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  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
        <publisher-loc>S&#227;o Paulo, SP, Brazil</publisher-loc>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v3">WNnrtXPvCwtwgMMgmByTGbt</article-id>
      <article-id pub-id-type="other">00001</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2007001500001</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(07)08900301</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2007001500001</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Artigos Originais</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Abla&#231;&#227;o da fibrila&#231;&#227;o atrial por cateter com radiofreq&#252;&#234;ncia guiada por mapeamento espectral endoc&#225;rdico dos "ninhos de FA" em ritmo sinusal</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Mateos</surname>
            <given-names>Jos&#233; Carlos Pach&#243;n</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Mateos</surname>
            <given-names>Enrique I. Pach&#243;n</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Lobo</surname>
            <given-names>Tasso J.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Pach&#243;n</surname>
            <given-names>Maria Z&#233;lia C.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Mateos</surname>
            <given-names>Ju&#225;n Carlos Pach&#243;n</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Pach&#243;n</surname>
            <given-names>Denilda Queiroz V.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Vargas</surname>
            <given-names>Remy Nelson A.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Piegas</surname>
            <given-names>Leopoldo S.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Jatene</surname>
            <given-names>Adib D.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <institution content-type="orgname">Hospital do Cora&#231;&#227;o</institution>
      </aff>
      <aff id="aff02">
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">S&#227;o Paulo</named-content>
        </addr-line>
        <institution content-type="orgname">Instituto Dante Pazzanese de Cardiologia</institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>09</month>
        <year>2007</year>
      </pub-date>
      <volume>89</volume>
      <issue>3</issue>
      <fpage>140</fpage>
      <lpage>150</lpage>
      <history>
        <date date-type="rev-recd">
          <day>01</day>
          <month>03</month>
          <year>2007</year>
        </date>
        <date date-type="received">
          <day>25</day>
          <month>02</month>
          <year>2007</year>
        </date>
        <date date-type="accepted">
          <day>07</day>
          <month>03</month>
          <year>2007</year>
        </date>
      </history>
      <permissions>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/" xml:lang="en">
          <license-p>This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>FUNDAMENTO: Atrav&#233;s de mapeamento espectral-(ME) endoc&#225;rdico em ritmo sinusal, observam-se dois tipos de mioc&#225;rdio atrial: o compacto de espectro liso e o fibrilar de espectro segmentado ("Ninho de FA" [NFA]). Durante a FA o compacto tem ativa&#231;&#227;o organizada e baixa freq&#252;&#234;ncia (passivo) enquanto o fibrilar apresenta ativa&#231;&#227;o bastante desorganizada e alta freq&#252;&#234;ncia (ativo/ressonante) sendo ambos ativados por uma taquicardia protegida de alta freq&#252;&#234;ncia, taquicardia de background (TB). OBJETIVO: Descrever o tratamento da FA pela abla&#231;&#227;o dos NFA e da TB. M&#201;TODOS: 1) Abla&#231;&#227;o por cateter-RF [4/8mm-60&#186;/30-40J/30s] dos NFA guiada por ME em ritmo sinusal, fora das veias pulmonares; 2) Estimula&#231;&#227;o atrial-300ppm; 3) Abla&#231;&#227;o adicional de NFA se induzida FA; 4) Abla&#231;&#227;o focal se induzida TB e/ou Flutter; 5) Seguimento cl&#237;nico+ECG+Holter. RESULTADOS: Foram tratados 50&#177;18 NFA/paciente. Ap&#243;s 11,3&#177;8m 81p (88%) estavam sem FA (28,3% com antiarr&#237;tmico). Ap&#243;s a abla&#231;&#227;o dos NFA: a FA n&#227;o foi reinduzida em 61p(71%); TB foi induzida e tratada em 24p(26%). Ocorreram 2 sangramentos peric&#225;rdicos (1 tratado clinicamente e 1 cirurgicamente) ocasionados por bainhas n&#227;o mais utilizadas. CONCLUS&#195;O: O ME em ritmo sinusal ablaciona os NFA. Durante a FA os NFA apresentam um padr&#227;o reativo-ressonante e o mioc&#225;rdio compacto apresenta-se passivo, estimulados pela alta freq&#252;&#234;ncia da TB. Ap&#243;s a abla&#231;&#227;o dos NFA e da TB n&#227;o foi poss&#237;vel reinduzir FA sustentada. A abla&#231;&#227;o dos NFA fora das VP se mostrou segura e altamente eficiente para a cura e/ou o controle cl&#237;nico da FA.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>Abla&#231;&#227;o por cateter</kwd>
        <kwd>fibrila&#231;&#227;o atrial</kwd>
        <kwd>an&#225;lise espectral</kwd>
        <kwd>freq&#252;&#234;ncia card&#237;aca</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>25</day>
        <month>09</month>
        <year>2007</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>ARTIGO ORIGINAL</bold>
    </p>
    <p>Abla&#231;&#227;o da fibrila&#231;&#227;o atrial por cateter com radiofreq&#252;&#234;ncia guiada por mapeamento espectral endoc&#225;rdico dos "ninhos de FA" em ritmo sinusal </p>
    <p>
      <bold>Jos&#233; Carlos Pach&#243;n Mateos; Enrique I. Pach&#243;n Mateos; Tasso J. Lobo; Maria Z&#233;lia C. Pach&#243;n; Ju&#225;n Carlos Pach&#243;n Mateos; Denilda Queiroz V. Pach&#243;n; Remy Nelson A. Vargas; Leopoldo S. Piegas; Adib D. Jatene</bold>
    </p>
    <p> Hospital do Cora&#231;&#227;o (HCor) e Instituto Dante Pazzanese de Cardiologia - S&#227;o Paulo, SP - Brasil</p>
    <p>
      <xref ref-type="corresp" rid="end">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p><bold>FUNDAMENTO:</bold> Atrav&#233;s de mapeamento espectral-(ME) endoc&#225;rdico em ritmo sinusal, observam-se dois tipos de mioc&#225;rdio atrial: o compacto de espectro liso e o fibrilar de espectro segmentado ("Ninho de FA" [NFA]). Durante a FA o compacto tem ativa&#231;&#227;o organizada e baixa freq&#252;&#234;ncia (passivo) enquanto o fibrilar apresenta ativa&#231;&#227;o bastante desorganizada e alta freq&#252;&#234;ncia (ativo/ressonante) sendo ambos ativados por uma taquicardia protegida de alta freq&#252;&#234;ncia, taquicardia de background (TB). </p>
    <p><bold>OBJETIVO:</bold> Descrever o tratamento da FA pela abla&#231;&#227;o dos NFA e da TB. </p>
    <p><bold>M&#201;TODOS:</bold> 1) Abla&#231;&#227;o por cateter-RF [4/8mm-60&#186;/30-40J/30s] dos NFA guiada por ME em ritmo sinusal, fora das veias pulmonares; 2) Estimula&#231;&#227;o atrial-300ppm; 3) Abla&#231;&#227;o adicional de NFA se induzida FA; 4) Abla&#231;&#227;o focal se induzida TB e/ou Flutter; 5) Seguimento cl&#237;nico+ECG+Holter. </p>
    <p><bold>RESULTADOS:</bold> Foram tratados 50&#177;18 NFA/paciente. Ap&#243;s 11,3&#177;8m 81p (88%) estavam sem FA (28,3% com antiarr&#237;tmico). Ap&#243;s a abla&#231;&#227;o dos NFA: a FA n&#227;o foi reinduzida em 61p(71%); TB foi induzida e tratada em 24p(26%). Ocorreram 2 sangramentos peric&#225;rdicos (1 tratado clinicamente e 1 cirurgicamente) ocasionados por bainhas n&#227;o mais utilizadas. </p>
    <p><bold>CONCLUS&#195;O:</bold> O ME em ritmo sinusal ablaciona os NFA. Durante a FA os NFA apresentam um padr&#227;o reativo-ressonante e o mioc&#225;rdio compacto apresenta-se passivo, estimulados pela alta freq&#252;&#234;ncia da TB. Ap&#243;s a abla&#231;&#227;o dos NFA e da TB n&#227;o foi poss&#237;vel reinduzir FA sustentada. A abla&#231;&#227;o dos NFA fora das VP se mostrou segura e altamente eficiente para a cura e/ou o controle cl&#237;nico da FA. </p>
    <p><bold>Palavras-chave:</bold> Abla&#231;&#227;o por cateter, fibrila&#231;&#227;o atrial, an&#225;lise espectral, freq&#252;&#234;ncia card&#237;aca.</p>
    <p>
      <bold>Introdu&#231;&#227;o</bold>
    </p>
