directly to arrhythmogenesis. On the other hand, CHF atria are prone to triggered activity due to abnormal Ca<sup>2+</sup> handling <xref rid="bib115" ref-type="bibr">[115]</xref>. The principle underlying abnormality appears to be increased cellular Ca<sup>2+</sup> load. While the underlying mechanisms are not completely clear, they likely include phospholamban hyperphosphorylation (which increases SR Ca<sup>2+</sup> up-take) and AP prolongation (which increases Ca<sup>2+</sup> loading by enhancing the period during which <sc>L</sc>-type Ca<sup>2+</sup> channels are open). The final phenotypic product of the CHF-induced Ca<sup>2+</sup>-handling abnormalities is focal ectopic activity due to aberrant diastolic Ca<sup>2+</sup>-release events from the SR, similar to abnormalities seen with paroxysmal and long-standing persistent AF <xref rid="bib116" ref-type="bibr">[116]</xref>.</p><p>Congestive heart failure also causes atrial hypocontractility, despite increased cytosolic Ca<sup>2+</sup> transient, indicating reduced contractile sensitivity to intracellular Ca<sup>2+</sup>, possibly because of reduced expression of total and phosphorylated myosin-binding protein C <xref rid="bib115" ref-type="bibr">[115]</xref>. This hypocon-tractility may be important in contributing to the increased likelihood of thromboembolic events in AF patients who also have CHF. Of the atrial changes that occur in CHF, many are also seen in the ventricle. However, the highly atrial-selective fibrosis may contribute to atrial cardiomyopathy in the absence of clear signs of disturbed ventricular function, particularly in patients with prior CHF events who later become well-compensated under therapy or after resolution of the underlying cause. Collagen depositions are prominent in CHF, leading most commonly to EHRAS Class II and III properties. However, EHRAS Class IVi and IVf may also be found in certain areas of the atria (see <xref rid="t0010" ref-type="table">Table 2</xref>).</p></sec><sec id="s0135"><label>4.6</label><title>Obstructive sleep apnoea</title><p>Obstructive sleep apnoea (OSA) is known to impair cardiac function and predispose to AF <xref rid="bib117" ref-type="bibr">[117]</xref>, <xref rid="bib118" ref-type="bibr">[118]</xref>, <xref rid="bib119" ref-type="bibr">[119]</xref>. Obstructive sleep apnoea prolongs atrial conduction times, slows atrial conduction, reduces atrial-electrogram voltages and increases electrogram complexity <xref rid="bib117" ref-type="bibr">[117]</xref>, <xref rid="bib118" ref-type="bibr">[118]</xref>. Signal-averaged P-wave duration is increased by OSA, and decreases significantly with continuous positive airway pressure treatment <xref rid="bib120" ref-type="bibr">[120]</xref>. In a rat model, repeated obstructive apnoea over a 4-week period increases AF vulnerability and slows atrial conduction by altering connexin-43 expression and inducing atrial fibrosis <xref rid="bib121" ref-type="bibr">[121]</xref>.</p></sec><sec id="s0140"><label>4.7</label><title>Atrial fibrillation-induced atrial remodelling</title><p>Atrial fibrillation itself induces atrial remodelling that contributes to the maintenance, progression, and stabilisation of AF <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>. The high atrial rate causes cellular Ca<sup>2+</sup> loading. This induces a decrease in I<sub>Ca,L</sub> due to down-regulation of the underlying Cav1.2 subunits, and an increase in constitutively active I<sub>K,Ach</sub><xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>, <xref rid="bib122" ref-type="bibr">[122]</xref>, <xref rid="bib123" ref-type="bibr">[123]</xref> MiR-328 up-regulation with consequent repression of Cav1.2-translation and Ca<sup>2+</sup> -dependent calpain acti-vation, causing proteolytic breakdown of <sc>L</sc>-type Ca<sup>2+</sup> channels <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>. The rate-dependent up-regulation of I<sub>K1</sub> results from a Ca<sup>2+</sup>/calcineurin/NFAT-mediated down-regulation of the inhibitory miR-26, removing translational–inhibition of Kir2.1 <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>. Increased I<sub>K1</sub> stabilizes AF by abbreviating and hyperpolarizing atrial cardiomyocyte Aps <xref rid="bib41" ref-type="bibr">[41]</xref>. Small-conductance Ca<sup>2+</sup>-activated K<sup>+</sup> (SK) currents (I<sub>SK</sub>) also play a role in AF <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>. Computational modelling shows that increased total inward-rectifier K<sup>+</sup> current in chronic atrial fibrillation (cAF) is the major contributor to the stabilisation of re-entrant circuits by shortening APD and hyperpolarizing the resting membrane potential <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>.</p><p>Atrial tachycardia remodelling reduces Ca<sup>2+</sup>-transient amplitude by a variety of mechanisms, contributing to atrial contractile dysfunction <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>, <xref rid="bib124" ref-type="bibr">[124]</xref>. Reduced atrial contractility causes atrial ‘stunning’ that may be involved in thromboembolic complications.</p><p>Long-term atrial tachycardia remodelling causes conduction slowing in several animal models, at least partly due to I<sub>Na</sub> down-regulaton <xref rid="bib122" ref-type="bibr">[122]</xref>. Heterogeneously distributed gap-junction uncoupling due to connexin remodelling likely contributes to atrial conduction slowing <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>. Heterogeneity in connexin-40 distribution correlates with AF stability in goats with repetitive burst-pacing-induced AF <xref rid="bib125" ref-type="bibr">[125]</xref>. Connexin-40 expression decreases in the PVs of dogs with AF-related remodelling, possibly due to tachycardia-induced connexin-degradation by calpains <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>.</p><p>Long-term atrial tachycardia/AF may itself cause atrial fibrosis that contributes to long-term persistence <xref rid="bib126" ref-type="bibr">[126]</xref>. Rapid atrial firing promotes fibroblast differentiation to collagen-secreting myofibroblasts through autocrine and paracrine mechanisms <xref rid="bib32" ref-type="bibr">[32]</xref>. Atrial tachycardia-induced NFAT-mediated decreases in fibroblast miR-26 may also contribute to structural remodelling. Atrial fibroblasts have non-selective cation channels of the transient receptor potential (TRP) family that carry Ca<sup>2+</sup> into the cell; the increased cell-Ca<sup>2+</sup> then triggers increased collagen production. Since miR-26 represses TRPC3 gene expression, miR-26 reductions increase TRPC3 expression, promoting fibroblast Ca<sup>2+</sup> entry that causes proliferation/myofibroblast differentiation <xref rid="bib127" ref-type="bibr">[127]</xref>. TRPM7 may similarly contribute to fibrotic changes in AF <xref rid="bib128" ref-type="bibr">[128]</xref>.</p><p>APD shortening in cAF patients also results from increased inward-rectifier K<sup>+</sup> currents <xref rid="bib129" ref-type="bibr">[129]</xref>, both I<sub>K1</sub> and a constitutive form of I<sub>K,Ach</sub><xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>. Agonist-activated I<sub>K,ACh</sub> is decreased in right atrium of AF patients because of a reduction in underlying Kir3.1 and Kir3.4 subunits <xref rid="bib129" ref-type="bibr">[129]</xref>, whereas agonist-independent current is increased <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>.</p><p>Atrial cardiomyocytes from patients with long-standing persistent AF show spontaneous diastolic SR Ca<sup>2+</sup>-release events (SCaEs) and delayed after depolarizations (DADs) <xref rid="bib130" ref-type="bibr">[130]</xref>. CaMKII-dependent RyR2 hyperphosphorylation underlies the SR Ca<sup>2+</sup> leak and SCaEs <xref rid="bib32" ref-type="bibr">[32]</xref>, <xref rid="bib106" ref-type="bibr">[106]</xref>, <xref rid="bib130" ref-type="bibr">[130]</xref>. Protein kinase A-dependent RyR2 hyperphosphorylation also occurs <xref rid="bib130" ref-type="bibr">[130]</xref>, likely promoting the dissociation of the inhibitory FKBP12.6 subunit from the RyR2 channel. Larger inward NCX current may also contribute to the stronger propensity for DADs <xref rid="bib130" ref-type="bibr">[130]</xref>.</p><p>Although initial work pointed to unchanged I<sub>Na</sub> or mRNA expression of the Nav1.5 a-subunit in AF patients, recent studies reported reduced peak I<sub>Na</sub><xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>. There is also evidence for increased I<sub>Na,late</sub>, although its functional consequences are less clear. Altered mRNA and protein levels of connexin-40/-43 may also contribute to re-entry-promoting conduction abnormalities in cAF patients. Reduced connexin-40 expression together with lateralization to the transverse cell membrane may cause heterogeneous conduction <xref rid="bib41" ref-type="bibr">[41]</xref>, <xref rid="bib116" ref-type="bibr">[116]</xref>.</p><p>Overall, ion-channel changes contribute to AF stabilisation and early recurrence after cardioversion. Ca<sup>2+</sup>-handling abnormalities are involved in atrial ectopy, and atrial fibrosis is important in the progression of long-term persistent AF to resistant forms. Atrial fibrillation-induced atrial myopathy has changes that depend on AF duration. Very short-term AF produces no ultrastructural alterations, while AF lasting several weeks causes EHRAS I alterations <xref rid="bib13" ref-type="bibr">[13]</xref>. Long-term persistent AF produces EHRA III changes <xref rid="bib126" ref-type="bibr">[126]</xref>.</p></sec><sec id="s0145"><label>4.8</label><title>Drug-related atrial fibrillation</title><p>A large number of drug classes have been associated with the induction of AF either in patients without heart disease or in individuals with pre-existing cardiac disorders (<xref rid="t0020" ref-type="table">Table 4</xref>) <xref rid="bib131" ref-type="bibr">[131]</xref>, but drug-induced AF (DIAF) has received less attention than that it might deserve. The overall incidence of DIAF is still unknown for several reasons: (a) the evidence associating specific drugs with AF has largely been based on anecdotal reports, with very few controlled prospective clinical trials, (b) DIAF is often paroxysmal and documentation may be difficult/poor, (c) while DIAF is easily recognised if it occurs just after i.v. drug administrations (e.g. adenosine or dobutamine), AF episodes can be missed if they appear after multiple exposures (e.g. chemotherapy), (d) patients often receive multiple drugs, making the specific culprit agent difficult to identify, (e) with non-cardiovascular drugs, DIAF is often diagnosed by non-cardiologists, often with an imprecise description of the arrhythmic event and clinical history <xref rid="bib132" ref-type="bibr">[132]</xref>. Multiple mechanisms have been suggested to explain the pathogenesis of DIAF: (a) direct atrial electrophysiological effects like abbreviated refractoriness, slowed conduction, or triggered activity due to Ca<sup>2+</sup> loading, (b) changes in autonomic tone, (c) myocardial ischaemia, (d) direct myocardial damage and other mechanisms such as release of pro-inflammatory cytokines, oxidative stress, hypotension, and electrolyte disturbances <xref rid="bib131" ref-type="bibr">[131]</xref>, <xref rid="bib132" ref-type="bibr">[132]</xref>.</p><p>In the majority of cases, DIAF is a benign self-limited disorder. However, DIAF may be clinically serious in polymedicated patients with underlying comorbidities <xref rid="bib132" ref-type="bibr">[132]</xref>. Discontinuation of the causative drug(s) usually leads to cardioversion in few minutes or hours. When AF persists, treatment is similar to that of non-DIAF patients <xref rid="bib133" ref-type="bibr">[133]</xref>, <xref rid="bib134" ref-type="bibr">[134]</xref>. Because of the wide range of mechanisms by which drugs cause AF, the histological changes associated with DIAF may vary substantially from EHRAS class I–IV (see <xref rid="t0010" ref-type="table">Table 2</xref> for reference). Future studies are warranted to assess specific effects of various drugs on atrial tissue.</p></sec><sec id="s0150"><label>4.9</label><title>Myocarditis</title><p>Myocarditis refers to an inflammatory disease of the heart, which occurs as a result of exposure to external triggers (e.g. infectious agents, toxins, or drugs) or internal ones like autoimmune disorders <xref rid="bib135" ref-type="bibr">[135]</xref>, <xref rid="bib136" ref-type="bibr">[136]</xref>.</p><p>The incidence is difficult to ascertain since it depends on the diagnostic criteria. A likely estimate is 8 to 10 per 100 000 population, representing the third leading cause of sudden death after hypertrophic cardiomyopathy and coronary artery disease <xref rid="bib137" ref-type="bibr">[137]</xref>. In autopsy series, the prevalence of myocarditis varies from 2% to 42% in young adults with sudden death <xref rid="bib138" ref-type="bibr">[138]</xref>, <xref rid="bib139" ref-type="bibr">[139]</xref>. Biopsy demonstrates an inflammatory infiltrate in 9–16% of patients with unexplained non-ischaemic dilated cardiomyopathy <xref rid="bib140" ref-type="bibr">[140]</xref>, <xref rid="bib141" ref-type="bibr">[141]</xref>.</p><p>Myocarditis is defined by the ‘Dallas criteria’ as the presence of a myocardial inflammatory infiltrate with necrosis and/or degeneration of adjacent cardiomyocytes of non-ischaemic nature <xref rid="bib142" ref-type="bibr">[142]</xref>. According to the type of inflammatory cell, myocarditis may be subdivided into lymphocytic, eosinophilic, polymorphic, giant-cell myocarditis, and cardiac sarcoidosis <xref rid="bib136" ref-type="bibr">[136]</xref>.</p><p>Atrial fibrillation is frequently part of the clinical presentation of myocarditis. In 245 patients with clinically suspected myocarditis, AF occurred in about 30% <xref rid="bib143" ref-type="bibr">[143]</xref>. Myocarditis with lone atrial involvement is rarly diagnosed <xref rid="bib144" ref-type="bibr">[144]</xref>, <xref rid="bib145" ref-type="bibr">[145]</xref>, <xref rid="bib146" ref-type="bibr">[146]</xref>. This may reflect the fact that atrial myocardium is not methodically sampled either at autopsy or in routine endomyocardial biopsy. In most such cases, AF dominated the clinical picture, suggesting a role for architectural remodelling that interferes with atrial conduction <xref rid="bib9" ref-type="bibr">[9]</xref>, <xref rid="bib147" ref-type="bibr">[147]</xref>. Giant-cell myocarditis is a distinct – and probably autoimmune – myocarditis characterised by diffuse infiltration by lymphocytes and numerous multinucleated giant-cells, frequent eosinophils, cardiomyocyte necrosis and, ultimately, fibrosis. The natural course is often fulminant and mortality is high if untreated. An isolated atrial variant of giant-cell myocarditis was first reported in 1964 <xref rid="bib148" ref-type="bibr">[148]</xref>. Since then, only a few cases have been described in the English language literature. The atrial variant appears to have a more favourable course compared with the classical form <xref rid="bib149" ref-type="bibr">[149]</xref>. The atrial giant-cell myocarditis may represent a distinct entity, potentially attributable to atrium-specific auto-antigens <xref rid="bib150" ref-type="bibr">[150]</xref>. EHRAS Class IVi is observed in patients with atrial myocarditis. As myocarditis persists and enters a chronic phase, characteristics may change to EHRAS Class III (see <xref rid="t0010" ref-type="table">Table 2</xref>).