    <p>O estudo eletrofisiol&#243;gico convencional baseia-se na an&#225;lise das varia&#231;&#245;es de amplitude no tempo (dom&#237;nio do tempo). Todavia, a an&#225;lise espectral de uma onda relaciona amplitude e/ou pot&#234;ncia com as freq&#252;&#234;ncias intr&#237;nsecas do sinal (dom&#237;nio da freq&#252;&#234;ncia), fornecendo grande n&#250;mero de informa&#231;&#245;es adicionais. A freq&#252;&#234;ncia card&#237;aca &#233; medida em batimentos por minuto (freq&#252;&#234;ncia extr&#237;nseca do sinal), ou seja, dom&#237;nio do tempo, ao passo que o pico da onda R normal, por exemplo, muda de voltagem de forma brusca pelo fato de ter altas freq&#252;&#234;ncias espectrais intr&#237;nsecas (dom&#237;nio da freq&#252;&#234;ncia), medidas em hertz (Hz, ciclos por segundo). Dessa forma, o termo freq&#252;&#234;ncia poder&#225; estar relacionado a grandezas temporais ou espectrais. Utilizando a an&#225;lise espectral em tempo real e em ritmo sinusal, verifica-se que as paredes atriais s&#227;o constitu&#237;das por dois tipos distintos de mioc&#225;rdio, o compacto e o fibrilar (<xref ref-type="fig" rid="fig01">fig. 1</xref>). O primeiro apresenta espectro cont&#237;nuo e organizado, com a maior parte da pot&#234;ncia agrupada &#224; esquerda (baixas freq&#252;&#234;ncias), e o segundo tem espectro segmentado, com boa parte de segmentos desviada &#224; direita (altas freq&#252;&#234;ncias, &gt; 80 Hz)<sup>1</sup>. O mioc&#225;rdio fibrilar geralmente est&#225; agrupado em pequenas &#225;reas mais ou menos extensas. Durante a fibrila&#231;&#227;o atrial (FA), o mioc&#225;rdio compacto apresenta comportamento organizado e ativa&#231;&#227;o el&#233;trica de grande amplitude, baixa freq&#252;&#234;ncia e discretamente irregular, sugerindo comportamento passivo. Contrariamente, o mioc&#225;rdio fibrilar apresenta atividade el&#233;trica de baixa amplitude, altamente desorganizada e de alta freq&#252;&#234;ncia, denotando, do ponto de vista el&#233;trico, comportamento ressonante. Ressonante &#233; o sistema que apresenta resson&#226;ncia. Resson&#226;ncia: estado de um sistema que vibra numa freq&#252;&#234;ncia pr&#243;pria, com amplitude geralmente decremental, como resultado de est&#237;mulos externos - pode ser: mec&#226;nica, como a do diapas&#227;o; el&#233;trica, como a de indutores, sintonizadores e osciladores; eletromagn&#233;tica, como a de forno de microondas e resson&#226;ncia nuclear magn&#233;tica; etc.</p>
    <fig id="fig01">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf01.jpg"/></fig>
    <p>Tem-se observado que a elimina&#231;&#227;o do mioc&#225;rdio fibrilar torna progressivamente mais dif&#237;cil a reindu&#231;&#227;o da FA. Al&#233;m disso, essas &#225;reas apresentam as maiores freq&#252;&#234;ncias durante essa arritmia. Por essa raz&#227;o, os pontos com alta densidade de mioc&#225;rdio fibrilar foram denominados "ninhos de FA"<sup>1,2</sup>. Adicionalmente, ap&#243;s a elimina&#231;&#227;o dos "ninhos de FA", tem sido poss&#237;vel induzir taquicardia atrial muito r&#225;pida e altamente protegida de revers&#227;o. Diversas evid&#234;ncias t&#234;m demonstrado que essa taquicardia existe em segundo plano durante a FA (taquicardia de <italic>background</italic>), sendo seu elemento mantenedor. Neste estudo, s&#227;o descritos o mapeamento e a abla&#231;&#227;o dos "ninhos de FA", seguidos de indu&#231;&#227;o e abla&#231;&#227;o da taquicardia de <italic>background</italic>.</p>
    <p><italic>Hip&#243;tese - </italic>Os "ninhos de FA" podem ser facilmente identificados, por meio do mapeamento espectral durante o ritmo sinusal, e eliminados com abla&#231;&#227;o por radiofreq&#252;&#234;ncia. Isso poderia enfraquecer um dos mecanismos de manuten&#231;&#227;o da FA, contribuindo para seu tratamento definitivo. Al&#233;m disso, permitiria visualizar a taquicardia de <italic>background</italic><sup>2</sup>, possibilitando seu mapeamento e a respectiva abla&#231;&#227;o.</p>
    <p><italic>Objetivos - </italic>Propor uma nova alternativa para o tratamento da FA baseada em mapeamento espectral durante o ritmo sinusal e descrever novos achados para melhor entendimento da fisiopatologia dessa arritmia.</p>
    <p><italic>Casu&#237;stica - </italic>Foram inclu&#237;dos 92 pacientes, 76 do sexo masculino, com m&#233;dia de idade de 52,4 &#177; 11 anos. Todos eram portadores de FA freq&#252;ente e refrat&#225;ria a pelo menos duas drogas antiarr&#237;tmicas, e 51 (55,4%) relatavam pelo menos uma cardiovers&#227;o el&#233;trica. Nesse grupo, todos os antiarr&#237;tmicos dispon&#237;veis em nosso meio, assim como a flecainamida, mostraram-se ineficazes em um ou mais pacientes. Com rela&#231;&#227;o ao tipo de FA, 56 casos (61%) eram da forma parox&#237;stica (3,6 &#177; 1,3, com duas a sete crises por ano), 25 (27%) eram da forma persistente (2,6 &#177; 1,2, com uma a seis crises por ano), e 11 (12%) eram da forma permanente. Epis&#243;dios muito freq&#252;entes de FA n&#227;o-sustentada ou incessante foram observados em nove pacientes. A maioria dos pacientes n&#227;o apresentava cardiopatia significativa. O di&#226;metro do &#225;trio esquerdo era normal ou moderadamente aumentado (41,9 &#177; 5 mm). A m&#233;dia da fra&#231;&#227;o de eje&#231;&#227;o era de 0,61 &#177; 0,8. As etiologias mais relevantes foram: idiop&#225;tica, 42%; hipertens&#227;o, 22%; cardiopatias cong&#234;nitas, 11%; cardiopatia reum&#225;tica, 10%; coronariopatia, 9%; e outras, 6%. </p>
    <p>
      <bold>M&#233;todos</bold>
    </p>
    <p>Os pacientes em uso de anticoagulantes orais foram internados 24 ou 48 horas antes para ajustar o <italic>International Normalized Ratio </italic>(INR) para <underline>&lt;</underline> 1,4. Todos os casos, principalmente aqueles com hist&#243;ria de tromboembolismo, somente foram tratados ap&#243;s confirma&#231;&#227;o da aus&#234;ncia de trombos card&#237;acos por meio de ecocardiografia transesof&#225;gica<sup>3-5</sup>. Utilizou-se monitora&#231;&#227;o convencional, com eletrocardiografia (ECG) de superf&#237;cie, placas adesivas radiotransparentes de desfibrila&#231;&#227;o, entuba&#231;&#227;o orotraqueal com ventila&#231;&#227;o mec&#226;nica e anestesia inalat&#243;ria, al&#233;m de passagem de transdutor de ecocardiografia transesof&#225;gica. Ap&#243;s assepsia, foram realizadas cinco pun&#231;&#245;es venosas (uma subcl&#225;via e quatro femorais). Foi introduzido um cateter decapolar pela veia subcl&#225;via para cateterizar o seio coronariano. Pela veia femoral foram introduzidos dois cateteres quadripolares para &#225;trio e ventr&#237;culo direitos, um cateter octapolar posicionado no His, sendo realizada pun&#231;&#227;o transeptal (cinco pacientes tinham forame oval patente). Foram utilizados os seguintes equipamentos: equipamento de anestesia C&#237;cero EM (Dr&#228;ger); monitor multiparam&#233;trico HP/Philips M1026A; ecocardi&#243;grafo HP/Philips modelo Sonos 2500; pol&#237;grafo de 32 canais TEB com <italic>software</italic> modificado para p&#243;s-an&#225;lise espectral (TEB-Pach&#243;n); espectr&#244;metro computadorizado (Pach&#243;n<sup>&#174;</sup>) para an&#225;lise espectral em tempo real (<xref ref-type="fig" rid="fig02">fig. 2</xref>); radioscopia Digital Siemens; gerador de radiofreq&#252;&#234;ncia Biotronik Abcontrol MDS; desfibrilador bif&#225;sico Philips Heartstart XL com marcapasso transcut&#226;neo; espectr&#244;metro de atividade cerebral-BIS (nos casos de maior risco tromboemb&#243;lico). As abla&#231;&#245;es foram realizadas com cateter Blazer EPT 4 mm ou 8 mm ou Medtronic Conductor 4 mm ou 8 mm. Todos os pacientes inclu&#237;dos foram informados sobre os m&#233;todos e as potenciais complica&#231;&#245;es e concordaram com os procedimentos por meio de consentimento escrito.</p>
    <fig id="fig02">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf02.jpg"/></fig>
    <p>Por meio de pun&#231;&#227;o transeptal foram introduzidos um cateter espiral (Supreme St. Jude ou Biotronik Lexx) e o cateter de abla&#231;&#227;o. Foi utilizada heparina por via endovenosa para manter o tempo de coagula&#231;&#227;o ativado entre 300 s e 400 s. Os endoc&#225;rdios atriais foram escaneados com an&#225;lise espectral em tempo real. Foram eliminados todos os "ninhos de FA" encontrados com aplica&#231;&#227;o de radiofreq&#252;&#234;ncia (30-40 W/30 s/60&#186;C) at&#233; o desaparecimento do padr&#227;o fibrilar (<xref ref-type="fig" rid="fig03">fig. 3</xref>). N&#227;o foi realizado isolamento completo intencional das veias pulmonares ou das linhas de bloqueio conforme as t&#233;cnicas convencionais existentes<sup>6</sup>. O cateter espiral foi utilizado para identificar com seguran&#231;a os limites atriais e para detectar "ninhos de FA" que s&#227;o menos evidentes com cateter de 8 mm. </p>
    <fig id="fig03">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf03.jpg"/></fig>