</p></sec><sec id="s0155"><label>4.10</label><title>Atrial cardiomyopathy associated with genetic repolarization disturbances</title><p>Atrial standstill, a severe form of atrial cardiomyopathy, is associated with combined heterozygous mutations of SCN5A and Connexin-40 genes <xref rid="bib151" ref-type="bibr">[151]</xref>. Gain-of-function mutations in K+-channel subunits (e.g. KCNQ1, KCNH2, KCND3, and KCNE5) or loss-of-function mutations in KCN5A have been identified in AF patients <xref rid="bib152" ref-type="bibr">[152]</xref>. Thus, either gain or loss of K<sup>+</sup>-channel function can cause AF, indicating that repolarization requires optimal tuning and deficits in either direction can be arrhythmogenic. Recently, early repolarization or J-wave syndrome has been associated with AF although, in middle-aged subjects, early repolarization in inferior leads did not predict AF <xref rid="bib153" ref-type="bibr">[153]</xref>. A gain-of-function mutation in KCNJ8, encoding the cardiac Kir 6.1 (KATP) channel, is associated with both increased AF susceptibility and early repolarization <xref rid="bib154" ref-type="bibr">[154]</xref>. There is an established association between atrial arrhythmias and primary ventricular arrhythmia syndromes, which was first reported among conditions that manifest with obvious structural abnormalities <xref rid="bib155" ref-type="bibr">[155]</xref>. Atrial fibrillation is relatively common in hypertrophic cardiomyopathy (prevalence×20%) <xref rid="bib156" ref-type="bibr">[156]</xref>. In arrhythmogenic right ventricular cardiomyopathy, an even higher proportion (up to 40%) of patients may manifest AF <xref rid="bib157" ref-type="bibr">[157]</xref>. The association with AF also extends to primary arrhythmia syndromes without obvious structural heart disease. Supraventricular tachycardias, primarily AF/AFl, have been reported in Brugada syndrome <xref rid="bib158" ref-type="bibr">[158]</xref>, <xref rid="bib159" ref-type="bibr">[159]</xref>. Among long QT syndrome (LQTS) patients, prolongation of action potentials leading to atrial fibrillation has been suggested to be an atrial form of ‘torsades de pointes’ <xref rid="bib152" ref-type="bibr">[152]</xref>. A subtle form of ‘cardiomyopathy’ that includes increased left atrial volumes occurs in ×12% of LQTS patients <xref rid="bib160" ref-type="bibr">[160]</xref>. The reports available mostly implicate genetic variants in Na<sup>+</sup>-channel genes <xref rid="bib161" ref-type="bibr">[161]</xref>. Patients with early-onset lone AF have a high prevalence of LQTS-associated SCN5A variants <xref rid="bib162" ref-type="bibr">[162]</xref>. A mouse model of LQT3 is prone to atrial arrhythmias due to EADs <xref rid="bib163" ref-type="bibr">[163]</xref>. There are sporadic reports of atrial arrhythmias in patients with CPVT <xref rid="bib164" ref-type="bibr">[164]</xref>. Taken together, the associations between AF and sudden death syndromes likely reflect common mechanisms between atrial and ventricular arrhythmogenesis.</p></sec><sec id="s0160"><label>4.11</label><title>Ageing</title><p>In elderly dogs, premature impulses show markedly slowed conduction, associated with a doubling of fibrous-tissue content APD prolongation and spatial heterogeneity in repolarization <xref rid="bib165" ref-type="bibr">[165]</xref>, <xref rid="bib166" ref-type="bibr">[166]</xref>. Clinical mapping studies have also demonstrated similar findings of conduction abnormalities, prolonged refractoriness, reduced myocardial voltage, and a greater number of double potentials and fractionated electrograms <xref rid="bib167" ref-type="bibr">[167]</xref>, <xref rid="bib168" ref-type="bibr">[168]</xref>. Perhaps as a result of these atrial changes, alteration of wavefront propagation velocities has been described with an inverse correlation to age <xref rid="bib169" ref-type="bibr">[169]</xref>. Histologically, fibrotic changes are the most obvious alteration (EHRAS Class II; see <xref rid="t0010" ref-type="table">Table 2</xref>).</p></sec><sec id="s0165"><label>4.12</label><title>Hypertension</title><p>Hypertension accounts for at least one in five incident AF cases <xref rid="bib170" ref-type="bibr">[170]</xref>. In hypertensive subjects, both left atrial enlargement and P-wave changes are predictive of AF occurrence <xref rid="bib171" ref-type="bibr">[171]</xref>, <xref rid="bib172" ref-type="bibr">[172]</xref>.</p><p>In small animal models, mimicking hypertension by partial aortic clamping induces LA hypertrophy, fibrosis, connexin-43 down-regulation and slow/inhomogeneous conduction <xref rid="bib173" ref-type="bibr">[173]</xref>. Prenatal corticosteroid exposure-induced hypertension in sheep causes atrial conduction abnormalities, wavelength shortening, and increased AF <xref rid="bib174" ref-type="bibr">[174]</xref>. Lau et al. utilised a one-kidney one-clip model to investigate the impact of short- and long-term hypertension on the evolution of an atrial cardiomyopathy <xref rid="bib175" ref-type="bibr">[175]</xref>, <xref rid="bib176" ref-type="bibr">[176]</xref>. Utilisation of this model intrinsically is more reflective of a disordered renin–angiotensin axis. Short-term hypertension progressively enlarged the LA, reduced LA emptying fraction, prolonged atrial refractoriness, slowed conduction, and caused LA interstitial fibrosis and inflammatory cell infiltration <xref rid="bib175" ref-type="bibr">[175]</xref>, <xref rid="bib176" ref-type="bibr">[176]</xref>. In patients with established hypertension and LV hypertrophy, there is global and regional conduction slowing associated with fractionated electrograms and double potentials along the crista terminalis, along with an increase in low-voltage areas <xref rid="bib177" ref-type="bibr">[177]</xref>.</p><p>Importantly, population studies show increased AF risk even with ‘pre-hypertension’ (systolic blood pressure 130–139 mmHg) <xref rid="bib178" ref-type="bibr">[178]</xref>. The ab-normal atrial substrate is reversible, with studies demonstrating improved electrical and structural parameters and reduced AF burden following treatment with renin–angiotensin–aldosterone system blockers <xref rid="bib179" ref-type="bibr">[179]</xref>, <xref rid="bib180" ref-type="bibr">[180]</xref>, <xref rid="bib181" ref-type="bibr">[181]</xref>. In patients with resistant hypertension and improved blood pressure following renal denervation, there was a global improvement in atrial conduction and reduced complex fractionated activity. Histologically, pressure overload induces hypertrophy of atrial myocytes (EHRAS Class I). Collagen deposition may also occur (EHRAS II–III) with more severe hypertension causing LV hypertrophy and diastolic dysfunction (see <xref rid="t0010" ref-type="table">Table 2</xref>).</p></sec><sec id="s0170"><label>4.13</label><title>Obesity</title><p>Several population-based studies have demonstrated a robust relationship between obesity and AF <xref rid="bib182" ref-type="bibr">[182]</xref>, <xref rid="bib183" ref-type="bibr">[183]</xref>, <xref rid="bib184" ref-type="bibr">[184]</xref>. A recent meta-analysis estimates a 3.5–5.3% excess risk of AF for every one unit of body mass index increase <xref rid="bib185" ref-type="bibr">[185]</xref>.</p><p>Left atrium dilation and dysfunction are known consequences of the cardiomyopathy due to obesity <xref rid="bib186" ref-type="bibr">[186]</xref>. In a sheep model of obesity, progressive weight gain over 8 months was associated with increased atrial volume, pressure, and pericardial fat volume along with atrial interstitial fibrosis, inflammation, and myocardial lipidosis <xref rid="bib187" ref-type="bibr">[187]</xref>. This was associated with decreased conduction velocity, increased heterogeneity of conduction and a greater inducibility of atrial fibrillation. With more sustained obesity, animals not only demonstrate progressive atrial changes but also in areas adjacent to pericardial fat there is infiltration of the atrial myocardium by fat cells <xref rid="bib188" ref-type="bibr">[188]</xref>.</p><p>Obese patients have higher left atrial volume and pressure with lower left atrial strain associated with shorter refractoriness in the LA and the PVs <xref rid="bib189" ref-type="bibr">[189]</xref>. A detailed evaluation of atrial changes associated with human obesity showed an increase in the left atrial epicardial fat, a global reduction in atrial conduction velocity, increased fractionation, and preserved overall voltage but greater low-voltage areas <xref rid="bib190" ref-type="bibr">[190]</xref>. The low-voltage areas were observed in regions adjacent to epicardial fat depots.</p><p>Pericardial fat volume has been shown to be associated with AF incidence, severity, and adversely effects ablation outcome <xref rid="bib191" ref-type="bibr">[191]</xref>, <xref rid="bib192" ref-type="bibr">[192]</xref>. Epicardial adiposity is associated with altered 3D atrial architecture, adipocyte infiltration into the myocardium, and atrial fibrosis that may contribute to conduction heterogeneity that promotes AF <xref rid="bib193" ref-type="bibr">[193]</xref>, <xref rid="bib194" ref-type="bibr">[194]</xref>, <xref rid="bib195" ref-type="bibr">[195]</xref>.</p><p>In the ovine model of chronic obesity, weight reduction is associated with reduction in total body fat, atrial dilatation, and interstitial fibrosis together with improved hemodynamics, atrial connexin-43 expression and conduction properties that result in reduced vulnerability to AF <xref rid="bib196" ref-type="bibr">[196]</xref>. In humans, aggressive management of weight and associated risk factors is associated with favourable changes in pericardial fat volume, atrial size, myocardial mass as well as electrophysiological and electroanatomical changes along with reduced AF inducibility and burden <xref rid="bib197" ref-type="bibr">[197]</xref>. Furthermore, weight loss in morbidly obese subjects is associated with reduced epicardial fat <xref rid="bib198" ref-type="bibr">[198]</xref>. Weight reduction in obese individuals can result in regression of LV hypertrophy, reduction in left atrial size and reduction in AF burden/severity <xref rid="bib199" ref-type="bibr">[199]</xref>, <xref rid="bib200" ref-type="bibr">[200]</xref>, <xref rid="bib201" ref-type="bibr">[201]</xref>. Histologically, fatty infiltrates (EHRAS Class IVf) as well as collagen depositions are present (EHRAS III; see <xref rid="t0010" ref-type="table">Table 2</xref>).</p></sec><sec id="s0175"><label>4.14</label><title>Diabetes mellitus</title><p>Diabetes is an independent risk factor for development and progression of AF <xref rid="bib202" ref-type="bibr">[202]</xref>. In a rat model of diabetes mellitus, atrial tissue fibrosis deposit is associated with decreased conduction velocity and greater AF inducibility <xref rid="bib203" ref-type="bibr">[203]</xref>. Patients with abnormal glucose metabolism have larger left atrial size, lower left atrial voltage, and longer left atrial activation time compared with controls <xref rid="bib204" ref-type="bibr">[204]</xref>. Insulin resistance is associated with increased left atrial size and structural heterogeneity <xref rid="bib205" ref-type="bibr">[205]</xref>, <xref rid="bib206" ref-type="bibr">[206]</xref>.</p><p>Mitochondrial function is impaired, leading to oxidative stress, in diabetic atria <xref rid="bib207" ref-type="bibr">[207]</xref>. Oxidative stress and activation of the advanced glycation end-product (AGE)-AGE-receptor (RAGE) system mediates atrial interstitial fibrosis up-regulation of circulating tissue growth factors and pro-inflammatory responses <xref rid="bib207" ref-type="bibr">[207]</xref>, <xref rid="bib208" ref-type="bibr">[208]</xref>. In addition, prolonged hyperglycaemic stress leads to accumulation of AGE-RAGE and nitric oxide inactivation, leading to endothelial dysfunction and myocardial inflammation <xref rid="bib209" ref-type="bibr">[209]</xref>.</p><p>Hyperglycaemia and AGE-RAGE ligand interactions lead to decreased phosphorylation of connexin-43, potentially impairing intercellular coupling <xref rid="bib210" ref-type="bibr">[210]</xref>. Advanced glycation is also related to alterations in myocardial calcium handling and hence contractility <xref rid="bib211" ref-type="bibr">[211]</xref>. These findings could explain the electrophysiological alterations that serve as a central mechanism of the vulnerability to AF in diabetes <xref rid="bib212" ref-type="bibr">[212]</xref>.</p><p>Aggressive treatment of diabetes and adequate glycemic control may prevent or delay the occurrence of AF, despite little direct evidence of the effects of anti-diabetic drugs on AF. Peroxisome proliferator-activated gamma receptor agonists may offer protection against AF beyond glycemic control, due to their anti-inflammatory, antioxidant, and anti-fibrotic effects <xref rid="bib213" ref-type="bibr">[213]</xref>. However, caution should be taken in extrapolating these experimental findings to patients with diabetic cardiomyopathy. Histologically, changes in the atrial myocytes are the initial findings without significant fibrosis (EHRAS I). Later on the disease tissue appearance may change to EHRAS Class III and EHRAS Class IV (see <xref rid="t0010" ref-type="table">Table 2</xref>).</p></sec><sec id="s0180"><label>4.15</label><title>Atrial cardiomyopathy due to valvular heart disease</title><p>Mitral valve disease (MVD) and aortic stenosis (AS) have been associated with atrial structural remodelling and a propensity for AF. Although secondary atrial cardiomyopathy is most often associated with age, hypertension, and heart failure in developed countries, RHD is responsible for over 40% of AF in the developing world <xref rid="bib214" ref-type="bibr">[214]</xref>.