    <p><italic>Reestudo p&#243;s-abla&#231;&#227;o - </italic>Ap&#243;s abla&#231;&#227;o dos "ninhos de FA", foi realizada estimula&#231;&#227;o atrial tanto programada (at&#233; tr&#234;s extra-est&#237;mulos) como progressiva (at&#233; 300 ppm). Se fosse induzida FA, novos "ninhos de FA" eram procurados e tratados. Caso fosse induzida taquicardia residual (taquicardia de <italic>background</italic><sup>2</sup>), esta era mapeada e tratada em seu foco de origem. Os autores deste estudo optaram pela denomina&#231;&#227;o taquicardia de <italic>background</italic> em detrimento de taquicardia de segundo plano, pelo fato de a palavra <italic>background</italic> j&#225; ter sido incorporada &#224; l&#237;ngua portuguesa, conforme vers&#227;o 5.11 do Novo Dicion&#225;rio Aur&#233;lio. Caso houvesse hist&#243;ria ou indu&#231;&#227;o de <italic>flutter</italic> era realizada abla&#231;&#227;o espec&#237;fica. Os crit&#233;rios para encerrar a abla&#231;&#227;o foram: 1) impossibilidade de reinduzir FA ou taquicardias; 2) indu&#231;&#227;o somente de taquicardia/FA n&#227;o-sustentada inferior a 10 segundos; e 3) impossibilidade de eliminar taquicardia residual ou procedimento prolongado (mais de cinco horas), caso em que era feita cardiovers&#227;o tor&#225;cica externa.</p>
    <p><italic>Medica&#231;&#227;o p&#243;s-abla&#231;&#227;o - </italic>Mesmo sendo ineficaz ou pouco eficaz na fase pr&#233;-abla&#231;&#227;o, a medica&#231;&#227;o antiarr&#237;tmica foi utilizada durante dois meses para reduzir a excitabilidade atrial em decorr&#234;ncia do processo de resolu&#231;&#227;o cicatricial. Anticoagulantes warfar&#237;nicos foram administrados durante tr&#234;s meses p&#243;s-abla&#231;&#227;o, mantendo-se o tempo de protrombina entre 2 e 3 INR. Ap&#243;s esse per&#237;odo, foram utilizados antiagregantes nos casos com risco de tromboembolismo (idade, insufici&#234;ncia card&#237;aca, disfun&#231;&#227;o mitral, &#225;trio esquedo dilatado, etc.), inclusive naqueles com recidiva sustentada ou n&#227;o-sustentada da FA e resposta farmacol&#243;gica adequada. Os antiarr&#237;tmicos foram retirados, exceto em 23 casos nos quais se mostraram necess&#225;rios para manter o ritmo sinusal.</p>
    <p><italic>Seguimento p&#243;s-abla&#231;&#227;o - </italic>Foi constitu&#237;do de controle cl&#237;nico e ECG (alta hospitalar, um m&#234;s, tr&#234;s e seis meses, e um ano) e Holter (um m&#234;s, seis meses e um ano) ou sempre que ocorressem sintomas. Adicionalmente, foi realizado controle constante por contato telef&#244;nico.</p>
    <p>
      <bold>Resultados</bold>
    </p>
    <p>Em m&#233;dia, foram tratados 50 &#177; 18 "ninhos de FA" por paciente. Ap&#243;s a abla&#231;&#227;o, n&#227;o foi poss&#237;vel induzir FA sustentada em 65 (71%) casos. Em 27 (29%) pacientes foi poss&#237;vel induzir epis&#243;dio n&#227;o-sustentado de taquicardia atrial ou FA (&lt; 10 s). Em 24 pacientes (26%) foi poss&#237;vel induzir taquicardia atrial com caracter&#237;sticas peculiares (induzida por estimula&#231;&#227;o atrial programada ou progressiva, alta freq&#252;&#234;ncia, altamente protegida por bloqueio de entrada, dif&#237;cil de induzir e muito dif&#237;cil de reverter por estimula&#231;&#227;o atrial), a qual foi denominada taquicardia de <italic>background</italic><sup>2</sup>. Em 18 pacientes (19%), havia antecedente de <italic>flutter</italic> comum ou o mesmo foi induzido, sendo tratado com bloqueio bidirecional do istmo cavotric&#250;spide. Ap&#243;s seguimento m&#233;dio de 11,3 &#177; 8 meses, 81 pacientes (88%) estavam em ritmo sinusal, 23 casos (28%) utilizando antiarr&#237;tmicos previamente ineficazes em doses reduzidas (amiodarona, 100 mg/dia a 300 mg/dia; sotalol, 60 mg/dia a 160 mg/dia; propafenona, 150 mg/dia a 600 mg/dia; quinidina, 200 mg/dia a 400 mg/dia). Em nove pacientes (9,8%) foram realizadas reabla&#231;&#245;es, em decorr&#234;ncia de dificuldade de controle cl&#237;nico da FA ou de taquicardias atriais na fase tardia p&#243;s-abla&#231;&#227;o (mais de seis meses de evolu&#231;&#227;o).</p>
    <p>Na fase inicial desse m&#233;todo, ocorreram dois sangramentos peric&#225;rdicos (sendo um de resolu&#231;&#227;o cl&#237;nica e outro drenado cirurgicamente), provavelmente relacionados &#224; manipula&#231;&#227;o simult&#226;nea de m&#250;ltiplas bainhas dentro do &#225;trio esquerdo, j&#225; que a ponta dos eletrodos envolvidos (EPT 4 mm <italic>large</italic>), ao contr&#225;rio das bainhas, &#233; bastante macia, sendo improv&#225;vel que tivesse ocasionado a les&#227;o. Al&#233;m do mais, essa complica&#231;&#227;o n&#227;o mais ocorreu depois que as bainhas passaram a ser retiradas do &#225;trio esquerdo durante a abla&#231;&#227;o, mesmo quando foram utilizados eletrodos mais r&#237;gidos de 8 mm. Nenhuma outra complica&#231;&#227;o foi observada.</p>
    <p>As localiza&#231;&#245;es mais freq&#252;entes dos "ninhos de FA" est&#227;o demonstradas na <xref ref-type="table" rid="tab01">tabela 1</xref>.</p>
    <table-wrap id="tab01">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gt01.jpg"/></table-wrap>
    <p>Em 11 pacientes (46%) dos 24 casos nos quais foi induzida taquicardia de <italic>background</italic>, o local de origem foi bem definido pelo mapeamento, sendo obtida revers&#227;o da taquicardia com aplica&#231;&#227;o de radiofreq&#252;&#234;ncia no local de melhor mapeamento (<xref ref-type="table" rid="tab02">tab. 2</xref>). Nos outros 13 casos (54%) foi realizada cardiovers&#227;o tor&#225;cica externa (10) ou revers&#227;o por <italic>overdrive</italic> (3), em decorr&#234;ncia de mapeamentos inconsistentes, freq&#252;&#234;ncia muito alta da taquicardia, mais de um foco de origem ou dura&#231;&#227;o prolongada dos procedimentos. </p>
    <table-wrap id="tab02">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gt02.jpg"/></table-wrap>
    <p>Os tempos m&#233;dios de procedimento e de radioscopia foram, respectivamente, de 4,3 &#177; 1,2 horas e de 53,8 &#177; 19 minutos.</p>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>Este estudo demonstra a aplica&#231;&#227;o do mapeamento espectral em tempo real, em ritmo sinusal, na identifica&#231;&#227;o e na abla&#231;&#227;o dos "ninhos de FA". Foi poss&#237;vel observar que quanto mais extensa a abla&#231;&#227;o dos "ninhos de FA" menor a possibilidade de indu&#231;&#227;o dessa arritmia por meio de estimula&#231;&#227;o. Al&#233;m do mais, elevada propor&#231;&#227;o desses pacientes (88%) permaneceu sem FA ou com FA controlada durante o seguimento, apesar dos 39% de casos de FA persistente e permanente, tipos normalmente relacionados a piores resultados<sup>7</sup>. Esses dados sugerem que, aparentemente, quanto menor o n&#250;mero de "ninhos de FA" mais est&#225;veis se tornam as paredes atriais, do ponto de vista el&#233;trico. Al&#233;m disso, sua elimina&#231;&#227;o permitiu identificar taquicardia com propriedades muito espec&#237;ficas, constituindo, provavelmente, um elo fundamental na fisiopatologia da FA.</p>
    <p><italic>Substrato da FA - </italic>Grandes contribui&#231;&#245;es foram feitas na identifica&#231;&#227;o de deflagradores da FA<sup>8-10</sup> assim como no tratamento dessa arritmia pela abla&#231;&#227;o ou pelo isolamento desses deflagradores<sup>11,12</sup>. Entretanto, pouco tem avan&#231;ado a identifica&#231;&#227;o do substrato. &#201; relativamente f&#225;cil entender uma arritmia como a FA em &#225;trio dilatado com fibrose e degenera&#231;&#227;o significativas; entretanto, como explicar essa arritmia em cora&#231;&#245;es aparentemente normais? As observa&#231;&#245;es iniciais deste estudo apontam para os "ninhos de FA" e para as taquicardias de <italic>background</italic>. Comparando pacientes normais com e sem FA parox&#237;stica, verificou-se que o n&#250;mero de "ninhos de FA" &#233; significativamente maior nos casos com FA espont&#226;nea ou induzida em laborat&#243;rio<sup>1,13</sup>.</p>
    <p><italic>Mioc&#225;rdio fibrilar e "ninhos de FA"</italic>: Os diferentes espectros dos mioc&#225;rdios compacto e fibrilar sugerem que a grande diferen&#231;a entre os dois tipos reside no grau de conex&#227;o entre as c&#233;lulas, o que lhes confere freq&#252;&#234;ncias de resson&#226;ncia el&#233;trica muito distintas. O mioc&#225;rdio compacto &#233; muito bem conectado e funciona como uma "grande c&#233;lula", ao passo que o fibrilar se comporta como um conjunto de feixes com velocidades de condu&#231;&#227;o e refratariedades diversas. Do ponto de vista espectral, os mioc&#225;rdios fibrilar e compacto t&#234;m alta e baixa freq&#252;&#234;ncias de resson&#226;ncia, respectivamente. Dessa forma, ao se estimular as paredes atriais com freq&#252;&#234;ncia progressiva, verifica-se que o mioc&#225;rdio fibrilar apresenta respostas repetitivas autolimitadas em freq&#252;&#234;ncia muito menor que o mioc&#225;rdio compacto (234 &#177; 28 x &gt; 300 ppm; p = 0,018), ou seja, o mioc&#225;rdio compacto &#233; muito mais resistente &#224; estimula&#231;&#227;o atrial r&#225;pida. Por causa dessa propriedade, durante a FA o mioc&#225;rdio fibrilar se mant&#233;m constantemente com freq&#252;&#234;ncia muito alta, irregular e desorganizada (elemento multiplicador), justificando a denomina&#231;&#227;o "ninho de FA", ao passo que o compacto mant&#233;m despolariza&#231;&#227;o organizada, freq&#252;&#234;ncia muito mais baixa e sem respostas repetitivas (elemento passivo) (<xref ref-type="fig" rid="a01fig04">fig. 4</xref>).</p>