</p><sec id="s0185"><label>4.15.1</label><title>Mitral stenosis</title><p>In atria from 24 patients with isolated MS and normal sinus rhythm undergoing mitral valvuloplasty, John et al <xref rid="bib215" ref-type="bibr">[215]</xref>. reported unchanged or an increased effective refractory period (ERP), widespread and site-specific conduction delay, myocyte loss and patchy electrical scar, suggesting that structural changes and their electrophysiological consequences precede the development of AF. Factors associated with these structural changes include direct myocardial effects (pathognomonic inflammatory Ashoff bodies), ultrastructural changes, atrial fibrosis, immunoactive cytokines, and matrix metalloproteinase remodelling (decreased MMP-1 and MMP-3) <xref rid="bib215" ref-type="bibr">[215]</xref>, <xref rid="bib216" ref-type="bibr">[216]</xref>, <xref rid="bib217" ref-type="bibr">[217]</xref>. Reverse atrial remodelling (an immediate reduction in LA pressure and volume and an improvement in biatrial voltage; and further increases in RA voltage 6 months later) was demonstrated in 21 patients with isolated MS undergoing commissurotomy <xref rid="bib218" ref-type="bibr">[218]</xref>. In contrast, atrial remodelling did not reverse in patients with lone AF undergoing successful AF ablation; indeed, substrate abnormalities progressed (decreased voltage and increased regional refractoriness) over the subsequent 6–14 months <xref rid="bib219" ref-type="bibr">[219]</xref>.</p><p>Atrial enlargement and fibrosis are important determinants for the development and maintenance of AF. Increases in collagen I and collagen III (the latter which increase in cultured fibroblasts exposed to mechanical stretch) <xref rid="bib220" ref-type="bibr">[220]</xref> were seen in patients with AF and MVD, but only type I was seen in patients with lone AF <xref rid="bib221" ref-type="bibr">[221]</xref>. Cellular decoupling and myocyte isolation, tissue anisotropy, and conduction inhomogeneities were considered the substrate for local re-entry and arrhythmia.</p></sec><sec id="s0190"><label>4.15.2</label><title>Mitral regurgitation</title><p>Verheule et al <xref rid="bib222" ref-type="bibr">[222]</xref>. found changes in atrial tissue structure and ultrastructure 1 month after creating severe mitral regurgitation (MR) by partial mitral valve avulsion. Effective refractory periods were increased homogeneously and sustained AF (.1 h) was inducible in 10 of 19 MR dogs; in this model, there were no differences in either atrial conduction pattern or velocities. Interstitial fibrosis, chronic inflammation, and cellular glycogen accumulation were noted in the dilated left atria, but myocyte hypertrophy, myolysis, and necrosis were absent. In contrast, myocyte hypertrophy, dedifferentiation, and degeneration and fibrosis are described in pigs with surgically created chronic MR <xref rid="bib223" ref-type="bibr">[223]</xref> and patients with MR <xref rid="bib12" ref-type="bibr">[12]</xref>, <xref rid="bib224" ref-type="bibr">[224]</xref>.</p><p>High-density oligonucleotide microarrays, enrichment analysis, and a differential proteomics approach were used to characterize the molecular regulatory mechanisms and biological processes involved in the atrial myopathy that is seen in pigs with moderate to severe chronic (6 and 12 months) MR <xref rid="bib225" ref-type="bibr">[225]</xref>. Renin-angiotensin-system and peroxisome proliferator-activated receptor signalling pathways and genes involved in the regulation of apoptosis, autophagy, oxidative stress, cell growth, and carbohydrate metabolism were differentially regulated <xref rid="bib225" ref-type="bibr">[225]</xref>. MLC2V (a marker of cardiac hypertrophy and important in the regulation of myocyte contractility) had the highest fold change in the MR pigs. Increased activity of a membrane-bound containing NADPH oxidase in atrial myocytes, which correlated with the degree of cellular hypertrophy and myolysis, was demonstrated in patients with isolated severe MR. The authors suggest that atrial stretch-induced NADPH oxidase activation and intracellular oxidative stress contributes to apoptosis, atrial contractile dysfunction, and atrial dilatation <xref rid="bib226" ref-type="bibr">[226]</xref>.</p><p>Correction of MR reverses many features of atrial remodelling and corrects functional abnormalities. Early LA reverse remodelling (45% reduction of mean LA maximal volume) and increased active atrial emptying was found in the early (30 day) postoperative period in 43 patients undergoing mitral valve surgery (successful repair or replacement) for chronic organic MR <xref rid="bib227" ref-type="bibr">[227]</xref> and a similar improvement at 6 months was reported by Dardas et al <xref rid="bib228" ref-type="bibr">[228]</xref>. Histologically, EHRAS Class III is the most prominent finding in MVD, although the histological appearance of the tissue may vary substantially over time and interindividually and, therefore, all EHRAS classes may be found in the tissue (see <xref rid="f0005" ref-type="fig">Fig. 1</xref>; <xref rid="t0010" ref-type="table">Table 2</xref>).</p></sec><sec id="s0195"><label>4.15.3</label><title>Aortic stenosis</title><p>Although AS is associated with chronic AF <xref rid="bib229" ref-type="bibr">[229]</xref>, animal models of AS and atrial remodelling are lacking. Kim et al <xref rid="bib173" ref-type="bibr">[173]</xref>. studied atrial electrical re-modelling in excised perfused hearts in a rat model of increased afterload simulating AS (ascending aortic banding), which produced LVH without systemic hypertension, heart failure, or neurohormonal activation. Banded hearts showed marked LA hypertrophy and fibrosis at 14 and 20 weeks post-operatively. The incidence and duration of pacing-induced AF was increased at 20 weeks and was associated with decreased mean vectorial conduction velocity and inhomogeneity of conduction, decreased expression of connexin-43, but without changes in ERP. Importantly, atrial remodelling was not present at 8 weeks, when the greatest degree of LVH was present <xref rid="bib173" ref-type="bibr">[173]</xref>.</p><p>Left atrium volumes are higher in patients with AS compared with controls and decrease significantly after valvuloplasty <xref rid="bib230" ref-type="bibr">[230]</xref>. Plasma natriuretic peptide (ANP) levels are higher in symptomatic than asymptomatic patients with AS <xref rid="bib231" ref-type="bibr">[231]</xref> and N-ANP levels predict atrial remodelling and late (2 month) post-operative AF after surgery for AS <xref rid="bib232" ref-type="bibr">[232]</xref>.</p><p>Taken together, these data support the notion that substrate-based AF is a consequence of the abnormal haemodynamics and atrial remodelling that accompany valvular heart disease. In this instance, atrial remodelling is the consequence of multiple biological processes that create structural and ultrastructural abnormalities and a change in conduction (as opposed to refractoriness) that favours the development and maintenance of AF. Histologically, EHRAS Class III is the most prominent finding, although the histological appearance of the tissue may vary substantially over time and interindividually (see <xref rid="f0005" ref-type="fig">Fig. 1</xref>, <xref rid="f0010" ref-type="fig">Fig. 2</xref>, <xref rid="f0015" ref-type="fig">Fig. 3</xref>; <xref rid="t0010" ref-type="table">Table 2</xref>). Atrial pathology often also affects specialised conduction system tissues like the sinus and AV nodes. However, these changes are beyond the scope of the present consensus report, which focuses on atrial cardiomyocytes and tissue.</p></sec></sec></sec><sec id="s0200"><label>5</label><title>Impact of atrial cardiomyopathies on occurrence of atrial fibrillation and atrial arrhythmia</title><p>Controversy about the mechanism of AF has been alive for over 100 years, yet given the continued increase in worldwide burden of AF <xref rid="bib233" ref-type="bibr">[233]</xref>, ongoing investigation will drive improved treatment and prevention. Currently, there are two opposing sides in the debate about re-entrant mechanisms in AF. On one side are those who promote variants of the original idea of Gordon Moe that fibrillation, whether atrial or ventricular, results from the continued random propagation of multiple independent electric waves that move independently throughout the atria <xref rid="bib234" ref-type="bibr">[234]</xref>, <xref rid="bib235" ref-type="bibr">[235]</xref>. On the other side are those who adhere to the theory that fibrillation is a consequence of the continued activity of a few vortices (rotors) that spin at high frequencies, generating ‘fibrillatory conduction’ <xref rid="bib236" ref-type="bibr">[236]</xref>, <xref rid="bib237" ref-type="bibr">[237]</xref>. In either case, arrhythmia maintenance is favoured by abbreviated APD/refractory period <xref rid="bib13" ref-type="bibr">[13]</xref>, <xref rid="bib238" ref-type="bibr">[238]</xref>, <xref rid="bib239" ref-type="bibr">[239]</xref>. Another pre-requisite of the multiple wavelet hypothesis is that there should be slow conduction, which is not the case for rotors. According to rotor theory, slowing of conduction is established dynamically by the curvature of the rotating wave front, which is steepest near the rotation centre, at which refractory period is briefest and conduction velocity is slowest <xref rid="bib240" ref-type="bibr">[240]</xref>. Which of the above two mechanisms prevails in human AF has not been fully established, yet <xref rid="bib241" ref-type="bibr">[241]</xref>.</p><p>Regardless of the mechanism that maintains it, AF leads to high-frequency atrial excitation, which if sustained, results in ion-channel remodelling that further abbreviates the APD and refractory period to boost its stabilisation. Such AF-induced electrical remodelling is reversible in the short term (minutes, hours, or days), but less so when lasting months or years. For a detailed discussion of AF-induced remodelling, see chapter 3. How these changes contribute to AF perpetuation in the long term has not been fully determined.</p><p>In a recent study using a sheep model of persistent AF induced by intermittent atrial tachypacing there was a progressive spontaneous increase in the dominant frequency (DF) of AF activation after the first detected AF episode <xref rid="bib240" ref-type="bibr">[240]</xref>, <xref rid="bib242" ref-type="bibr">[242]</xref>. The results suggested that, unlike the tachypacing induced electrical remodelling that can occur over minutes or hours, there existed a protracted, slowly progressing electrical and structural remodelling secondary to AF that sustains for days or weeks <xref rid="bib240" ref-type="bibr">[240]</xref>, <xref rid="bib242" ref-type="bibr">[242]</xref>. In addition, a consistent left-vs.-right atrial DF difference correlated with the presence of rotors, DF gradients, and outward propagation from the posterior LA during sustained AF in the explanted, Langendorff-perfused sheep hearts <xref rid="bib242" ref-type="bibr">[242]</xref>, and an underlying basis is seen in humans <xref rid="bib243" ref-type="bibr">[243]</xref>. The DF of non-sustained AF increases progressively at a rate (dDF/dt) that accurately predicts the transition from episodic, non-sustained AF to persistent, long-lasting AF <xref rid="bib126" ref-type="bibr">[126]</xref>. Although fibrosis developed progressively <xref rid="bib126" ref-type="bibr">[126]</xref>, it is unknown what role if any fibrosis played in rotor acceleration or stabilisation. Other studies using different animal models have also demonstrated that long-term atrial tachypacing results in atrial fibrosis <xref rid="bib244" ref-type="bibr">[244]</xref>, with concomitant release of cytokines that are known to modify atrial electrical function <xref rid="bib245" ref-type="bibr">[245]</xref>. In the sheep model, atrial structural changes leading to PLA enlargement likely made rotors less likely to collide with anatomic boundaries, thus contributing to their stabilisation and AF persistence <xref rid="bib242" ref-type="bibr">[242]</xref>, <xref rid="bib246" ref-type="bibr">[246]</xref>.</p><p>Distinct stresses of the atrial myocardium could contribute to the transformation of atrial cardiomyopathy into an arrhythmogenic substrate for AF. For instance, mechanical stress is a major regulator of cardiac electrical properties. The two atria are particularly sensitive to changes in mechanical coupling due to their ‘reservoir’ position and their function of ‘pressure sensor’ with a specific endocrine role, i.e. the secretion of natriuretic peptides. Many mechanosensors are expressed in the atrial myocardium and contribute to the interplay between membrane electrical properties, mechanical stresses, and myocardial wall deformation <xref rid="bib247" ref-type="bibr">[247]</xref>. Recently, it has been reported that shear stress of atrial cardiomyocytes regulates the surface expression of voltage-gated potassium channels via the stimulation of the integrins that link myocytes to the extracellular matrix <xref rid="bib248" ref-type="bibr">[248]</xref>, <xref rid="bib249" ref-type="bibr">[249]</xref>. During atrial haemodynamic overload, the mechano-sensor signalling pathways, are constitutively activated, such that myocytes are no longer able to respond to shear stress. This process results in the acceleration of atrial repolarization and could contribute to AF vulnerability <xref rid="bib249" ref-type="bibr">[249]</xref>.</p><p>Oxidative stress is also thought to be important in AF-induced atrial remodelling leading to cardiomyopathy and AF perpetuation <xref rid="bib250" ref-type="bibr">[250]</xref>. How-ever, the manner in which reactive oxygen species (ROS) mediate atrial ionic remodelling is inadequately understood. NOX2/4 activity increases in fibrillating atria and is a potential source of ROS in AF. Mitochondrial ROS is potentially another important source of oxidative stress; mitochondrial dysfunction has been demonstrated in AF. It remains to be determined whether atrial oxidative stress directly affects atrial APD and refractoriness and thus contributes to rotor acceleration and stability in AF. Several sarcolemmal ionic currents are directly or indirectly modulated by ROS <xref rid="bib251" ref-type="bibr">[251]</xref>, but the relevance of these mechanisms to human AF has not been demonstrated.</p><p>Sustained AF activates the release of pro-inflammatory cytokines and hormones related to cardiovascular disease and tissue injury, including angiotensin-II (Ang-II), tumour necrosis factor (TNF)-a, interleukin (IL)-6, and IL-8 <xref rid="bib252" ref-type="bibr">[252]</xref>. Pro-inflammatory stimuli such as NOX-derived ROS, growth factors, and other hormones has been demonstrated to have a role in Ang-II function <xref rid="bib253" ref-type="bibr">[253]</xref>. However, the precise molecular modifications of the putative signalling targets of ROS after Ang-II stimulation are yet to be identified. Knowing which NOXs are activated by Ang-II in the normal atria may help generate better interventions aimed at preventing AF associated with Ang-II activation. Ang-II is a well-known trigger of fibroblast activation and differentiation into myofibroblasts, which are key factors in the generation of fibrosis. Pro-inflammatory cytokines also promote ion-channel dysfunction, which together with myocyte apoptosis and extracellular matrix remodelling predisposes patients to AF.