    <p content-type="asset">
      <fig id="a01fig04">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf04.jpg"/></fig>
    </p>
    <p><italic>Resson&#226;ncia dos "ninhos de FA" - </italic>Durante a FA, freq&#252;entemente, os "ninhos de FA" alternam per&#237;odos de baixa amplitude e alta-freq&#252;&#234;ncia-desorganizada com grande amplitude e baixa-freq&#252;&#234;ncia-organizada (<xref ref-type="fig" rid="a01fig04">fig. 4</xref>). Isso acontece por causa de uma instabilidade el&#233;trica peri&#243;dica que promove altern&#226;ncia de altas e baixas freq&#252;&#234;ncias. Nesse caso, "ninhos de FA" pr&#243;ximos e em fases diferentes podem se realimentar, favorecendo a manuten&#231;&#227;o da FA (<xref ref-type="fig" rid="fig05">fig. 5</xref>). Essa periodicidade de organiza&#231;&#227;o/desorganiza&#231;&#227;o el&#233;trica &#233; denominada resson&#226;ncia el&#233;trica (propriedade biol&#243;gica conhecida observada em algumas c&#233;lulas do sistema nervoso de mam&#237;feros e anf&#237;bios), j&#225; que seu comportamento &#233; compar&#225;vel ao de um ressonador eletr&#244;nico<sup>14</sup>, capaz de multiplicar o est&#237;mulo inicial. A microrreentrada e/ou a reflex&#227;o entre feixes celulares pr&#243;ximos, assim como per&#237;odos de atividade deflagrada autolimitada decorrente de fen&#244;meno transiente de c&#225;lcio, podem explicar essa propriedade dos "ninhos de FA"<sup>15,16</sup>.</p>
    <fig id="fig05">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf05.jpg"/></fig>
    <p><italic>Prov&#225;vel origem dos "ninhos de FA" - </italic>No grupo de pacientes avaliado neste estudo foi poss&#237;vel relacionar os "ninhos de FA" com as seguintes condi&#231;&#245;es:</p>
    <p>1. Cong&#234;nita: entrada da inerva&#231;&#227;o (interpola&#231;&#227;o de fibras)<sup>20</sup>.</p>
    <p>2. Constitucional: redu&#231;&#227;o de conexinas, com predom&#237;nio de conex&#245;es t&#233;rmino-terminais (<italic>crista terminalis</italic>)<sup>21</sup>.</p>
    <p>3. Transi&#231;&#227;o atriovenosa (interpola&#231;&#227;o de tecidos na inser&#231;&#227;o das veias pulmonares).</p>
    <p>4. Estiramento mec&#226;nico do mioc&#225;rdio atrial (separa&#231;&#227;o das c&#233;lulas por condi&#231;&#245;es patol&#243;gicas, tais como aneurisma do septo interatrial, etc.).</p>
    <p>5. Redu&#231;&#227;o da express&#227;o das conexinas (insufici&#234;ncia card&#237;aca congestiva, envelhecimento, condi&#231;&#245;es cong&#234;nitas).</p>
    <p>6. Patol&#243;gica: degenera&#231;&#227;o, isquemia, inflama&#231;&#227;o ou doen&#231;a infiltrativa com remodela&#231;&#227;o e redu&#231;&#227;o das conexinas.</p>
    <p>Recentemente foi observado que a elimina&#231;&#227;o dos "ninhos de FA" torna negativa a resposta &#224; atropina em pacientes que antes apresentavam resposta normal, denotando estreita rela&#231;&#227;o entre "ninhos de FA" e inerva&#231;&#227;o vagal<sup>20</sup> (<xref ref-type="fig" rid="fig06">fig. 6</xref>).</p>
    <fig id="fig06">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf06.jpg"/></fig>
    <p><italic>Tratando a fibrila&#231;&#227;o atrial em ritmo sinusal por meio de abla&#231;&#227;o com radiofreq&#252;&#234;ncia dos "ninhos de FA" - </italic>A vantagem do conceito dos "ninhos de FA" foi permitir a abla&#231;&#227;o por cateter durante o ritmo sinusal<sup>1</sup> (<xref ref-type="fig" rid="a01fig04">fig. 4</xref>) sem realizar as cl&#225;ssicas linhas de bloqueio. Tem sido observado que quanto maior o n&#250;mero de "ninhos de FA" mais freq&#252;ente e mais prolongada &#233; a FA espont&#226;nea ou induzida. Pacientes que apresentam n&#250;mero muito reduzido de "ninhos de FA" s&#227;o tipicamente resistentes &#224; indu&#231;&#227;o da arritmia pela estimula&#231;&#227;o atrial. Al&#233;m disso, se induzida, a FA tende a ter dura&#231;&#227;o curta e revers&#227;o espont&#226;nea. Neste estudo, observou-se que &#224; medida que o n&#250;mero de "ninhos de FA" foi reduzido por meio de abla&#231;&#227;o com radiofreq&#252;&#234;ncia, tornou-se mais dif&#237;cil reinduzir a arritmia. </p>
    <p><italic>Taquicardia de </italic>background<italic> - </italic>Um fen&#244;meno extremamente interessante observado durante a abla&#231;&#227;o espectral dos "ninhos de FA" foi a taquicardia de <italic>background</italic>"<sup>2</sup>. Trata-se de uma taquicardia atrial somente vista ap&#243;s a abla&#231;&#227;o dos "ninhos de FA" e obtida nas seguintes condi&#231;&#245;es: durante FA, pela abla&#231;&#227;o progressiva de "ninhos de FA" ou durante ritmo sinusal, por meio de estimula&#231;&#227;o atrial programada e/ou progressiva (at&#233; 300 ppm), ap&#243;s a maioria dos "ninhos de FA" ter sido submetida a abla&#231;&#227;o.</p>
    <p><italic>Principais caracter&#237;sticas da taquicardia de </italic>background:</p>
    <p>1. Taquicardia atrial regular ou ligeiramente irregular.</p>
    <p>2. Freq&#252;&#234;ncia muito alta (256 &#177; 34 bpm).</p>
    <p>3. Originada por reentrada (geralmente microrreentrada induzida por estimula&#231;&#227;o atrial r&#225;pida e/ou programada e revertida por <italic>overdrive</italic>).</p>
    <p>4. Foco de origem altamente protegido (muito dif&#237;cil de ser revertida por <italic>overdrive</italic>) (<xref ref-type="fig" rid="fig07">fig. 7</xref>).</p>
    <fig id="fig07">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf07.jpg"/></fig>
    <p>5. Pode ser identificada por meio de subtra&#231;&#227;o digital do QRS no ECG de superf&#237;cie e an&#225;lise espectral do tra&#231;ado da FA pura (FFT), antes da abla&#231;&#227;o.</p>
    <p><italic>Rela&#231;&#227;o entre taquicardia de </italic>background<italic> e fibrila&#231;&#227;o atrial - </italic>Neste estudo foi poss&#237;vel visualizar a taquicardia de <italic>background</italic> ap&#243;s a limpeza dos "ninhos de FA". Observou-se que a FA vai se organizando e se transforma em taquicardia de <italic>background</italic> com a progressiva elimina&#231;&#227;o dos "ninhos de FA". Esses dados sugerem ser essa taquicardia pe&#231;a fundamental na fisiopatologia da FA. Trata-se de uma taquicardia regular (originada por reentrada), que, aparentemente, existe num segundo plano (<italic>background</italic>) durante a FA. Sua freq&#252;&#234;ncia muito alta estimula os "ninhos de FA", promovendo sua desorganiza&#231;&#227;o, sua resson&#226;ncia e sua realimenta&#231;&#227;o. A presen&#231;a de bloqueio de entrada protege o foco da taquicardia de <italic>background</italic> de forma que ela n&#227;o &#233; revertida pelos est&#237;mulos vindos da ativa&#231;&#227;o dos "ninhos de FA". Quanto maior o bloqueio de entrada (mais dif&#237;cil de reverter com estimula&#231;&#227;o atrial) mais prolongada a FA. A fus&#227;o da taquicardia de <italic>background</italic> com a freq&#252;&#234;ncia muito alta e desorganizada dos "ninhos de FA" constitui a atividade el&#233;trica aparentemente ca&#243;tica que caracteriza a morfologia cl&#225;ssica das ondas f no ECG da FA franca. Muitas vezes, ocorre altern&#226;ncia peri&#243;dica da resson&#226;ncia dos "ninhos de FA", fazendo com que uma taquicardia de <italic>background</italic> pare&#231;a ciclicamente mais ou menos organizada, constituindo a condi&#231;&#227;o freq&#252;entemente conhecida como "fibrilo-<italic>flutter</italic>". Do ponto de vista el&#233;trico, essa taquicardia &#233; o oscilador mestre da FA<sup>2</sup>.</p>
    <p><italic>Abla&#231;&#227;o da taquicardia de </italic>background - Ap&#243;s a abla&#231;&#227;o dos "ninhos de FA", procurou-se localizar e realizar a abla&#231;&#227;o do foco da taquicardia de <italic>background</italic> induzida por estimula&#231;&#227;o atrial (<xref ref-type="fig" rid="fig08">fig. 8</xref>). Eventualmente, o foco dessa taquicardia pode ter sido eliminado de forma indireta durante a abla&#231;&#227;o dos "ninhos de FA". Neste estudo, a evolu&#231;&#227;o dos pacientes que tiveram a taquicardia de <italic>background</italic> tratada ou daqueles nos quais foi imposs&#237;vel induzi-la comparativamente &#224; do grupo no qual essa taquicardia n&#227;o foi tratada foi muito diferente. No primeiro grupo, o sucesso foi de 88,9%; no segundo grupo, por&#233;m, a FA foi eliminada em apenas 73% (p = 0,008). Entretanto, em decorr&#234;ncia de mecanismos de prote&#231;&#227;o, muitas vezes a taquicardia de <italic>background</italic> pode n&#227;o ser induzida. Adicionalmente, seu mapeamento &#233; dificultado pela alta freq&#252;&#234;ncia. </p>
    <fig id="fig08">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf08.jpg"/></fig>
    <p><italic>Fisiopatologia da fibrila&#231;&#227;o atrial baseada nos "ninhos de FA" - </italic>Este estudo sugere que a FA resulta da fus&#227;o de arritmias constitu&#237;das essencialmente por uma taquicardia atrial protegida (taquicardia de <italic>background</italic>), que excita os ninhos e os mant&#233;m em constante estado de respostas repetitivas (<xref ref-type="fig" rid="fig08">fig. 8</xref>). A observa&#231;&#227;o desse grupo de pacientes, das respectivas abla&#231;&#245;es e da hist&#243;ria cl&#237;nica de cada caso permite estabelecer uma fisiopatologia espec&#237;fica para a FA baseada nos seguintes componentes:</p>
    <p>1. Modulador: sistema nervoso aut&#244;nomo (extensamente modificado pela abla&#231;&#227;o dos "ninhos de FA"<sup>20</sup>).</p>
    <p>2. Deflagrador: extra-s&#237;stoles e taquicardias n&#227;o-sustentadas das veias pulmonares<sup>9,22-24</sup>.</p>
    <p>3. Substrato (elemento multiplicador): "ninhos de FA" que respondem com alta freq&#252;&#234;ncia &#224; estimula&#231;&#227;o atrial r&#225;pida, por causa das propriedades ressonantes (microrreentrada e/ou atividade deflagrada). A capacidade de multiplicar os est&#237;mulos &#233; um dos fatores que sustentam a FA.</p>
    <p>4. Mantenedor: taquicardia de <italic>background</italic> que funciona como um marcapasso atrial assincr&#244;nico, com freq&#252;&#234;ncia muito alta, capaz de acionar os "ninhos de FA", mantendo-os na faixa de respostas repetitivas. &#201; o an&#225;logo do marcapasso artificial utilizado por Wijffels e cols.<sup>25</sup> e Moreira e cols.<sup>26</sup> para produzir FA, estimulando com freq&#252;&#234;ncias muito altas.</p>
    <p>Essa fisiopatologia explica os diversos quadros cl&#237;nicos classicamente conhecidos (<xref ref-type="table" rid="tab03">tab. 3</xref>).</p>
    <table-wrap id="tab03">
      <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gt03.jpg"/></table-wrap>
    <p><italic>Compara&#231;&#227;o com outros m&#233;todos de abla&#231;&#227;o de fibrila&#231;&#227;o atrial - </italic>A cura da FA &#233; um grande desafio para todas as t&#233;cnicas dispon&#237;veis<sup>27</sup>. Apesar de publicada em 2004<sup>1</sup>, a abla&#231;&#227;o dos "ninhos de FA" foi desenvolvida no final da d&#233;cada de 1990, sem nenhum embasamento em t&#233;cnicas anteriores. A proposta inicial dos autores deste estudo foi utilizar o mapeamento espectral para buscar o substrato da FA mesmo no cora&#231;&#227;o aparentemente normal, inclusive em pacientes que ainda n&#227;o tinham hist&#243;ria de FA e, certamente, sem fibrose atrial. Os "ninhos de FA" s&#227;o freq&#252;entes no antro das veias pulmonares. Durante sua elimina&#231;&#227;o, pode ocorrer o isolamento el&#233;trico dessas estruturas. Contudo, como o isolamento orientado pelo espectro busca as freq&#252;&#234;ncias &gt; 80 Hz, na maioria das vezes as veias pulmonares n&#227;o s&#227;o totalmente isoladas pela abla&#231;&#227;o dos "ninhos de FA", havendo condu&#231;&#227;o el&#233;trica de potenciais &lt; 80 Hz. Isso diferencia essa t&#233;cnica dos m&#233;todos desenvolvidos por Haissaguerre e cols.<sup>11</sup>, Natale e cols.<sup>28</sup>, Pappone e cols.<sup>19,29</sup> e Oral e cols.<sup>30,31</sup>, entre outros, caracterizados pelo isolamento completo das veias pulmonares com a utiliza&#231;&#227;o de extensas abla&#231;&#245;es e grandes quantidades de energia. A elimina&#231;&#227;o exclusiva das altas freq&#252;&#234;ncias do espectro permite preservar o mioc&#225;rdio mais compacto da parede atrial, evitando les&#245;es profundas e reduzindo o risco de perfura&#231;&#227;o, de f&#237;stulas atrioesof&#225;gicas<sup>29,32</sup> e de estenose de veias pulmonares<sup>33,34</sup>, fato que tamb&#233;m diferencia a t&#233;cnica de outros m&#233;todos baseados em extensas e profundas linhas de bloqueio<sup>19</sup>. </p>
    <p>Assim como as t&#233;cnicas que eliminam diretamente os g&#226;nglios paracard&#237;acos<sup>35,36</sup>, a abla&#231;&#227;o dos "ninhos de FA", de forma mais simplificada, promove importante denerva&#231;&#227;o parassimp&#225;tica pela elimina&#231;&#227;o direta dos neur&#244;nios intramurais e pela elimina&#231;&#227;o indireta dos g&#226;nglios paracard&#237;acos. Dessa forma, al&#233;m de atuar diretamente no sistema nervoso aut&#244;nomo, elimina grande parte da interface neuromioc&#225;rdica, que tem propriedades ressonantes (decorrentes de sua microestrutura) e caracter&#237;sticas espectrais espec&#237;ficas<sup>20</sup> (interpola&#231;&#227;o de fibras). A elimina&#231;&#227;o do neur&#244;nio intramural e da fibrose da jun&#231;&#227;o neuromioc&#225;rdica reduz sensivelmente a extens&#227;o da reinerva&#231;&#227;o. </p>
    <p>O m&#233;todo desenvolvido por Nademanee e cols.<sup>37</sup>, tamb&#233;m publicado em 2004, descreve a abla&#231;&#227;o durante a FA orientada por potenciais complexos (<italic>complex fractionated electrograms</italic> &#150; CFAEs), que s&#227;o &#225;reas de atividade el&#233;trica altamente fracionada e identificadas diretamente pelo dom&#237;nio do tempo. Sabe-se, entretanto, que durante a FA, pela grande quantidade de colis&#245;es entre frentes de ondas, formam-se muitas &#225;reas virtuais de potenciais complexos, problema que n&#227;o existe durante o ritmo sinusal e, portanto, na abla&#231;&#227;o dos "ninhos de FA". Provavelmente por causa desse fato, sabe-se que &#233; dif&#237;cil reverter uma FA persistente ou cr&#244;nica com a abla&#231;&#227;o de CFAEs. Somente a FA parox&#237;stica pode ser revertida mais facilmente, e a revers&#227;o, nesse caso, pode ser ocasional e n&#227;o necessariamente eletrofisiol&#243;gica. </p>
    <p>Na realidade, a maioria dos m&#233;todos tem evolu&#237;do no sentido de provocar les&#245;es transmurais cada vez mais extensas na parede atrial. Obviamente, quanto maior a &#225;rea destru&#237;da maior o n&#250;mero de "ninhos de FA" eliminados, o que poder&#225; influenciar os resultados<sup>38</sup>, independentemente do m&#233;todo. Al&#233;m disso, tem-se observado que a origem da taquicardia de <italic>background</italic> pode ser inadvertidamente eliminada nessas abla&#231;&#245;es extensas, favorecendo o resultado de longo prazo. Esse aspecto &#233; altamente desej&#225;vel; contudo, tomando como base o mapeamento espectral, entende-se que &#233; prefer&#237;vel dirigir as abla&#231;&#245;es racionalmente para o substrato, eliminar somente as freq&#252;&#234;ncias ressonantes (mioc&#225;rdio fibrilar), preservando o m&#250;sculo compacto, aplicar a menor quantidade de energia poss&#237;vel para prevenir complica&#231;&#245;es, e tentar induzir a taquicardia de <italic>background</italic> com subseq&#252;ente abla&#231;&#227;o de seu foco de origem.</p>
    <p>
      <bold>Conclus&#245;es</bold>
    </p>
    <p>Os "ninhos de FA" foram facilmente encontrados em ritmo sinusal por meio do mapeamento espectral, permitindo que fossem tratados por abla&#231;&#227;o com radiofreq&#252;&#234;ncia convencional, independentemente do isolamento das veias pulmonares. Durante a FA, esse tipo de mioc&#225;rdio (fibrilar) apresenta padr&#227;o reativo-ressonante de alta freq&#252;&#234;ncia, que realimenta a arritmia. Ao contr&#225;rio, o mioc&#225;rdio compacto responde de forma organizada e com baixa freq&#252;&#234;ncia. Ap&#243;s a abla&#231;&#227;o dos "ninhos de FA", tornou-se progressivamente mais dif&#237;cil a reindu&#231;&#227;o da FA, demonstrando que est&#227;o diretamente relacionados com a fisiopatologia da arritmia. Al&#233;m disso, a retirada dos "ninhos de FA" permitiu visualizar uma taquicardia residual com bloqueio de entrada e freq&#252;&#234;ncia alta, a taquicardia de <italic>background</italic>. O tratamento dessa taquicardia foi acompanhado de melhora significativa dos resultados. Essas observa&#231;&#245;es, al&#233;m de contribu&#237;rem para o melhor entendimento da fisiopatologia da FA, permitem concluir que a abla&#231;&#227;o dos "ninhos de FA" seguida do tratamento da taquicardia de <italic>background</italic> &#233; um m&#233;todo seguro, poss&#237;vel e altamente eficiente para curar ou para controlar clinicamente a FA.</p>
    <p>
      <bold> Potencial Conflito de Interesses</bold>
    </p>
    <p>Declaro n&#227;o haver conflitos de interesses pertinentes.</p>
    <p>
      <bold> Fontes de Financiamento</bold>
    </p>
    <p>O presente estudo n&#227;o teve fontes de financiamento externas.</p>
    <p>
      <bold>Vincula&#231;&#227;o Acad&#234;mica</bold>
    </p>
    <p>Esse artigo &#233; parte de tese de livre-doc&#234;ncia de Jos&#233; Carlos Pach&#243;n Mateos, pela Universidade de S&#227;o Paulo.</p>