</p><p>Recently, atrial adipose tissue has emerged as a potential player in the pathophysiology of AF <xref rid="bib3" ref-type="bibr">[3]</xref>, <xref rid="bib254" ref-type="bibr">[254]</xref>. In addition to its paracrine effects <xref rid="bib192" ref-type="bibr">[192]</xref>, adi-pose tissue can infiltrate the subepicardium of the atrial myocardium and become fibrotic <xref rid="bib255" ref-type="bibr">[255]</xref> contributing to the functional dissociation of electrical activity between epicardial layer and the endocardial bundle network, favouring wavebreak, and rotor formation. Lone AF or rapid atrial pacing promotes adipogenesis through the regulation of genes specific to metabolic adaptation. Therefore, it is possible that the accumulation and infiltration of adipose tissue reflects metabolic stress secondary to excessive work of the atrial myocardium <xref rid="bib191" ref-type="bibr">[191]</xref>. Furthermore, adipose tissue can induce fibrosis and alter gene-expression patterns <xref rid="bib195" ref-type="bibr">[195]</xref>, <xref rid="bib256" ref-type="bibr">[256]</xref>.</p></sec><sec id="s0205"><label>6</label><title>Atrial cardiomyopathies, systemic biomarkers, and atrial thrombogenesis</title><sec id="s0210"><label>6.1</label><title>Atrial cardiomyopathies and systemic biomarkers</title><sec id="s0215"><label>6.1.1</label><title>Atrial inflammation and inflammatory biomarkers</title><p>Infiltration of neutrophils, macrophages, and lymphocytes accompanies surgical injury or pericarditis, promoting the development of atrial fibrosis, resulting in heterogeneous and slowed conduction, a risk factor for re-entrant arrhythmia <xref rid="bib257" ref-type="bibr">[257]</xref>, <xref rid="bib258" ref-type="bibr">[258]</xref>, <xref rid="bib259" ref-type="bibr">[259]</xref>, <xref rid="bib260" ref-type="bibr">[260]</xref>, <xref rid="bib261" ref-type="bibr">[261]</xref>. This provides a mechanistic link between inflammatory activation and atrial arrhythmogenesis. Anti-inflammatory interventions such as prednisone are effective in preventing neutrophil infiltration in sterile pericarditis and in suppressing pacing-inducible atrial flutter <xref rid="bib262" ref-type="bibr">[262]</xref>, and steroid pre-treatment has been found to reduce the incidence of postoperative AF in an appropriately powered randomized, clinical trial <xref rid="bib263" ref-type="bibr">[263]</xref>. An ongoing trial studies the effect of colchicine (NCT 001128427).</p><p>In a mouse model of persistent hypertension, Ang-II infusion promotes increased atrial abundance of myeloperoxidase (MPO, a neutrophil and macrophage oxidant-generating enzyme) and promotes atrial fibrosis <xref rid="bib261" ref-type="bibr">[261]</xref>. In MPO knockout mice, the profibrotic response to A-II infusion was eliminated. Angiotensin II and endothelin-1 are linked to inflammatory and proarrhythmogenic atrial remodelling <xref rid="bib2" ref-type="bibr">[2]</xref>, <xref rid="bib264" ref-type="bibr">[264]</xref>, <xref rid="bib265" ref-type="bibr">[265]</xref>, <xref rid="bib266" ref-type="bibr">[266]</xref>. This evidence suggests that inflammatory cell infiltration has an important role in promoting the creation of a substrate for AF, as a result of conduction heterogeneity and slowing, both in the setting of cardiac surgery and beyond.</p></sec><sec id="s0220"><label>6.1.2</label><title>Systemic inflammatory activation in atrial fibrillation</title><p>In addition to haemodynamic stress-induced cellular inflammation of the atria, a cross-sectional study demonstrated that AF was associated with higher plasma levels of C-reactive protein (CRP), a sensitive but non-specific biomarker of systemic inflammation produced by the liver <xref rid="bib267" ref-type="bibr">[267]</xref>. A follow-up secondary analysis of the participants Cardiovascular Health Study participants further revealed that elevated CRP predicted incident AF <xref rid="bib268" ref-type="bibr">[268]</xref>.</p><p>Subsequent studies have demonstrated relationships between several different serologic markers of inflammation and AF, including IL-6 <xref rid="bib269" ref-type="bibr">[269]</xref>, TNF-a <xref rid="bib270" ref-type="bibr">[270]</xref>, aldosterone <xref rid="bib271" ref-type="bibr">[271]</xref> and simple white blood cell counts <xref rid="bib272" ref-type="bibr">[272]</xref>. Analyses of multiple inflammatory biomarkers within the same study have suggested that IL-6 and osteoprotegerin <xref rid="bib273" ref-type="bibr">[273]</xref> may be especially important. The relationship between IL-6 and AF may be mediated by left atrial enlargement <xref rid="bib269" ref-type="bibr">[269]</xref>.</p><p>While evidence that inflammatory markers presage the development of AF has been replicated <xref rid="bib268" ref-type="bibr">[268]</xref>, <xref rid="bib274" ref-type="bibr">[274]</xref>, there are also multiple studies to dem-onstrate that atrial arrhythmias likely contribute to inflammation: specifically, cardioversion of AF <xref rid="bib275" ref-type="bibr">[275]</xref> as well as ablation of either AF <xref rid="bib276" ref-type="bibr">[276]</xref> or atrial flutter <xref rid="bib277" ref-type="bibr">[277]</xref> has resulted in a decrease in inflammation. Indeed, Marcus et al. demonstrated that the rhythm at the time of the blood draw (AF vs. sinus) was an important determinant in detecting an elevated CRP or IL-6 level <xref rid="bib278" ref-type="bibr">[278]</xref>. Taken together, these data suggest that the relationship between inflammation and AF may be bidirectional and progressive.</p></sec><sec id="s0225"><label>6.1.3</label><title>Intra-atrial sampling studies</title><p>As the enhanced risk of stroke in the setting of AF has been attributed to status of blood flow and in particular thromboemboli originating in the left atrial appendage, there has been an interest in determining whether peripheral blood can adequately reflect the hypercoagulability that may be present locally within the atria (see <xref rid="f0050" ref-type="fig">Fig. 10</xref>) <xref rid="bib279" ref-type="bibr">[279]</xref>. The first intra-atrial sampling study failed to identify evidence of statistically significant differences between several markers of hypercoagulability in right and left atrial vs. femoral vein and arterial samples among persistent AF patients with MS <xref rid="bib280" ref-type="bibr">[280]</xref>; of note, the same markers revealed statistically significant differences when compared with normal controls without AF <xref rid="bib279" ref-type="bibr">[279]</xref>. In contrast, a subsequent study demonstrated that platelet activation acutely increased in coronary sinus blood in AF, while systemic platelet activation (obtained from the femoral vein) revealed no such change <xref rid="bib281" ref-type="bibr">[281]</xref>.</p><p>A similar approach to multi-site sampling has also been applied to better understand the relationship between inflammation and AF. Liuba et al. found higher levels of IL-8 in the femoral vein, right atrium, and coronary sinus than the left and right upper PVs among eight permanent AF patients (without any such differences 10 paroxysmal AF patients or 10 controls) <xref rid="bib280" ref-type="bibr">[280]</xref>.</p></sec><sec id="s0230"><label>6.1.4</label><title>Practical implications and use of systemic biomarkers</title><p>Systemic biomarkers have been used to predict development of AF and/or its complications (<xref rid="t0025" ref-type="table">Table 5</xref>). Various studies have examined the role of inflammatory indices, natriuretic peptides, injury markers, etc. in predicting incident AF, especially in the post-surgery setting. Many of these bio-markers are non-specific, and high levels may reflect infection or sepsis, an acute phase reaction, etc <xref rid="bib282" ref-type="bibr">[282]</xref>, <xref rid="bib283" ref-type="bibr">[283]</xref>, <xref rid="bib284" ref-type="bibr">[284]</xref>.</p><p>Adding BNP and CRP to a prediction score derived from CHARGE-AF (which included data from the Atherosclereosis Risk in Communities Study (ARIC), Cardiovascular Health Study (CHS), the Framingham Heart Study, the Age, Gene/Environment Susceptibility Reykjavik Study (AGES), and the Rotterdam Study) and utilising age, race, height, weight, systolic and diastolic blood pressure, current smoking, use of antihypertensive medication, diabetes, history of myocardial infarction and history of heart failure <xref rid="bib285" ref-type="bibr">[285]</xref> improved the statistical model <xref rid="bib286" ref-type="bibr">[286]</xref>. Once again, the addition of CRP did not meaningfully improve the model.</p><p>In another study evaluating the relationship of extracellular matrix modulators (matrix metalloproteinases, MMPs, and their tissue inhibitors, TIMPs) and AF risk, only elevated MMP9 levels were significantly associated with AF risk <xref rid="bib287" ref-type="bibr">[287]</xref>. Proteases having desintegrin and metalloprotease activities (ADAM) are related to atrial dilatation and thereby influence mechanical performance of the atria <xref rid="bib288" ref-type="bibr">[288]</xref>.</p><p>The clinical benefit of considering biomarkers associated with AF is questionable unless there is clear evidence of a direct benefit in AF risk prediction and management- this has not been achieved to date.</p></sec></sec><sec id="s0235"><label>6.2</label><title>Prothrombotic indices – coagulation, platelets</title><p>Over 150 years ago, Virchow proposed a triad of abnormalities that contributed to thrombus formation (thrombogenesis), that is, abnormalities of vessel wall, abnormal blood flow and abnormal blood constituents (<xref rid="f0050" ref-type="fig">Fig. 10</xref>). In the setting of AF, abnormalities of vessel walls are evident by the association of thromboembolism with structural heart disease (eg. mitral valve stenosis) and complex aortic plaque, as well as endothelial damage/dysfunction, whether recognised by biomarkers (eg. von Willebrand factor (vWF), tissue plasminogen activator, tPA), immunohistochemistry studies of the left atrial wall, electron microscopy, or by functional studies (eg. flow mediated dilatation) <xref rid="bib289" ref-type="bibr">[289]</xref>. Abnormal blood flow in AF can be visualised by spontaneous echocontrast in the LA, as well as low left atrial appendage Doppler velocities. Abnormal blood constituents in AF are evident from abnormalities of coagulation, platelets, fibrinolysis, inflammation, extracellular matrix turnover, etc. that are all directly or indirectly associated with thrombogenesis, or a predisposition to the latter. While abnormalities of platelets are often evident in AF, they may be more reflective of associated vascular disease or comorbidities than of AF per se <xref rid="bib290" ref-type="bibr">[290]</xref>, <xref rid="bib291" ref-type="bibr">[291]</xref>. Indeed, thrombus obtained in AF is largely fibrin-rich (‘red clot’) compared with arterial thrombus, which is largely platelet-rich (‘white clot’), providing a mechanistic explanation for the role of anticoagulation therapy, rather than antiplatelet therapy for AF-related thromboembolism <xref rid="bib291" ref-type="bibr">[291]</xref>, <xref rid="bib292" ref-type="bibr">[292]</xref>.</p><p>The concept of AF being a prothrombotic or hypercoagulable state was first proposed in 1995 <xref rid="bib293" ref-type="bibr">[293]</xref>. Many prothrombotic indices in AF have been related to subsequent stroke and thromboembolism, whether in non-anticoagulated or anticoagulated subjects (<xref rid="f0050" ref-type="fig">Fig. 10</xref>). Initial studies showed that coagulation-related factors, such as fibrin <sc>D</sc>-dimer (an index of fibrin turnover and thrombogenesis) were related to stroke risk strata as well as an adverse prognosis from thromboembolism, whether or not patients were anticoagulated <xref rid="bib294" ref-type="bibr">[294]</xref>, <xref rid="bib295" ref-type="bibr">[295]</xref>, <xref rid="bib296" ref-type="bibr">[296]</xref>, <xref rid="bib297" ref-type="bibr">[297]</xref>. In contrast, there was no prognostic advantage of platelet indices <xref rid="bib295" ref-type="bibr">[295]</xref>, <xref rid="bib298" ref-type="bibr">[298]</xref>, <xref rid="bib299" ref-type="bibr">[299]</xref>.</p><sec id="s0240"><label>6.2.1</label><title>Prediction of thrombogenesis</title><p>Addition of vWf refines clinical risk stratification in AF, first shown in the non-anticoagulated or suboptimally anticoagulated patients from the SPAF study <xref rid="bib300" ref-type="bibr">[300]</xref>. More recently, vWf has been related to thromboembolism as well as bleeding risks in anticoagulated AF patients <xref rid="bib301" ref-type="bibr">[301]</xref>. Ancillary studies from large Phase 3 anticoagulation trials have reported prognostic implications for increased levels of <sc>D</sc>-dimer, troponin, natriuretic peptides, and novel biomarkers (e.g. GDF15) <xref rid="bib302" ref-type="bibr">[302]</xref>, <xref rid="bib303" ref-type="bibr">[303]</xref>, <xref rid="bib304" ref-type="bibr">[304]</xref>. Many of these studies have been performed in selected clinical trial cohorts, and the prognostic role in risk stratification requires prospective testing in unselected large ‘real-world’ cohorts with a broad range of stroke risk and renal function. As in the case of AF prediction, evidence for the additive value of biomarkers for stroke risk prediction from large prospective non-anticoagulated ‘real-world’ cohorts is limited <xref rid="bib305" ref-type="bibr">[305]</xref>. Endocardial thrombogenic alterations in diseased atria, which appear to be related to oxidative stress, appear to contribute to clot formation, particularly in the left atrial appendage <xref rid="bib306" ref-type="bibr">[306]</xref>, <xref rid="bib307" ref-type="bibr">[307]</xref>, <xref rid="bib308" ref-type="bibr">[308]</xref>, <xref rid="bib309" ref-type="bibr">[309]</xref>, <xref rid="bib310" ref-type="bibr">[310]</xref>. Thus, the impact and the relation between EHRAS Classses and the extend of endocardial thrombogenic alterations have to be assessed in future studies. Interestingly, duration of AF does not correlate with the extent of abserved endocardial changes <xref rid="bib309" ref-type="bibr">[309]</xref>.</p></sec></sec></sec><sec id="s0245"><label>7</label><title>Imaging techniques to detect atrial cardiomyopathies mapping and ablation in atrial cardiomyopathies</title><p>It is well established that an enlarged LA is associated with adverse cardiovascular outcomes <xref rid="bib311" ref-type="bibr">[311]</xref>, <xref rid="bib312" ref-type="bibr">[312]</xref>, <xref rid="bib313" ref-type="bibr">[313]</xref>, <xref rid="bib314" ref-type="bibr">[314]</xref>, <xref rid="bib315" ref-type="bibr">[315]</xref>, <xref rid="bib316" ref-type="bibr">[316]</xref>. In the absence of MVD, an increase in LA size most commonly reflects increased wall tension as a result of increased LA pressure <xref rid="bib317" ref-type="bibr">[317]</xref>, <xref rid="bib318" ref-type="bibr">[318]</xref>, <xref rid="bib319" ref-type="bibr">[319]</xref>, <xref rid="bib320" ref-type="bibr">[320]</xref>, as well as impairment in LA function secondary to atrial myopathy <xref rid="bib321" ref-type="bibr">[321]</xref>, <xref rid="bib322" ref-type="bibr">[322]</xref>. A clear relationship exists between an enlarged LA and the incidence of atrial fibrillation and stroke <xref rid="bib323" ref-type="bibr">[323]</xref>, <xref rid="bib324" ref-type="bibr">[324]</xref>, <xref rid="bib325" ref-type="bibr">[325]</xref>, <xref rid="bib326" ref-type="bibr">[326]</xref>, <xref rid="bib327" ref-type="bibr">[327]</xref>, <xref rid="bib328" ref-type="bibr">[328]</xref>, <xref rid="bib329" ref-type="bibr">[329]</xref>, <xref rid="bib330" ref-type="bibr">[330]</xref>, <xref rid="bib331" ref-type="bibr">[331]</xref>, <xref rid="bib332" ref-type="bibr">[332]</xref>, risk for overall mortality after myocardial infarction <xref rid="bib321" ref-type="bibr">[321]</xref>, <xref rid="bib322" ref-type="bibr">[322]</xref>, <xref rid="bib333" ref-type="bibr">[333]</xref>, <xref rid="bib334" ref-type="bibr">[334]</xref>, risk for death and hospitalisation in patients with dilated cardiomyopathy <xref rid="bib335" ref-type="bibr">[335]</xref>, <xref rid="bib336" ref-type="bibr">[336]</xref>, <xref rid="bib337" ref-type="bibr">[337]</xref>, <xref rid="bib338" ref-type="bibr">[338]</xref>, <xref rid="bib339" ref-type="bibr">[339]</xref>, <xref rid="bib340" ref-type="bibr">[340]</xref>, <xref rid="bib341" ref-type="bibr">[341]</xref>, <xref rid="bib342" ref-type="bibr">[342]</xref>, <xref rid="bib343" ref-type="bibr">[343]</xref>, <xref rid="bib344" ref-type="bibr">[344]</xref>, and major cardiac events or death in patients with diabetes mellitus <xref rid="bib345" ref-type="bibr">[345]</xref>. left atrium enlargement is a marker of both the severity and chronicity of diastolic dysfunction and magnitude of LA pressure elevation <xref rid="bib317" ref-type="bibr">[317]</xref>, <xref rid="bib318" ref-type="bibr">[318]</xref>, <xref rid="bib319" ref-type="bibr">[319]</xref>, <xref rid="bib320" ref-type="bibr">[320]</xref>. A recent consensus report on multi-modality imaging for AF patients summarizes the current status of atrial imaging in more detail <xref rid="bib346" ref-type="bibr">[346]</xref>.</p><sec id="s0250"><label>7.1</label><title>Echocardiography</title><p>Echocardiography is the imaging modality of choice for screening and serially following patients with diseases involving the LA morphology and function <xref rid="bib347" ref-type="bibr">[347]</xref>.</p><p>For assessment of atrial size, most widely reported is the linear dimension in the parasternal long-axis view using M-mode or 2 delayed enhancement (DE) <xref rid="bib324" ref-type="bibr">[324]</xref>, <xref rid="bib325" ref-type="bibr">[325]</xref>, <xref rid="bib326" ref-type="bibr">[326]</xref>, <xref rid="bib327" ref-type="bibr">[327]</xref>, <xref rid="bib328" ref-type="bibr">[328]</xref>, <xref rid="bib329" ref-type="bibr">[329]</xref>, <xref rid="bib330" ref-type="bibr">[330]</xref>, <xref rid="bib331" ref-type="bibr">[331]</xref>, <xref rid="bib332" ref-type="bibr">[332]</xref>, <xref rid="bib333" ref-type="bibr">[333]</xref>, <xref rid="bib334" ref-type="bibr">[334]</xref>, <xref rid="bib335" ref-type="bibr">[335]</xref>, <xref rid="bib336" ref-type="bibr">[336]</xref>, <xref rid="bib337" ref-type="bibr">[337]</xref>, <xref rid="bib338" ref-type="bibr">[338]</xref>, <xref rid="bib339" ref-type="bibr">[339]</xref>, <xref rid="bib345" ref-type="bibr">[345]</xref>, <xref rid="bib347" ref-type="bibr">[347]</xref>, <xref rid="bib348" ref-type="bibr">[348]</xref>, <xref rid="bib349" ref-type="bibr">[349]</xref>. However, due to the complex 3D nature of the atrium and the non-uniform nature of atrial remodelling, this measurement frequently does not provide an accurate picture of LA size <xref rid="bib350" ref-type="bibr">[350]</xref>, <xref rid="bib351" ref-type="bibr">[351]</xref>, <xref rid="bib352" ref-type="bibr">[352]</xref>, <xref rid="bib353" ref-type="bibr">[353]</xref>, <xref rid="bib354" ref-type="bibr">[354]</xref>. Thus, when assessing LA size and remodelling, the measurement of LA volume is a more powerful prognostic indicator in a variety of cardiac disease states <xref rid="bib329" ref-type="bibr">[329]</xref>, <xref rid="bib331" ref-type="bibr">[331]</xref>, <xref rid="bib333" ref-type="bibr">[333]</xref>, <xref rid="bib334" ref-type="bibr">[334]</xref>, <xref rid="bib335" ref-type="bibr">[335]</xref>, <xref rid="bib336" ref-type="bibr">[336]</xref>, <xref rid="bib337" ref-type="bibr">[337]</xref>, <xref rid="bib338" ref-type="bibr">[338]</xref>, <xref rid="bib339" ref-type="bibr">[339]</xref>, <xref rid="bib345" ref-type="bibr">[345]</xref>, <xref rid="bib347" ref-type="bibr">[347]</xref>, <xref rid="bib348" ref-type="bibr">[348]</xref>, <xref rid="bib349" ref-type="bibr">[349]</xref>, <xref rid="bib350" ref-type="bibr">[350]</xref>, <xref rid="bib351" ref-type="bibr">[351]</xref>, <xref rid="bib352" ref-type="bibr">[352]</xref>, <xref rid="bib353" ref-type="bibr">[353]</xref>, <xref rid="bib354" ref-type="bibr">[354]</xref>, <xref rid="bib355" ref-type="bibr">[355]</xref>, <xref rid="bib356" ref-type="bibr">[356]</xref>, <xref rid="bib357" ref-type="bibr">[357]</xref>, <xref rid="bib358" ref-type="bibr">[358]</xref>, <xref rid="bib359" ref-type="bibr">[359]</xref>, <xref rid="bib360" ref-type="bibr">[360]</xref>. Two-dimensional echocardiographic LA volumes are typically smaller than those reported from computed tomography or cardiac magnetic resonance imaging (CMR) <xref rid="bib361" ref-type="bibr">[361]</xref>, <xref rid="bib362" ref-type="bibr">[362]</xref>, <xref rid="bib363" ref-type="bibr">[363]</xref>, <xref rid="bib364" ref-type="bibr">[364]</xref>, <xref rid="bib365" ref-type="bibr">[365]</xref>. Left atrium volume from 2D images is best measured using the disk summation algorithm because it includes fewer geometric assumptions <xref rid="bib366" ref-type="bibr">[366]</xref>, <xref rid="bib367" ref-type="bibr">[367]</xref>. The advent of 3-D ECHO has improved the accuracy of ECHO volume measurements which correlate well with cardiac computed tomography <xref rid="bib368" ref-type="bibr">[368]</xref>, <xref rid="bib369" ref-type="bibr">[369]</xref> and magnetic resonance imaging <xref rid="bib370" ref-type="bibr">[370]</xref>, <xref rid="bib371" ref-type="bibr">[371]</xref>. Compared with 2D assessment of LA volume, 3DE also has superior prognostic prediction <xref rid="bib372" ref-type="bibr">[372]</xref>, <xref rid="bib373" ref-type="bibr">[373]</xref>.</p><p>The recommended upper normal indexed LA volume is 34 mL/m<sup>2</sup> for both genders which fits well with a risk-based approach for determination of cut-off between a normal and an enlarged LA <xref rid="bib323" ref-type="bibr">[323]</xref>, <xref rid="bib357" ref-type="bibr">[357]</xref>, <xref rid="bib358" ref-type="bibr">[358]</xref>, <xref rid="bib359" ref-type="bibr">[359]</xref>.</p></sec><sec id="s0255"><label>7.2</label><title>Left atrial function by Doppler echocardiography</title><p>Left atrium function can be assessed by pulsed-wave Doppler measurements of late (mitral A) diastolic filling. Multiple studies have used this parameter as an index of LA function assessment, but it is affected by age and loading conditions <xref rid="bib317" ref-type="bibr">[317]</xref>, <xref rid="bib374" ref-type="bibr">[374]</xref>, <xref rid="bib375" ref-type="bibr">[375]</xref>, <xref rid="bib376" ref-type="bibr">[376]</xref>, <xref rid="bib377" ref-type="bibr">[377]</xref>, <xref rid="bib378" ref-type="bibr">[378]</xref>, <xref rid="bib379" ref-type="bibr">[379]</xref>, <xref rid="bib380" ref-type="bibr">[380]</xref>, <xref rid="bib381" ref-type="bibr">[381]</xref>, <xref rid="bib382" ref-type="bibr">[382]</xref>. The PV atrial reversal velocity has also been used as a measurement of LA function <xref rid="bib317" ref-type="bibr">[317]</xref>, <xref rid="bib377" ref-type="bibr">[377]</xref>, <xref rid="bib379" ref-type="bibr">[379]</xref>, <xref rid="bib380" ref-type="bibr">[380]</xref>, <xref rid="bib381" ref-type="bibr">[381]</xref>, <xref rid="bib382" ref-type="bibr">[382]</xref>. In the presence of reduced LV compliance and elevated filling pressures, atrial contraction results in significant flow reversal into the PVs <xref rid="bib80" ref-type="bibr">[80]</xref>, <xref rid="bib81" ref-type="bibr">[81]</xref>. Studies have also demonstrated that Doppler tissue imaging can be used as an accurate marker of atrial function <xref rid="bib383" ref-type="bibr">[383]</xref>, <xref rid="bib384" ref-type="bibr">[384]</xref>.</p><sec id="s0260"><label>7.2.1</label><title>New echocardiographic techniques</title><p>Two-dimensional speckle-tracking echo has been used as a more sensitive marker to detect early functional remodelling before anatomical alterations occur <xref rid="bib385" ref-type="bibr">[385]</xref>, <xref rid="bib386" ref-type="bibr">[386]</xref>, <xref rid="bib387" ref-type="bibr">[387]</xref>, <xref rid="bib388" ref-type="bibr">[388]</xref>, <xref rid="bib389" ref-type="bibr">[389]</xref>, <xref rid="bib390" ref-type="bibr">[390]</xref>, <xref rid="bib391" ref-type="bibr">[391]</xref>, <xref rid="bib392" ref-type="bibr">[392]</xref>, <xref rid="bib393" ref-type="bibr">[393]</xref>, <xref rid="bib394" ref-type="bibr">[394]</xref>, <xref rid="bib395" ref-type="bibr">[395]</xref>, <xref rid="bib396" ref-type="bibr">[396]</xref>, <xref rid="bib397" ref-type="bibr">[397]</xref>, <xref rid="bib398" ref-type="bibr">[398]</xref>, <xref rid="bib399" ref-type="bibr">[399]</xref>, <xref rid="bib400" ref-type="bibr">[400]</xref>.</p><p>Strain (S) and strain rate (SR) imaging provide data on myocardial deformation by estimating spatial gradients in myocardial velocities <xref rid="bib385" ref-type="bibr">[385]</xref>, <xref rid="bib388" ref-type="bibr">[388]</xref>, <xref rid="bib392" ref-type="bibr">[392]</xref>, <xref rid="bib393" ref-type="bibr">[393]</xref>, <xref rid="bib401" ref-type="bibr">[401]</xref>, <xref rid="bib402" ref-type="bibr">[402]</xref>, <xref rid="bib403" ref-type="bibr">[403]</xref>, <xref rid="bib404" ref-type="bibr">[404]</xref>, <xref rid="bib405" ref-type="bibr">[405]</xref>. This technique has been used as a surrogate of LA structural remodelling and fibrosis <xref rid="bib388" ref-type="bibr">[388]</xref>, <xref rid="bib389" ref-type="bibr">[389]</xref>, <xref rid="bib390" ref-type="bibr">[390]</xref>, <xref rid="bib391" ref-type="bibr">[391]</xref>, <xref rid="bib392" ref-type="bibr">[392]</xref>, <xref rid="bib393" ref-type="bibr">[393]</xref>. Interestingly, LA dysfunction with changes in strain and strain rate has been observed in patients with amyloidosis in the absence of other echocardiographic features of cardiac involvement <xref rid="bib402" ref-type="bibr">[402]</xref>. Abnormalities in atrial strain have been observed in diverse conditions, including AF, valvular pathology, heart failure, hypertension, diabetes, and cardiomyopathies <xref rid="bib388" ref-type="bibr">[388]</xref>, <xref rid="bib389" ref-type="bibr">[389]</xref>, <xref rid="bib396" ref-type="bibr">[396]</xref>, <xref rid="bib397" ref-type="bibr">[397]</xref>, <xref rid="bib398" ref-type="bibr">[398]</xref>, <xref rid="bib399" ref-type="bibr">[399]</xref>, <xref rid="bib400" ref-type="bibr">[400]</xref>. Population-based studies have demonstrated the prognostic value of LA strain analysis for long-term outcome <xref rid="bib388" ref-type="bibr">[388]</xref>, <xref rid="bib394" ref-type="bibr">[394]</xref>.</p><p>Less research and fewer clinical outcomes data are available on the quantification of RA size. Right atrial volumes are also underestimated with 2D echocardiographic techniques compared with 3DE <xref rid="bib343" ref-type="bibr">[343]</xref>, <xref rid="bib406" ref-type="bibr">[406]</xref>, <xref rid="bib407" ref-type="bibr">[407]</xref>.</p></sec></sec><sec id="s0265"><label>7.3</label><title>Cardiac computed tomography</title><p>Cardiac CT may be used for accurate assessment of atrial volumes. Volumetric data from cardiac computed tomography (CCT) are comparable to data generated by CMR and 3D echocardiographic imaging and is superior to 2D echocardiography <xref rid="bib371" ref-type="bibr">[371]</xref>. The LA volume prior to catheter ablation and the presence of asymmetry of chamber geometry predicts the likelihood of maintaining sinus rhythm post-procedure <xref rid="bib408" ref-type="bibr">[408]</xref>. As the LA enlarges, the shape of the LA roof initially becomes flat and then becomes coved, and this progression may correlate with development of non-PV substrate in patients undergoing AF ablation <xref rid="bib409" ref-type="bibr">[409]</xref>.</p><p>CCT may also be used to screen for thrombus prior to AF ablation. The diagnostic accuracy of CT has been studied by multiple groups, with a systematic review of 19 studies and 2955 patients reporting a sensitivity and specificity of 96 and 92%, respectively, translating to a positive predictive value of 41% and a negative predictive value of 99% <xref rid="bib410" ref-type="bibr">[410]</xref>. Diagnostic accuracy increased to 99%, with 100% specificity, when delayed imaging was performed. An advantage of using CT imaging to exclude thrombus is that CCT is frequently performed prior to AF ablation for integration into the electroanatomic mapping systems routinely used during AF ablation procedures. CCT can also provide accurate information about PV anatomy and variants and correlates well with CMR in that regard <xref rid="bib411" ref-type="bibr">[411]</xref>.