    <p>
      <bold>Refer&#234;ncias</bold>
    </p>
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    <p>
      <fn id="end" fn-type="corresp">
        <p>Correspond&#234;ncia:</p>
        <p> Jos&#233; Carlos Pach&#243;n Mateos </p>
        <p> Av. A&#231;oc&#234;, 515/31 </p>
        <p> 04075-000 </p>
        <p> S&#227;o Paulo, SP - Brasil </p>
        <p> E-mail: </p>
        <p>
          <email xlink:href="jcpachon@hotmail.com">jcpachon@hotmail.com </email>
        </p>
      </fn>
    </p>
    <p>Artigo recebido em 25/02/07; revisado recebido em 01/03/07; aceito em 07/03/07.</p>
  </body>
  <back>
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  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Original Articles</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">Radiofrequency catheter ablation of atrial fibrillation guided by spectral mapping of atrial fibrillation nests in sinus rhythm</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>BACKGROUND: Two types of myocardia can be observed through the endocardial spectral mapping (SM) in sinus rhythm: the compact type with a smooth spectrum and the fibrillar type with a segmented spectrum (atrial fibrillation nests). During the atrial fibrillation (AF), the compact type has an organized activation and low frequency (passive), whereas the fibrillar type has a rather disorganized activation and high frequency (active/resonant), with both being activated by high-frequency sustained tachycardia - the background tachycardia (BT). OBJECTIVE: To describe the treatment of AF by the ablation of the AF nests and BT. METHODS: 1) Catheter ablation of the AF nests with RF [4/8mm-60&#186;/30-40J/30s] guided by SM in sinus rhythm, outside the pulmonary vein; 2) atrial stimulation -300ppm; 3) Additional ablation of the AF nests if AF is induced; 4) Focal ablation if BT and/or Flutter is induced; 5)Clinical follow-up+ ECG+ Holter. RESULTS: A total of 50&#177;18 AF nests/patient were treated. After 11.3&#177;8m, 81 patients (88%) did not present AF (28.3% with antiarrhythmic drugs). After the ablation of the AF nests, AF was not reinduced in 61 patients (71%) and BT was induced and treated in 24 patients (26%). There were two episodes of pericardial bleeding (1 treated clinically and 1 surgically), caused by sheaths that are no longer used CONCLUSION: The SM in sinus rhythm can be used in the ablation of AF nests. During the AF, the AF nests present a reactive-resonant pattern and the compact myocardium is passive, stimulated by the high frequency of the BT. After the ablation of the AF nests and the BT, it was not possible to reinduce the sustained AF. The Ablation of AF nests outside the pulmonary veins showed to be safe and highly effective in the cure and/or clinical control of the AF.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Catheter ablation</kwd>
        <kwd>atrial fibrillation</kwd>
        <kwd>spectrum analysis</kwd>
        <kwd>heart rate</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ORIGINAL ARTICLE</bold>
      </p>
      <p>Radiofrequency catheter ablation of atrial fibrillation guided by spectral mapping of atrial fibrillation nests in sinus rhythm </p>
      <p>
        <bold>Jos&#233; Carlos Pach&#243;n Mateos; Enrique I. Pach&#243;n Mateos; Tasso J. Lobo; Maria Z&#233;lia C. Pach&#243;n; Ju&#225;n Carlos Pach&#243;n Mateos; Denilda Queiroz V. Pach&#243;n; Remy Nelson A. Vargas; Leopoldo S. Piegas; Adib D. Jatene</bold>
      </p>
      <p>Hospital do Cora&#231;&#227;o (HCor) and Instituto Dante Pazzanese de Cardiologia - S&#227;o Paulo, SP - Brazil</p>
      <p>
        <xref ref-type="corresp" rid="end-body2">Mailing address</xref>
      </p>
      <p>
        <bold>SUMMARY</bold>
      </p>
      <p><bold>BACKGROUND:</bold> Two types of myocardia can be observed through the endocardial spectral mapping (SM) in sinus rhythm: the compact type with a smooth spectrum and the fibrillar type with a segmented spectrum (atrial fibrillation nests). During the atrial fibrillation (AF), the compact type has an organized activation and low frequency (passive), whereas the fibrillar type has a rather disorganized activation and high frequency (active/resonant), with both being activated by high-frequency sustained tachycardia - the background tachycardia (BT).</p>
      <p><bold>OBJECTIVE:</bold> To describe the treatment of AF by the ablation of the AF nests and BT.</p>
      <p><bold>METHODS:</bold> 1) Catheter ablation of the AF nests with RF [4/8mm-60&#186;/30-40J/30s] guided by SM in sinus rhythm, outside the pulmonary vein; 2) atrial stimulation -300ppm; 3)Additional ablation of the AF nests if AF is induced; 4) Focal ablation if BT and/or Flutter is induced; 5)Clinical follow-up+ ECG+ Holter.</p>
      <p><bold>RESULTS:</bold> A total of 50&#177;18 AF nests/patient were treated. After 11.3&#177;8m, 81 patients (88%) did not present AF (28.3% with antiarrhythmic drugs). After the ablation of the AF nests, AF was not reinduced in 61 patients (71%) and BT was induced and treated in 24 patients (26%). There were two episodes of pericardial bleeding (1 treated clinically and 1 surgically), caused by sheaths that are no longer used.</p>
      <p><bold>CONCLUSION:</bold> The SM in sinus rhythm can be used in the ablation of AF nests. During the AF, the AF nests present a reactive-resonant pattern and the compact myocardium is passive, stimulated by the high frequency of the BT. After the ablation of the AF nests and the BT, it was not possible to reinduce the sustained AF. The Ablation of AF nests outside the pulmonary veins showed to be safe and highly effective in the cure and/or clinical control of the AF.</p>
      <p><bold>Key words: </bold>Catheter ablation; atrial fibrillation; spectrum analysis; heart rate.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>The conventional electrophysiological study is based on the analysis of amplitude variations over time (time domain). However, the spectral analysis of a wave correlates amplitude and/or potency with the intrinsic signal frequencies (frequency domain), supplying a large amount of additional information. The heart rate is measured in beats per minute (extrinsic signal frequency), i.e., time domain, whereas the normal R wave peak, for instance, changes voltage abruptly due to the fact that it has high intrinsic spectral frequencies (frequency domain), measured in hertz (Hz, cycles per second). Therefore, the term frequency can be related to temporal or spectral values. Using real-time spectral analysis in sinus rhythm, it is observed that the atrial walls are constituted by two distinct types of myocardia, the compact and the fibrillar types (<xref ref-type="fig" rid="fig01-body2">Fig. 1</xref>). The first type presents a continuous and organized spectrum, with most of the potency grouped to the left (low frequency). The second type presents a segmented spectrum, with a large amount of the segments shifted to the right (high frequencies, &gt; 80 Hz)<sup>1</sup>. The fibrillar myocardium is usually grouped in small areas, which are more or less extensive. During the atrial fibrillation (AF), the compact myocardium presents an organized behavior and high-amplitude electrical activation, low frequency, slightly irregular, suggesting a passive behavior. On the other hand, the fibrillar myocardium presents low-amplitude electrical activity, which is highly disorganized and has high frequency, showing, from an electrical point of view, a resonant behavior. </p>
      <fig id="fig01-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf01-en.jpg"/></fig>
      <p> Resonant is the system that presents resonance. The resonance - the state of a system that vibrates in its own frequency, generally with decremental amplitude, as the result of external stimuli - can be mechanical, such as that of a tuning fork; electrical, such as that of inducers, tuners and oscillators; electromagnetic, such as that of a microwave oven and magnetic resonance imaging, etc.</p>
      <p>It has been observed that the elimination of the fibrillar myocardium makes it progressively more difficult to reinduce AF. Additionally, these areas present he highest frequencies during this type of arrhythmia. Therefore, the places with high density of fibrillar myocardium were called AF "nests"<sup>1,2</sup>. Moreover, after the elimination of the AF nests, it has been possible to induce very rapid atrial tachycardia that is highly protected from reversion. Some evidence has demonstrated that this tachycardia occurs secondarily during the AF (background tachycardia), being its maintenance element. The present study describes the mapping and the ablation of the AF nests, followed by the induction and ablation of the background tachycardia.</p>
      <p><italic>Hypothesis - </italic>The AF nests can be easily identified through spectral mapping during the sinus rhythm and eliminated with ablation by radiofrequency. This could weaken one of the mechanisms of AF maintenance, contributing to its ultimate treatment. Additionally, it would allow the visualization of background tachycardia<sup>2</sup>, permitting its mapping and respective ablation. </p>
      <p><italic>Objectives - </italic>To propose a new alternative for the treatment of AF based on a spectral mapping during sinus rhythm and describe new findings, aiming at a better understanding of the physiopathology of this arrhythmia. </p>
      <p><italic>Patients - </italic>A total of 92 patients, 76 males, whose mean age was 52.4 &#177; 11 yrs were included in the study. All patients had frequent AF that was refractory to at least two antiarrhythmic drugs and 51 (55.4%) reported at least one electrical cardioversion. In this group, all the antiarrhythmic drugs available in our country, as well as flecainamide, showed to be ineffective in one or more patients. Regarding the type of AF, 56 cases (61%) presented the paroxysmal type (3.6 &#177; 1.3, with 2 to 7 crises per year), 25 (27%) presented the persistent type (2.6 &#177; 1.2, with 1 to 6 crises per year) and 11 (12%) presented the permanent type. Very frequent episodes of non-sustained or incessant AF were observed in 9 patients. Most of the patients did not present any significant cardiopathy. The left atrium diameter was normal or moderately increased (41.9 &#177; 5 mm). The mean ejection fraction was 0.61 &#177; 0.8. The most relevant etiologies were: idiopathic, 42%; hypertension, 22%; congenital cardiopathy, 11%; rheumatic cardiopathy, 10%; coronaropathy, 9%; and others, 6%.</p>
      <p>
        <bold>Methods</bold>
      </p>
      <p>The patients using oral anticoagulants were admitted at the hospital 24 or 48 to have the <italic>International Normalized Ratio </italic>(INR) adjusted for <underline>&lt;</underline> 1.4. All cases, especially those with a history of thromboembolism, were treated only after the confirmation of the absence of cardiac thrombi through transesophageal echocardiography<sup>3-5</sup>. The conventional monitoring with surface electrocardiography (ECG) radiotransparent defibrillation adhesive plaques, orotracheal intubation with mechanical ventilation and inhalation anesthesia was used, as well as the passing of a transesophageal echocardiography transducer. After asepsis, five venipunctures were performed (one subclavian and four femoral ones). A decapolar catheter was introduced through the subclavian vein to catheterize the coronary sinus. Two quadripolar catheters were introduced through the femoral vein into the right atrium and ventricle, an octapolar catheter was positioned at the His and a transeptal punction was performed (five patients had a patent foramen ovale). The following equipment were utilized: C&#237;cero EM anesthesia equipment (Dr&#228;ger); HP/Philips M1026A multiparametric monitor; HP/Philips echocardiography equipment model Sonos 2500; 32-channel TEB polygraph with modified software for real-time spectral post-analysis (TEB-Pach&#243;n); computerized spectrometer (Pach&#243;n<sup>&#174;</sup>) for real-time spectral analysis (<xref ref-type="fig" rid="fig02-body2">Fig. 2</xref>); Digital Siemens radioscopy; Biotronik Abcontrol MDS; radiofrequency generator; Philips Heartstart XL biphasic defibrillator with transcutaneous pacemaker; brain-activity spectrometer-BIS (in cases with higher thromboembolic risk). The ablations were carried out with a Blazer EPT 4-mm or 8-mm catheter or 4-mm or 8-mm Medtronic Conductor. All patients received information about the methods and potential complications and agreed with the procedures by signing the informed consent form. </p>
      <fig id="fig02-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf02-en.jpg"/></fig>
      <p>Through a transeptal punction a spiral catheter (Supreme St. Jude or Biotronik Lexx) and the ablation catheter were introduced. Heparin was administered IV to maintain the activated coagulation time between 300 and 400 s. The atrial endocardia were scanned with real-time spectral analysis. All AF nests found were eliminated by applying radiofrequency (30-40 W/30 s/60&#186;C) until the fibrillar pattern disappeared (<xref ref-type="fig" rid="fig03-body2">Fig. 3</xref>). No complete intentional isolation of the pulmonary veins or blockage lines was carried out, according to the existing conventional techniques<sup>6</sup>. The spiral catheter was used to safely identify the atrial limits and detect AF nests, which are less evident with an 8-mm catheter.</p>
      <fig id="fig03-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf03-en.jpg"/></fig>
      <p><italic>Post-ablation re-study - </italic>After the ablation of the AF nests, programmed (up to three extra-stimuli) as well as progressive (up to 300 ppm) atrial stimulation were performed. If AF were induced, new AF nests would be sought and treated. If residual tachycardia were induced (background tachycardia<sup>2</sup>), it would be mapped and treated at its focus of origin. The authors of the present study chose to use the term "background tachycardia", instead of secondary tachycardia, as the term "background" has been incorporated into the Brazilian Portuguese language, according to version 5.11 of <italic>Novo Dicion&#225;rio Aur&#233;lio</italic>. In case of history or induction of flutter, the specific ablation was carried out. The criteria to finish the ablation were: 1. Impossibility to re-induce AF or tachycardias; 2. Induction only of non-sustained tachycardia/AF &lt; 10 sec; and 3. Impossibility to eliminate residual tachycardia or prolonged procedure (more than five hrs); in these cases, the external thoracic cardioversion was carried out. </p>
      <p><italic>Post-ablation medication - </italic>Even being ineffective or little effective in the pre-ablation phase, the antiarrhythmic medication was used for two months to reduce the atrial excitability caused by the cicatricial process. Warfarin anticoagulants were administered for three months post-ablation, keeping the prothrombin time between 2 and 3 INR. After this period, several anti-aggregants were used in cases that presented thromboembolism risk (age, heart failure, mitral dysfunction, dilated left atrium, etc), including those patients with sustained or non-sustained AF recurrence and adequate pharmacological response. The antiarrhythmic medication was withdrawn, except in 23 cases in whom it was necessary to maintain the sinus rhythm.</p>
      <p><italic>Post-ablation follow-up - </italic>The follow-up consisted of clinical control and ECG (at hospital discharge, after one, three and six months and after one year) and Holter (one month, six months and one year) or whenever there were symptoms. Additionally, a continuous control was kept through telephone calls. </p>
      <p>
        <bold>Results</bold>
      </p>
      <p>On average, 50 &#177; 18 AF nests were treated per patient. After the ablation, it was not possible to induce sustained AF in 65 (71%) cases. In 27 cases (29%), it was possible to induce a non-sustained episode of atrial tachycardia or AF (&lt; 10 s). In 24 patients (26%), it was possible to induce atrial tachycardia with special characteristics (induced by programmed or progressive high-frequency atrial stimulation, highly protected by inflow blockage, difficult to induce and very difficult reversion through atrial stimulation), which was called "background tachycardia"<sup>2</sup>. Eighteen patients (19%) presented a history of common flutter or it was induced, being treated with the bidirectional blockage of the cavotricuspid isthmus. After a mean follow-up of 11.3 &#177; 8 months, 81 patients (88%) were in sinus rhythm, 23 cases (28%) using previously ineffective antiarrhythmic drugs at reduced doses (amiodarone, 100 mg/day to 300 mg/day; sotalol, 60 mg/day to 160 mg/day; propafenone, 150 mg/day to 600 mg/day; quinidina, 200 mg/day to 400 mg/day). Nine patients (9.8%) underwent re-ablation due to the difficulty in the clinical control of AF or atrial tachycardia in the late phase post-ablation (more than six months of evolution).</p>
      <p>At the initial phase of this method, two episodes of pericardial bleeding occurred (one that resolved clinically and another that had to be surgically drained), probably related to the simultaneous manipulation of multiple sheaths inside the left atrium, as the tip of the involved electrodes (EPT 4 mm <italic>large</italic>), differently from the sheaths, is very malleable, being unlikely that it would have caused the lesion. Additionally, this complication did not occur after the sheaths started to be removed from the left atrium during the ablation, even when more rigid 8-mm electrodes were used. No other complication was observed. </p>