</p></sec><sec id="s0270"><label>7.4</label><title>Magnetic resonance imaging of the atrium</title><p>Over recent years CMR has been used in clinical and research settings to provide gold standard volumetric assessments of chamber structure and function. Drawbacks are that CMR is expensive and has more limited availability than echocardiography. Recently, contrast-enhanced CMR with gadolinium has been used as a technique to detect atrial fibrosis <xref rid="bib412" ref-type="bibr">[412]</xref>. Although these methods are still in relatively early stages and have not been extensively reproduced, the ability to identify early degrees of atrial structural change would no doubt enhance our ability to detect varying degrees of remodelling that may not be as clear from volumetric or functional assessment. In addition to late-gadolinium-enhanced (LGE) CMR to detect replacement fibrosis, post-contrast T1 mapping <xref rid="bib413" ref-type="bibr">[413]</xref>, <xref rid="bib414" ref-type="bibr">[414]</xref> has been used to quantify diffuse interstitial fibrosis. Both techniques have been correlated with bipolar voltage measured during invasive mapping <xref rid="bib412" ref-type="bibr">[412]</xref>. However, these techniques require specialised post-imaging processing. While they are commonly used for ventricular imaging, they have not been widely employed for atrial imaging because of the technical challenges in achieving adequate image resolution in the thin-walled atrium <xref rid="bib415" ref-type="bibr">[415]</xref>.</p><p>Using a systematic scoring system for the extent of delayed enhancement, a recently-published multicentre study has related the extent of LGE CMR detected fibrosis to the outcome of AF ablation <xref rid="bib416" ref-type="bibr">[416]</xref>. The risk of recurrent AF increased from 15% for stage I fibrosis (,10% of the atrial wall) to 69% for stage IV fibrosis (≥30% of the atrial wall). The authors suggested that CMR quantification of fibrosis may play a role in the appropriate selection of patients most likely to benefit from AF ablation. Late-gadolinium-enhanced CMR has also been used to predict development of sinus node dysfunction <xref rid="bib417" ref-type="bibr">[417]</xref>, stroke risk <xref rid="bib418" ref-type="bibr">[418]</xref>, and progression of atrial fibrillation from paroxysmal to persistent <xref rid="bib419" ref-type="bibr">[419]</xref>. However, various studies have highlighted the need to further improve the methods of accurately identifying replacement fibrosis and to improve reproducibility of data analysis before LGE CMR can be considered a routine clinical tool <xref rid="bib420" ref-type="bibr">[420]</xref>, <xref rid="bib421" ref-type="bibr">[421]</xref>.</p><p>Recently, a number of studies have used CMR DE late gadolinium enhancement (LGE) in order to non-invasively characterize the extent and distribution of scarring present following AF ablation <xref rid="bib422" ref-type="bibr">[422]</xref>, <xref rid="bib423" ref-type="bibr">[423]</xref>, <xref rid="bib424" ref-type="bibr">[424]</xref>. Several studies observed that patients with more extensive scar at 3 months (or greater percentage scar around the PV circumference) had a lower AF recurrence rate <xref rid="bib423" ref-type="bibr">[423]</xref>, <xref rid="bib425" ref-type="bibr">[425]</xref>. Another study showed a correlation between measured contact force at the time of ablation, and the extent of CMR determined scar development <xref rid="bib426" ref-type="bibr">[426]</xref>. Other studies have shown a concordance between scar around the PVs and low-voltage regions on invasive electroanatomic mapping (EAM) <xref rid="bib427" ref-type="bibr">[427]</xref>, <xref rid="bib428" ref-type="bibr">[428]</xref>. Isolation of PVs at repeat procedures could be achieved guided by the imported MR image to identify the gaps <xref rid="bib427" ref-type="bibr">[427]</xref>, <xref rid="bib428" ref-type="bibr">[428]</xref>. However, other studies found no association between CMR scar gaps and mapped PV reconnection sites. A study in 50 paroxysmal AF patients undergoing either wide area or ostial ablation found that the proportion of patients in whom CMR could correctly identify the distribution of ablation lesions varied from as low as 28% to 54% depending on the technique used <xref rid="bib429" ref-type="bibr">[429]</xref>. These authors concluded that LGE imaging of atrial scar was not yet sufficiently accurate to reliably identify ablation lesions or to determine their distribution. Whether CMR will have the resolution to detect such focal regions where scar is incomplete remains uncertain. Of note, Harrison et al. used an animal model to correlate lesion size on CMR with lesion volume at pathology. The correlation depended critically on the definition of pixel intensity used to define scar with small changes in definition leading to large changes in estimated scar volume <xref rid="bib415" ref-type="bibr">[415]</xref>.</p></sec><sec id="s0275"><label>7.5</label><title>Imaging with electroanatomic mapping</title><p>Electroanatomic mapping systems have become the standard for invasive substrate characterisation of atrial cardiomyopathies. Using various technologies, these systems allow for rapid characterisation and reproduction of atrial anatomy with 3-D display rendering. Anatomic variations in PV anatomy, including common ostium or additional veins, may be identified. Visualisation software allows for accurate measurements of atrial distances <xref rid="bib430" ref-type="bibr">[430]</xref> and gross volumetric data but assessment of venous diameter may be suboptimal owning to venous susceptibility to distortion. Anatomic imaging of the atria may be enhanced with the co-registration of DICOM images from previously acquired cardiac MRI or CT or with the use of real-time contrast angiography or intracardiac echocardiogram.</p><p>While EAM allows for anatomic reproduction of the atria, it also enables the assessment of the atrial substrate through the geographic display of unipolar and bipolar signal amplitude data, as well as other signal characteristics, on rendered atrial surfaces. Regions of low-voltage, electrical silence, fractionation, or double potentials are reputed to correlate with underlying atrial fibrosis, surgical patches, or scar. In the same way, electrical activation of the atrium may be imaged allowing for assessment of regional changes in conduction velocity <xref rid="bib431" ref-type="bibr">[431]</xref> that may be proarrhythmic and support the perpetuation of atrial fibrillation. The use of EAM for activation mapping of atrial arrhythmia will be discussed in the subsequent section on ablation techniques.</p><p>Electroanatomic mapping has been used to image the electroanatomic substrate of atrial cardiomyopathy associated with sinus node disease <xref rid="bib432" ref-type="bibr">[432]</xref>, rheumatic MS <xref rid="bib215" ref-type="bibr">[215]</xref>, atrial septal defect <xref rid="bib218" ref-type="bibr">[218]</xref>, <xref rid="bib431" ref-type="bibr">[431]</xref>, CHF <xref rid="bib433" ref-type="bibr">[433]</xref>, obstructive sleep apnoea <xref rid="bib117" ref-type="bibr">[117]</xref>, and ageing <xref rid="bib167" ref-type="bibr">[167]</xref>. It has been a powerful research tool that has enhanced our understanding of the atrial substrate in patients with paroxysmal and persistent atrial fibrillation and <xref rid="bib74" ref-type="bibr">[74]</xref>, <xref rid="bib434" ref-type="bibr">[434]</xref> those who have failed initial PV antrum isolation <xref rid="bib435" ref-type="bibr">[435]</xref>.</p><p>Unlike cardiac MR, CT, or echocardiography, EAM requires invasive catheterization and mapping. However, despite recent advances in MRI techniques that allow for imaging atrial scar, EAM imaging arguably has a great clinical feasibility and superior ability to image and to define the atrial substrate that leads to the development of atrial fibrillation. A recent consensus report on multi-modality imaging for AF patients is a useful detailed reference <xref rid="bib346" ref-type="bibr">[346]</xref>.</p></sec><sec id="s0280"><label>7.6</label><title>Ablation of atrial tachyarrhythmia</title><p>Numerous single-centre, randomized studies and larger multicentre observational registries have demonstrated the superiority of AF ablation over drug therapy for maintenance of sinus rhythm. However, late recurrences are common and associated with more advanced atrial substrate associated with structural heart disease <xref rid="bib436" ref-type="bibr">[436]</xref>, <xref rid="bib437" ref-type="bibr">[437]</xref>, <xref rid="bib438" ref-type="bibr">[438]</xref>, <xref rid="bib439" ref-type="bibr">[439]</xref>, <xref rid="bib440" ref-type="bibr">[440]</xref>, <xref rid="bib441" ref-type="bibr">[441]</xref>, <xref rid="bib442" ref-type="bibr">[442]</xref>, <xref rid="bib443" ref-type="bibr">[443]</xref>, <xref rid="bib444" ref-type="bibr">[444]</xref>, <xref rid="bib445" ref-type="bibr">[445]</xref>, <xref rid="bib446" ref-type="bibr">[446]</xref>.</p><p>It is in this context that it is important to consider the various types of underlying atrial cardiomyopathy and how they may affect ablation outcomes. This is timely, as it has recently been observed that lone AF is a rapidly disappearing entity as we recognise conditions such as sleep apnoea, obesity, endurance exercise etc. previously not suspected of being causally associated with atrial fibrillation <xref rid="bib447" ref-type="bibr">[447]</xref>. In addition, emerging data suggest that treating these underlying causes may be central to improving long-term ablation outcomes <xref rid="bib199" ref-type="bibr">[199]</xref>, <xref rid="bib200" ref-type="bibr">[200]</xref>, <xref rid="bib448" ref-type="bibr">[448]</xref>, <xref rid="bib449" ref-type="bibr">[449]</xref>. In addition, LA ablation procedures may alter atrial size, structure, and mechanical atrial function. Catheter ablation may thus influence ongoing pathologies and atrial thrombogenesis <xref rid="bib450" ref-type="bibr">[450]</xref>, <xref rid="bib451" ref-type="bibr">[451]</xref>.</p><p>Mapping studies have demonstrated a common electrophysiological endpoint for a range of such conditions affecting the atrium either primarily or secondarily, many of which have been shown to be associated with atrial remodelling characterised by conduction slowing and myocardial voltage reduction suggesting fibrosis <xref rid="bib117" ref-type="bibr">[117]</xref>, <xref rid="bib167" ref-type="bibr">[167]</xref>, <xref rid="bib177" ref-type="bibr">[177]</xref>, <xref rid="bib433" ref-type="bibr">[433]</xref>, <xref rid="bib452" ref-type="bibr">[452]</xref>, <xref rid="bib453" ref-type="bibr">[453]</xref>. Magnetic resonance imaging techniques attempting to characterize the extent of myocardial fibrosis have demonstrated that this appears to be the strongest independent predictor of AF recurrence after ablation <xref rid="bib416" ref-type="bibr">[416]</xref>, <xref rid="bib454" ref-type="bibr">[454]</xref>. Whether the EHRAS classification has value for informing catheter ablation in human atria remains to be determined.</p></sec><sec id="s0285"><label>7.7</label><title>Age and atrial fibrillation ablation</title><p>Increasing age has been shown to be associated with increasing atrial fibrosis in both basic and clinical studies <xref rid="bib167" ref-type="bibr">[167]</xref>, <xref rid="bib455" ref-type="bibr">[455]</xref>. Numerous studies have evaluated ablation outcomes in ageing patients (variously defined as .65 through to .80) <xref rid="bib444" ref-type="bibr">[444]</xref>, <xref rid="bib445" ref-type="bibr">[445]</xref>, <xref rid="bib456" ref-type="bibr">[456]</xref>, <xref rid="bib457" ref-type="bibr">[457]</xref>, <xref rid="bib458" ref-type="bibr">[458]</xref>, <xref rid="bib459" ref-type="bibr">[459]</xref>, <xref rid="bib460" ref-type="bibr">[460]</xref>, <xref rid="bib461" ref-type="bibr">[461]</xref>, <xref rid="bib462" ref-type="bibr">[462]</xref>. Observational studies have consistently reported high multiple procedure success rates at 12 months of up to 80% in older patients. Conflicting data exist regarding outcomes in comparative studies with one study demonstrating a reduced success rate in patients over 65 years while another study showed similar efficacy in patients over the age of 80 years to the younger cohort <xref rid="bib461" ref-type="bibr">[461]</xref>, <xref rid="bib463" ref-type="bibr">[463]</xref>.</p></sec><sec id="s0290"><label>7.8</label><title>Hypertension</title><p>Hypertension is another well-recognised risk factor for development of atrial fibrillation. Mapping studies have demonstrated the presence of a more advanced atrial substrate in hypertensive patients compared with controls <xref rid="bib177" ref-type="bibr">[177]</xref>, <xref rid="bib464" ref-type="bibr">[464]</xref>. Hypertension has been shown to be a risk factor for recurrence of AF after AF ablation in numerous studies on univariate analysis, but it is less clear whether this is independent of factors such as atrial size. Recent preliminary studies have suggested that aggressive treatment of hypertension improves post-ablation outcomes <xref rid="bib200" ref-type="bibr">[200]</xref>, <xref rid="bib464" ref-type="bibr">[464]</xref>, <xref rid="bib465" ref-type="bibr">[465]</xref>.</p></sec><sec id="s0295"><label>7.9</label><title>Heart failure and atrial fibrillation ablation</title><p>Contractile dysfunction has similarly been associated with advanced atrial remodelling and predisposition to atrial fibrillation both in basic and in clinical studies <xref rid="bib113" ref-type="bibr">[113]</xref>, <xref rid="bib433" ref-type="bibr">[433]</xref>. Numerous studies have evaluated the efficacy of catheter ablation of both paroxysmal and persistent atrial fibrillation with significant impairment of systolic function <xref rid="bib437" ref-type="bibr">[437]</xref>, <xref rid="bib466" ref-type="bibr">[466]</xref>, <xref rid="bib467" ref-type="bibr">[467]</xref>, <xref rid="bib468" ref-type="bibr">[468]</xref>, <xref rid="bib469" ref-type="bibr">[469]</xref>, <xref rid="bib470" ref-type="bibr">[470]</xref>, <xref rid="bib471" ref-type="bibr">[471]</xref>, <xref rid="bib472" ref-type="bibr">[472]</xref>, <xref rid="bib473" ref-type="bibr">[473]</xref>. The weight of evidence is that sinus rhythm can be successfully achieved in 50–80% of patients although repeat procedures are common and follow-up periods are usually not more than 12 months. Successful ablation has been associated with significant improvements in ejection fraction and reduction in atrial size in the majority of studies <xref rid="bib470" ref-type="bibr">[470]</xref>, <xref rid="bib474" ref-type="bibr">[474]</xref>.</p></sec><sec id="s0300"><label>7.10</label><title>Metabolic syndrome and obesity</title><p>A number of studies have evaluated the impact of the metabolic syndrome on catheter ablation outcomes in atrial fibrillation patients <xref rid="bib475" ref-type="bibr">[475]</xref>, <xref rid="bib476" ref-type="bibr">[476]</xref>, <xref rid="bib477" ref-type="bibr">[477]</xref>, <xref rid="bib478" ref-type="bibr">[478]</xref>, <xref rid="bib479" ref-type="bibr">[479]</xref>, <xref rid="bib480" ref-type="bibr">[480]</xref>. Although the data are mixed, the weight of studies and a systematic review <xref rid="bib477" ref-type="bibr">[477]</xref> suggest a higher risk of AF recurrence. In the ARREST AF study, patients with BMI over 27 undergoing AF ablation had a much lower risk of recurrence if weight loss was achieved and maintained <xref rid="bib200" ref-type="bibr">[200]</xref>. Observational studies have demonstrated a significantly lower risk of recurrent AF in patients with treated compared with untreated OSA <xref rid="bib481" ref-type="bibr">[481]</xref>.</p></sec><sec id="s0305"><label>7.11</label><title>Impact of diabetes on ablation outcomes</title><p>Several studies have documented an increased recurrence rate of atrial fibrillation after an ablation procedure in patients with diabetes mellitus <xref rid="bib204" ref-type="bibr">[204]</xref>, <xref rid="bib475" ref-type="bibr">[475]</xref>, <xref rid="bib482" ref-type="bibr">[482]</xref>. An abnormal atrial substrate and non-PV triggers have been shown to underlie this worse outcome.</p></sec><sec id="s0310"><label>7.12</label><title>Role of myocarditis</title><p>Markers of inflammation such as CRP and IL-6 have been linked to risk of AF <xref rid="bib267" ref-type="bibr">[267]</xref>, <xref rid="bib483" ref-type="bibr">[483]</xref>, <xref rid="bib484" ref-type="bibr">[484]</xref>, <xref rid="bib485" ref-type="bibr">[485]</xref>. Recently, giant-cell myocarditis involving only the atria has been shown to result in atrial fibrillation with enlarged atria <xref rid="bib149" ref-type="bibr">[149]</xref>. Patients with apparently lone atrial fibrillation frequently demonstrate histological findings consistent with an atrial myocarditis <xref rid="bib486" ref-type="bibr">[486]</xref>; and those with past myocarditis may have atrial electrical scar, conduction abnormalities, or atrial standstill <xref rid="bib146" ref-type="bibr">[146]</xref>, <xref rid="bib487" ref-type="bibr">[487]</xref>, <xref rid="bib488" ref-type="bibr">[488]</xref>, <xref rid="bib489" ref-type="bibr">[489]</xref>. Baseline CRP levels have been associated with the risk of recurrent AF after catheter ablation <xref rid="bib278" ref-type="bibr">[278]</xref>. Recently, colchicine has been used to prevent atrial fibrillation recurrence after PV isolation <xref rid="bib490" ref-type="bibr">[490]</xref>. It is also possible that AF in itself can result in inflammation and the development of an ‘atrial myocarditis’ <xref rid="bib491" ref-type="bibr">[491]</xref>.</p></sec><sec id="s0315"><label>7.13</label><title>Impact of atrial fibrillation duration on atrial myopathy and atrial fibrillation ablation outcomes</title><p>Longitudinal studies in AF patients have demonstrated clinical progression of AF over time in a significant proportion with risk strongly associated with drivers such as increasing age, structural heart disease, and hypertension <xref rid="bib492" ref-type="bibr">[492]</xref>. Chronic AF results in structural change with a recent study showing that in proportion to AF burden, atrial remodelling may progress significantly even over a time period as short as 1 year.</p><p>Numerous studies have demonstrated that atrial size and occasionally mechanical function may improve following ablation <xref rid="bib493" ref-type="bibr">[493]</xref>, but at least one invasive study showed no improvement in atrial electrophysiology 6 months after successful ablation <xref rid="bib219" ref-type="bibr">[219]</xref>. Overwhelmingly, studies evaluating long-term outcomes after ablation of persistent atrial fibrillation have demonstrated lower rates of procedural reversion to sinus rhythm and higher late recurrence rates reflecting more advanced atrial substrate.</p></sec><sec id="s0320"><label>7.14</label><title>Impact of ongoing atrial fibrillation on electrical and structural remodelling</title><p>It is now well known that in the presence of an appropriate heterogenous AF substrate, a focal trigger can result in sustained high-frequency re-entrant AF drivers, named rotors. The waves that emerge from these rotors undergo spatially distributed fragmentation and so give rise to fibrillatory conduction. When high-frequency atrial activation is maintained for at least 24 h, ion-channel remodelling changes the electrophysiologic substrate, promoting perpetuation of re-entry and increasing the activity of triggers, further contributing to AF permanence <xref rid="bib494" ref-type="bibr">[494]</xref>. Atrial fibrillation itself leads to remodelling, causing electrophysiological (electrical), contractile, and structural changes <xref rid="bib495" ref-type="bibr">[495]</xref>, <xref rid="bib496" ref-type="bibr">[496]</xref>. Although AF can typically be reversed in its early stages, it becomes more difficult to eliminate over time due to such remodelling <xref rid="bib238" ref-type="bibr">[238]</xref>, <xref rid="bib497" ref-type="bibr">[497]</xref>. Dominant-frequency analysis points to an evolution of mechanisms in AF patients, with PV sources becoming less predominant as AF becomes more persistent and atrial remodelling progresses <xref rid="bib498" ref-type="bibr">[498]</xref>. The data suggest that in patients with long-standing persistent AF, atrial remodelling augments the number of AF drivers and shifts their location away from the PV/ostial region.</p></sec><sec id="s0325"><label>7.15</label><title>Impact of catheter ablation on atrial pathology</title><p>Several studies have examined LA size before and after catheter ablation and have demonstrated a 10–20% decrease in the dimensions of the LA after catheter ablation of AF <xref rid="bib499" ref-type="bibr">[499]</xref>, <xref rid="bib500" ref-type="bibr">[500]</xref>. Although the precise mechanism of this decrease in size is not known, it appears consistent with reverse remodelling. It has been suggested that earlier aggressive intervention to maintain sinus rhythm, including AF ablation if needed, may aid to prevent ‘chronicization’ of AF and improve long-term outcomes <xref rid="bib501" ref-type="bibr">[501]</xref>. A large-scale multicentre trial is presently testing this idea <xref rid="bib502" ref-type="bibr">[502]</xref>.</p><p>The true impact of atrial cardiomyopathies on the success of catheter ablation has not been elucidated. Nevertheless, it is very likely that atrial pathology affects energy delivery to tissue and specific forms of cardiomyopathy may differentially affect ablation procedures. However, the true impact and interaction of various energy sources with different atrial pathologies need to be studied.</p></sec></sec><sec id="s0330"><label>8</label><title>Conclusion</title><p>Atrial cardiomyopathies as defined in this consensus paper have a significant impact on atrial function and arrhythmogenesis. The EHRAS classification (EHRAS Class I–IV) is a first attempt to characterize atrial pathologies into discrete cohorts. Because disease-related histological changes in atrial tissue are often poorly characterised, not necessarily specific and vary considerably over time their classification is challenging. Further studies are needed to implement and validate the EHRAS classification and to assess its value in guiding clinical understanding and management of AF. 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pub-id-type="pmid">16179272</pub-id></element-citation></ref></ref-list><fn-group><fn id="d32e905"><label>☆</label><p id="ntp0010">Endorsed by EHRA, APHRS, SOLAECE in May 2016, by HRS, AHA, ACC in June 2016.</p></fn><fn id="d32e910"><label>☆☆</label><p id="ntp0015">Developed in partnership with the European Heart Rhythm Association (EHRA), (a registered branch of the European Society of Cardiology (ESC)) the Heart Rhythm Society (HRS), the Asia Pacific Heart Rhythm Society (APHRS), the Sociedad Latino Americana de Estimulación Cardíaca y Electrofisiología (SOLAECE), and in collaboration with the American College of Cardiology (ACC), the American Heart Association (AHA). Endorsed by SOLAECE in May 2016, pending endorsement by HRS, APHRS, AHA, and ACC.</p></fn></fn-group></back><floats-group><fig id="f0005"><label>Fig. 1</label><caption><p>Histological and pathopysiological classification of atrial cardiomyopathies (EHRA/HRS/APHRS/SOLAECE): EHRAS classification. The EHRAS class may vary over time in the cause of the disease and may differ at various atrial sites. Of note, the nature of the classification is purely descriptive. EHRAS I–IV is not intended to describe disease progression from EHRAS I to EHRAS IV.</p></caption><alt-text id="at0005">Fig. 1</alt-text><graphic xlink:href="gr1"></graphic></fig><fig id="f0010"><label>Fig. 2</label><caption><p>(A) EHRAS Class I (biopsy): there are severe changes affecting ‘primarily’ the cardiomyocytes in terms of cell hypertrophy and myocytolysis; fibrosis is much less evident than myocyte modifications. (B) EHRAS Class II (biopsy): cardiomyocyte alterations are relatively modest compared with severe fibrotic changes; in this case, interstitial changes are much more prevalent than myocyte ones. (C) EHRAS Class III (biopsy): this is a combination of cardiomyocyte changes and collagen fibre deposition. (D) EHRAS Class IV (autopsy heart): primarily neutro-philic myocarditis.</p></caption><alt-text id="at0010">Fig. 2</alt-text><graphic xlink:href="gr2"></graphic></fig><fig id="f0015"><label>Fig. 3</label><caption><p>EHRAS Class IV (autopsy heart): this image shows a myocardial interstitial with some fibrosis but prominent amyloid (AL type) deposition (left-hand side, congo red staining under regular light microscope; right-hand side, congo red staining under polarised light microscope).</p></caption><alt-text id="at0015">Fig. 3</alt-text><graphic xlink:href="gr3"></graphic></fig><fig id="f0020"><label>Fig. 4</label><caption><p>Schematic representations and heart dissections to show the arrangement of the myocardial strands in the superficial parts of the walls. (A) The dissection viewed from the anterior aspect display the interatrial muscle Bachmann bundle and its bifurcating branches leftward and rightward. (B) A view of the roof and posterior wall of the left and right atriums. The right pulmonary veins (PVs) passes behind the intercaval area. The subepicardial dissection shows the abrupt changes in fibre orientation and the myocardial strands (septopulmonary bundle) in the region between the left and right PVs. The red arrows show multiple muscle bridges connecting the two atria. ICV, inferior caval vein; LAA, left atrial appendage; LSPV, left superior pulmonary vein; MV, mitral valve; RAA, right atrial appendage; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein; SCV, superior caval vein; TV, tricuspid valve (see text for details).</p></caption><alt-text id="at0020">Fig. 4</alt-text><graphic xlink:href="gr4"></graphic></fig><fig id="f0025"><label>Fig. 5</label><caption><p>Normal histology of the left atrium and relevant pathological changes in mitral valve disease-associated atrial fibrillation. (A) Medium-power view of a normal left atrial myocardium which is composed of large bands of homogeneous cardiomyocytes. (B) In the same atrium as in (A), the Van Gieson staining show that collagen fibres (red colour) are primarily seen in the adventitial spaces of blood vessels (arrow). (C) Low-power view of a left atrium from a patient with mitral valve disease-associated atrial fibrillation. Large bands of cardiomyocytes are separated by significant amounts of pathologic fibrous tissue (arrows). (D) In the same atrium as in (C), the Van Gieson staining shows that the pathologic fibrous significantly thickens the perivascular spaces (perivascular fibrosis, arrow) and separates single or small groups of cardiomyocytes (interstitial fibrosis, arrowhead). (E) In atrial fibrillation, a variable number of cardiomyocytes undergo loss of contractile elements starting from the perinuclear area and resulting in so-called myocytolysis. These spaces may be empty (arrow) or filled with glycogen (arrowhead). (F) A higher-power view of myocytolysis with both glycogen rich (arrow) and optically empty (arrowhead) cardiomyocytes. (G) Ultrastructural view of a myolytic cardiomyocyte with significant loss of contractile elements around the nucleus (asterisk). In this empty area, there is very often accumulation of mitochondria (arrowhead) while the adjacent myofibrils display signs of abnormal contraction (arrow). (H) An LA from a patient with atrial fibrillation where the myocardial microcirculation (arrow) is slightly reduced and irregularly distributed. Stainings. (A and C) haematoxylin–eosin staining; (B and D) Van Gieson staining for collagen; (E and F) Periodic acid Schiff staining; (G) ultrastructural image; (H) immunohistochemical analysis with an anti-CD31 antibody. Original magnifications. (A, B, E, and H) ×20; (C and D) ×4; (F) ×40; (G) ×2800.</p></caption><alt-text id="at0025">Fig. 5</alt-text><graphic xlink:href="gr5"></graphic></fig><fig id="f0030"><label>Fig. 6</label><caption><p>(A) Comparison of atrial and ventricular action potential properties and underlying ionic currents. Resting potentials (2 mV) are more negative (averaging 280–285 mV) in ventricular vs. atrial (270–275 mV) myocytes. (B) Connexin distribution differs between atria and ventricles, with connexin-43 only expressed in ventricular cardiomyocytes (CMs) but atrial CMs having both connexin-40 and connexin-43. (C) Ralistic reconstruction of the structure of sheep atria. The right atrium (RA), left atrium (LA), pectinate muscles (PM), Bachmann׳s bundle (BB) and pulmonary veins (PV) are colour coded. From Ref. <xref rid="bib43" ref-type="bibr">[43]</xref> with permission.</p></caption><alt-text id="at0030">Fig. 6</alt-text><graphic xlink:href="gr6"></graphic></fig><fig id="f0035"><label>Fig. 7</label><caption><p>Left atrial pressure–volume loop. (A) Analogue recordings of left atrial pressure and dimensions in the time domain. Vertical lines indicate time of mitral valve opening (A), end of passive atrial emptying and onset of atrial diastasis (B), atrial end-diastole (C), and atrial end-systole (D). a and v represent respective venous pressure waves. (B) Left atrial pressure–volume loop from a single beat illustrating characteristic figure-of-eight configuration. Arrows indicate the direction of loop as a function of time. A loop represents active atrial contraction. V loop represents passive filling and emptying of the LA. MVO, time of mitral valve opening; MVC, approximate time of mitral valve closure; LA, left atrial end-systole; and LAd, left atrial end-diastole. Reproduced from Ref. <xref rid="bib49" ref-type="bibr">[49]</xref> with permission.</p></caption><alt-text id="at0035">Fig. 7</alt-text><graphic xlink:href="gr7"></graphic></fig><fig id="f0040"><label>Fig. 8</label><caption><p>LA functions colour-coded displays of atrial functions (red, reservoir; blue, conduit; yellow, booster pump) related to events in the cardiac cycle. Displayed are pulmonary venous (PV) velocity, LA strain, LA strain rate, LA volume and pressure, and mitral spectral and tissue Doppler. Reproduced from Ref. <xref rid="bib1" ref-type="bibr">[1]</xref> with permission.</p></caption><alt-text id="at0040">Fig. 8</alt-text><graphic xlink:href="gr8"></graphic></fig><fig id="f0045"><label>Fig. 9</label><caption><p>Excitation–contraction coupling in atria vs. ventricles. Schematic representation of the cell structure and major Ca<sup>2+</sup> handling proteins, along with related currents and ion transporters (A). Illustration of action potential (top), Ca<sup>2+</sup> transient (middle) and confocal linescan image of intracellular Ca<sup>2+</sup> wave propagation towards cell centre (bottom) in a ventricular (left) vs. atrial (right) cardiomyocyte (B). Arrows indicate differences in expression and/or function of Ca<sup>2+</sup> handling proteins in atrial vs. ventricular cardiomyocytes. I<sub>Na</sub>, Na<sup>+</sup> current; FKPB12.6, FK506-binding protein 12.6; JPH2, Junctophilin-2; MyBP-CMyosin bindig protein C; TnI, Troponin-I; for further abbreviations, see text.</p></caption><alt-text id="at0045">Fig. 9</alt-text><graphic xlink:href="gr9"></graphic></fig><fig id="f0050"><label>Fig. 10</label><caption><p>Concept of ‘endocardial remodelling’ in fibrillating atria. In accordance to Virchow׳s triad hypercoagulability, flow abnormalities, and endothelial changes must co-exist to induce thrombogenesis at the atrial endocardium. Molecular studies have revealed substantial endocardial changes in left atrial tissue samples. Prothrombogenic factors (vWF, adhesion molecules like VCAM-1, P-selectin etc; green) are expressed at the surface of endothelial cells causing an increased adhesiveness of platelets and leucocytes to the atrial endocardium. This initiates atrial thrombogenesis at the atrial endocardium. Several clinical factors like diabetes mellitus, heart failure ageing etc. (CHA2DS2VASc Parameters) increase molecular alterations (oxidative stress pathways etc.) within myocytes and endothelial cells, and thereby, increase the expression of prothrombogenic factors. These alterations are not directly related to the presence of absensce of atrial fibrillation in the surface ECG, and therefore, help to explain, why thrombogenesis is increased even during episodes of sinus rhythm.</p></caption><alt-text id="at0050">Fig. 10</alt-text><graphic xlink:href="gr10"></graphic></fig><table-wrap id="t0005" position="float"><label>Table 1</label><caption><p>Definition of atrial cardiomyopathy.</p></caption><alt-text id="at0055">Table 1</alt-text><table frame="hsides" rules="groups"><tbody><tr><td>‘Any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations’.</td></tr></tbody></table></table-wrap><table-wrap id="t0010" position="float"><label>Table 2</label><caption><p>EHRAS classification of atrial cardiomyopathy.</p></caption><alt-text id="at0060">Table 2</alt-text><table frame="hsides" rules="groups"><thead><tr><th>EHRAS class</th><th>Histological characterisation</th></tr></thead><tbody><tr><td>I <xref rid="bib11" ref-type="bibr">[11]</xref>, <xref rid="bib12" ref-type="bibr">[12]</xref>, <xref rid="bib13" ref-type="bibr">[13]</xref>, <xref rid="bib14" ref-type="bibr">[14]</xref>, <xref rid="bib15" ref-type="bibr">[15]</xref>, <xref rid="bib503" ref-type="bibr">[503]</xref></td><td>Morphological or molecular changes affecting ‘primarily’ the cardiomyocytes in terms of cell hypertrophy and myocytolysis; no significant pathological tissue fibrosis or other interstitial changes</td></tr><tr><td>II <xref rid="bib8" ref-type="bibr">[8]</xref>, <xref rid="bib12" ref-type="bibr">[12]</xref>, <xref rid="bib14" ref-type="bibr">[14]</xref>, <xref rid="bib504" ref-type="bibr">[504]</xref>, <xref rid="bib505" ref-type="bibr">[505]</xref>, <xref rid="bib506" ref-type="bibr">[506]</xref></td><td>Predominantly fibrotic changes; cardiomyocytes show normal appearance</td></tr><tr><td>III <xref rid="bib9" ref-type="bibr">[9]</xref>, <xref rid="bib11" ref-type="bibr">[11]</xref>, <xref rid="bib12" ref-type="bibr">[12]</xref>, <xref rid="bib217" ref-type="bibr">[217]</xref>, <xref rid="bib266" ref-type="bibr">[266]</xref></td><td>Combination of cardiomyocyte changes (e.g. cell hypertrophy, myocytolysis) and fibrotic changes Alteration of interstitial matrix without prominent</td></tr><tr><td>IV <xref rid="bib17" ref-type="bibr">[17]</xref>, <xref rid="bib18" ref-type="bibr">[18]</xref>, <xref rid="bib19" ref-type="bibr">[19]</xref></td><td>collagen fibre accumulation</td></tr><tr><td>Iva</td><td>Accumulation of amyloid</td></tr><tr><td>IVf</td><td>Fatty infiltration</td></tr><tr><td>IVi</td><td>Inflammatory cells</td></tr><tr><td>IVo</td><td>Other interstitial alterations</td></tr></tbody></table></table-wrap><table-wrap id="t0015" position="float"><label>Table 3</label><caption><p>Hereditary muscular dystrophies with cardiac involvement.</p></caption><alt-text id="at0065">Table 3</alt-text><table frame="hsides" rules="groups"><thead><tr><th>Muscular dystrophy</th><th>Protein/gene</th><th>Primary cardiac disease</th></tr></thead><tbody><tr><td>Duchenne</td><td>dystrophin</td><td>DCM</td></tr><tr><td>Becker</td><td>dystrophin</td><td>DCM</td></tr><tr><td>Myotonic dystrophy, type 1</td><td>DMPK</td><td>CSD</td></tr><tr><td>Emery-Dreifuss</td><td>Emerin</td><td>CSD</td></tr><tr><td></td><td>Lamin A/C</td><td>(DCM)</td></tr><tr><td>Limb-Girdle</td><td>Lamin A/C</td><td>CSD</td></tr><tr><td></td><td>Sarcoglycans</td><td>CM</td></tr><tr><td></td><td>others</td><td></td></tr><tr><td>Facioscapulohumeral</td><td>Dux 4</td><td>CSD (rare)</td></tr></tbody></table><table-wrap-foot><fn><p>DCM, dilated cardiomyopathy; CSD, conduction system disease; DMPK, myotonic dystrophy protein kinase.</p></fn></table-wrap-foot></table-wrap><table-wrap id="t0020" position="float"><label>Table 4</label><caption><p>Drugs reported to induce atrial fibrillation.</p></caption><alt-text id="at0070">Table 4</alt-text><table frame="hsides" rules="groups"><thead><tr><th>Drug group</th><th>Drugs</th><th>Mechanism</th></tr></thead><tbody><tr><td>Bisphosphonates</td><td>Alendronate, zoledronic acid</td><td></td></tr><tr><td>Cardiovascular</td><td></td><td></td></tr><tr><td>Inotropics</td><td>Dopamine, dobutamine, dopexamine, arbutamine, enoximone, milrinone, levosimendan</td><td>Adrenergic stimulation</td></tr><tr><td>Vasodilators</td><td>Isosorbide, losartan, flosequinan</td><td>Hypotension with probable adrenergic reflex</td></tr><tr><td>Cholinergics</td><td>Acetylcholine</td><td>Vagal stimulation</td></tr><tr><td>Diuretics</td><td>Thiazides</td><td>Hypokaliemia</td></tr><tr><td>Respiratory System</td><td></td><td></td></tr><tr><td>Sympathicomimetics</td><td>Pseudoephedrine, albuterol, oriciprenaline, salbutamol, salmetrol</td><td>Adrenergic stimulation</td></tr><tr><td>Xanthines</td><td>Aminophylline, teophylline</td><td>Adrenergic stimulation</td></tr><tr><td>Central Nervous System</td><td></td><td></td></tr><tr><td>Anticholinergics</td><td>Atropine</td><td>Adrenergic stimulation</td></tr><tr><td>Anticonvulsants</td><td>Lacosamide, paliperidone</td><td></td></tr><tr><td>Antidepressants</td><td>Fluoexetine, tranylcypromine, trazodone</td><td>Direct cardiodepressant effect, sympathetic tone</td></tr><tr><td>Antimigraine</td><td>Ondasetron, sumatriptan</td><td>coronary spasm</td></tr><tr><td>Antipsychotics</td><td>Clozapine, loxapine, olanzapine</td><td>Direct cardiodepressant effect, sympathetic tone</td></tr><tr><td>Cholinergics</td><td>Physostigmine, donepezil</td><td>Vagal stimulation</td></tr><tr><td>Dopamine agonists</td><td>Apomorphine</td><td>Vagal activity</td></tr><tr><td>Chemotherapeutics</td><td></td><td>Cardiac injury, coronary vasospasm, hypertension, reactive oxygen species, changes in mitochondrial calcium transport, electrolyte disturbances, inflammation</td></tr><tr><td>Alylating agents</td><td>Cisplatin, cyclophosphamide, ifosfamide, melphalan</td><td></td></tr><tr><td>Anthracyclines</td><td>Doxorubicin, mitoxantrone</td><td></td></tr><tr><td>Anti-metabolites</td><td>Capecitabine, 5-fluorouracil, gemcitabine</td><td></td></tr><tr><td>Antimicrotubule agents</td><td>Docetaxel, paclitaxel</td><td></td></tr><tr><td>Tyrosine kinase inhibitors</td><td>cetuximab, soratenib, sunitinib</td><td></td></tr><tr><td>Topoisomerase inhibitors</td><td>amsacrine, etoposide</td><td></td></tr><tr><td>Monoclonal antibodies Cytokines and immunomodulators</td><td>alemtuzumab, bevacizumab, rituximab, trastuzumab azathioprine, interferon-gamma, interleukin-2, lenalidomide</td><td></td></tr><tr><td>Genitourinary System</td><td></td><td></td></tr><tr><td>Drugs for erectile</td><td>sildenafil, tadalafil, vardenafil</td><td>Hypotension with adrenergic reflex dysfunction</td></tr><tr><td>Tocolytic drugs</td><td>b2-adrenoceptor agonists (hexoprenalin, terbutaline), magnesium sulphate</td><td></td></tr><tr><td>Hormones</td><td></td><td></td></tr><tr><td>Anabolic-androgenic</td><td></td><td>Structural changes, changes in autonomic activity steroids</td></tr></tbody></table></table-wrap><table-wrap id="t0025" position="float"><label>Table 5</label><caption><p>Coagulations markers in atrial fibrillation.</p></caption><alt-text id="at0075">Table 5</alt-text><table frame="hsides" rules="groups"><thead><tr><th>Study</th><th>AF group(s)</th><th>Control group(s)</th><th>Significant abnormalities found in AF (increase in coagulation markers)<xref rid="tbl5fna" ref-type="table-fn">a</xref></th></tr></thead><tbody><tr><td>Gustafsson (1990) <xref rid="bib507" ref-type="bibr">[507]</xref></td><td>20 (with stroke)</td><td>40 (normal without stroke)</td><td><sc>D</sc>-dimers, vWF irrespectively of history of stroke</td></tr><tr><td></td><td>20 (without stroke)</td><td>20 (with stroke)</td><td></td></tr><tr><td>Kumagai (1990) <xref rid="bib508" ref-type="bibr">[508]</xref></td><td>73</td><td>73</td><td><sc>D</sc>-dimers</td></tr><tr><td>Asakura (1992) <xref rid="bib509" ref-type="bibr">[509]</xref></td><td>83</td><td>(normal)</td><td>PF1+2, TATIII complex</td></tr><tr><td>Sohara (1994) <xref rid="bib510" ref-type="bibr">[510]</xref></td><td>13 (paroxysmal)</td><td>(normal)</td><td>TATIII complex (no difference in <sc>D</sc>-dimers),</td></tr><tr><td>Lip (1995) <xref rid="bib511" ref-type="bibr">[511]</xref></td><td>87</td><td>158</td><td><sc>D</sc>-dimers, vWF</td></tr><tr><td>Lip (1996) <xref rid="bib512" ref-type="bibr">[512]</xref></td><td>51</td><td>26 (healthy)</td><td><sc>D</sc>-dimers</td></tr><tr><td>Kahn (1997) <xref rid="bib513" ref-type="bibr">[513]</xref></td><td>50 (without prior stroke)</td><td>31(without prior stroke)</td><td>Fibrinogen in AF without stroke vs. controls without stroke (no difference was seen between groups with prior stroke)</td></tr><tr><td></td><td>25 (with prior stroke)</td><td>11 (with prior stroke)</td><td></td></tr><tr><td>Heppell (1997) <xref rid="bib514" ref-type="bibr">[514]</xref></td><td>19 with thrombus in LA</td><td>not applicable</td><td><sc>D</sc>-dimers, vWF, TATIII complex if LA thrombus</td></tr><tr><td></td><td>90 without thrombus in LA</td><td></td><td></td></tr><tr><td>Shinohara (1998) <xref rid="bib515" ref-type="bibr">[515]</xref></td><td>45 (non-valvular)</td><td>not applicable</td><td><sc>D</sc>-dimers, TATIII complex in patients with low vs. high LAA velocity</td></tr><tr><td>Feinberg (SPAF III) (1999) <xref rid="bib516" ref-type="bibr">[516]</xref></td><td>1531</td><td>not applicable</td><td>No association of PF1+2 with thromboembolism</td></tr><tr><td>Mondillo (2000) <xref rid="bib517" ref-type="bibr">[517]</xref></td><td>45</td><td>35 (healthy)</td><td><sc>D</sc>-dimers, vWF, s-thrombomodulin</td></tr><tr><td>Fukuchi (2001) <xref rid="bib518" ref-type="bibr">[518]</xref></td><td>16</td><td>27 (cardiac without AF)</td><td>vWF in LA appendage tissue</td></tr><tr><td>Conway (2002) <xref rid="bib296" ref-type="bibr">[296]</xref></td><td>1321</td><td></td><td>vWF in high-risk group for stroke</td></tr><tr><td>Kamath (2002) <xref rid="bib519" ref-type="bibr">[519]</xref></td><td>93</td><td>50 (normal)</td><td><sc>D</sc>-dimers</td></tr><tr><td>Vene (2003) <xref rid="bib520" ref-type="bibr">[520]</xref></td><td>113</td><td></td><td><sc>D</sc>-dimers in patients having cardiovascular events vs. no event</td></tr><tr><td>Nakamura (2003) <xref rid="bib521" ref-type="bibr">[521]</xref></td><td>LA appendage tissue of 7 non-valvular</td><td>4 non-cardiac death</td><td>vWF, TF</td></tr><tr><td>Conway (2003) <xref rid="bib297" ref-type="bibr">[297]</xref></td><td>994</td><td>not applicable</td><td>vWF not associated of with risk of stroke, vWF independently associated with vascular events</td></tr><tr><td>Kamath (2003) <xref rid="bib522" ref-type="bibr">[522]</xref></td><td>31 (acute onset)</td><td>31 (healthy)</td><td>Haematocrit raised in acute AF</td></tr><tr><td></td><td>93 (permanent)</td><td></td><td><sc>D</sc>-dimers in permanent AF (but not in acute AF)</td></tr><tr><td>Sakurai (2004) <xref rid="bib523" ref-type="bibr">[523]</xref></td><td>28 (AFL)</td><td>27</td><td><sc>D</sc>-dimers if impaired LAA function</td></tr><tr><td>Inoue (2004) <xref rid="bib524" ref-type="bibr">[524]</xref></td><td>246 (non-valvular)</td><td>111</td><td><sc>D</sc>-dimers in patients having risk factors, PF1+2 (NS)</td></tr><tr><td>Kumagai (2004) <xref rid="bib525" ref-type="bibr">[525]</xref></td><td>16 (post mortem)</td><td></td><td>vWF and protein in patients with enlarged atrium</td></tr><tr><td>Marin (2004) <xref rid="bib526" ref-type="bibr">[526]</xref></td><td>24 (acute onset)</td><td>24 (CAD patients in sinus rhythm)</td><td><sc>D</sc>-dimers, vWF, s-thrombomodulin (no longer different after cardioversion)</td></tr><tr><td></td><td>24 (chronic)</td><td>24 (healthy)</td><td></td></tr><tr><td>Nozawa (2004) <xref rid="bib527" ref-type="bibr">[527]</xref></td><td>509</td><td>111 (healthy)</td><td><sc>D</sc>-dimers, PF1+2 (NS)</td></tr><tr><td>Freestone (2005) <xref rid="bib528" ref-type="bibr">[528]</xref></td><td>59</td><td>40 (healthy)</td><td>vWF</td></tr><tr><td>Nozawa (2006) <xref rid="bib295" ref-type="bibr">[295]</xref></td><td>509 (non-valvular)</td><td></td><td><sc>D</sc>-dimers (but not PF1+2) predictive for thromboembolic events <sc>D</sc>-dimers, PF1+2, platelet factor 4, b-thromboglobulin</td></tr><tr><td>Ohara (2007) <xref rid="bib294" ref-type="bibr">[294]</xref></td><td>591 (non-valvular)</td><td>129</td><td><sc>D</sc>-dimers, PF1+2 (correlated with presence of risk factors for stroke)</td></tr></tbody></table><table-wrap-foot><fn><p>AF, atrial fibrillation; AFL, atrial flutter; CAD, coronary artery disease; LA, left atrial; LAA, left atrial appendage; NS, non-significant; vWf, von Willebrand factor; PF1+2, prothrombin fragment 1+2; TATIII, thrombin-antithrombin III; TF, tissue factor; s-thrombomodulin, soluble-thrombomodulin.</p></fn></table-wrap-foot><table-wrap-foot><fn id="tbl5fna"><label>a</label><p id="ntp0005">Significantly different in AF group, unless otherwise indicated.</p></fn></table-wrap-foot></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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