      <p>The most common locations of "AF nests" are shown in <xref ref-type="table" rid="tab01-body2">Table 1</xref>.</p>
      <table-wrap id="tab01-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gt01-en.jpg"/></table-wrap>
      <p>In 11 patients (46%) of the 24 cases in whom background tachycardia was induced, the focus was well defined by mapping, with tachycardia reversion following the use of radiofrequency at the place of better mapping (<xref ref-type="table" rid="tab02-body2">Table 2</xref>). In the other 13 cases (54%), the external thoracic cardioversion (10) or reversion by overdrive (3) was carried out due to inconsistent mappings, very high tachycardia frequency, more than one focus or prolonged procedures. </p>
      <table-wrap id="tab02-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gt02-en.jpg"/></table-wrap>
      <p>The mean procedure and radioscopy duration were, respectively: 4.3 &#177; 1.2 hrs and 53.8 &#177; 19 minutes.</p>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>This study demonstrates the use of real-time spectral mapping, in sinus rhythm, in the identification and ablation of AF nests. It was possible to observe that the more extensive the ablation of the AF nests, the lower the possibility of inducing this arrhythmia through stimulation. Additionally, a large number of these patients (88%) remained without AF or had controlled AF during follow-up, despite the 39% of cases with persistent and permanent AF, types that are normally associated to poorer outcomes<sup>7</sup>. These data suggest that, apparently, the lower the number of AF nests, more stable the atrial walls become, from an electrical point of view. Additionally, their elimination allowed the identification of tachycardia with very specific characteristics, likely constituting an essential connection in the physiopathology of AF. </p>
      <p><italic>AF substrate - </italic>Large contributions have been made in the identification of AF triggers<sup>8-10</sup> as well as in the treatment of this arrhythmia by the ablation or isolation of these triggers<sup>11,12</sup>. However, the identification of the substrate has advanced very little. It is relatively easy to understand an arrhythmia such as the AF in a dilated atrium with significant fibrosis and degeneration; however, how does one explain this arrhythmia in apparently normal hearts? The initial observations of the present study indicate the AF nests and the background tachycardias. When comparing normal patients with and without paroxysmal AF, it was observed that the number of AF nests is significantly higher in cases with spontaneous or laboratory-induced AF<sup>1,13</sup>.</p>
      <p><italic>Fibrillar myocardium and AF nests</italic>: The different spectrums of compact and fibrillar myocardia suggest that the great difference between the two types lies in the degree of connection among the cells, which gives those very distinct electrical resonance frequencies. The compact myocardium is very well connected and functions as a "large cell", whereas the fibrillar type behaves as a set of bundles with varied velocities of conduction and refractoriness. From the spectral point of view, the fibrillar and compact myocardia have high and low resonance frequencies, respectively. Therefore, when the atrial walls are stimulated with progressive frequencies, it is observed that the fibrillar myocardium presents autolimited repetitive responses at a much lower frequency than the compact myocardium (234 &#177; 28 x &gt; 300 ppm; p = 0.018), i.e., the compact myocardium is much more resistant to rapid atrial stimulation. Due to this property, during the AF the fibrillar myocardium constantly maintains a very high, irregular and disorganized frequency (multiplying element), justifying the name "AF nests", whereas the compact myocardium maintains an organized depolarization, much lower frequency and no repetitive responses (passive element) (<xref ref-type="fig" rid="fig04-body2">Fig. 4</xref>). </p>
      <fig id="fig04-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf04-en.jpg"/></fig>
      <p><italic>Resonance of the AF nests - </italic>During the AF, the AF nests frequently alternate periods of low amplitude and disorganized high frequency with high amplitude and organized low frequency (<xref ref-type="fig" rid="fig04-body2">Fig. 4</xref>). This happens due to a periodical electrical instability that promotes the alternateness of high and low frequencies. In this case, AF nests that are close and at different phases can feed again, favoring the maintenance of AF (<xref ref-type="fig" rid="fig05-body2">Fig. 5</xref>). This periodicity of electrical organization/disorganization is called electrical resonance (a known biological property observed in some cells of the mammalian and amphibian nervous system), as its behavior is comparable to that of an electronic resonator<sup>14</sup>, capable of multiplying the initial stimulation. The microreentry and/or reflection between close cell bundles, as well as periods of autolimited triggered activity due to a transitory calcium phenomenon, can explain this property of AF nests<sup>15,16</sup>.</p>
      <fig id="fig05-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf05-en.jpg"/></fig>
      <p><italic>Probable focus of the AF nests - </italic>In the group of patients assessed in the present study, it was possible to associate the AF nests with the following conditions: </p>
      <p>1. Congenital: innervation entry (fiber interpolation)<sup>20</sup>.</p>
      <p>2. Constitutional: reduction of conexins, with a predominance of termino-terminal connections (<italic>crista terminalis</italic>)<sup>21</sup>.</p>
      <p>3. Atriovenous transition (interpolation of tissues at the insertion of the pulmonary veins).</p>
      <p>4. Mechanical stretching of the atrial myocardium (separation of cells due to pathological conditions, such as interatrial septum aneurysm, etc). </p>
      <p>5. Decreased expression of conexins (congestive heart failure, aging, congenital conditions).</p>
      <p>6. Pathological: degeneration, ischemia, inflammation or infiltrative disease com remodeling and reduction of conexins.</p>
      <p>Recently it was observed that the elimination of the AF nests makes the response to atropine negative in patients who presented a previously normal response, showing a close association between AF nests and vagal innervation<sup>20</sup> (<xref ref-type="fig" rid="fig06-body2">Fig. 6</xref>).</p>
      <fig id="fig06-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf06-en.jpg"/></fig>
      <p><italic>Treating atrial fibrillation in sinus rhythm through ablation with radiofrequency of AF nests - </italic>The advantage of the concept of AF nests was to allow the ablation by catheter during sinus rhythm<sup>1</sup> (<xref ref-type="fig" rid="fig04-body2">Fig. 4</xref>) without performing the classical blockage lines. It has been observed that the higher the number of AF nests, more frequent and prolonged is the AF, whether spontaneous or induced. Patients that present a very reduced number of AF nests are typically resistant to arrhythmia induction by atrial stimulation. Additionally, when induced, the AF tends to be short and present spontaneous reversion. In the present study, we observed that as the number of AF nests was reduced through ablation with radiofrequency, it became more difficult to re-induce arrhythmia.</p>
      <p><italic>Background Tachycardia - </italic>An extremely interesting phenomenon observed during the spectral ablation of AF nests was the background tachycardia<sup>2</sup>. The latter is an atrial tachycardia observed only after the ablation of AF nests and attained at the following conditions: during AF, by progressive ablation of AF nests or during sinus rhythm, through programmed and/or progressive atrial stimulation (up to 300 ppm) after most of the AF nests have been submitted to ablation. </p>
      <p>
        <italic>Main characteristics of background tachycardia: </italic>
      </p>
      <p>1. Regular or slightly irregular atrial tachycardia.</p>
      <p>2. Very high frequency (256 &#177; 34 bpm).</p>
      <p>3. Originated by reentry (generally microreentry induced by rapid and/or programmed atrial stimulation and reversed by overdrive).</p>
      <p>4. Highly protected focus (very difficult to be reversed by overdrive) (<xref ref-type="fig" rid="fig07-body2">Fig. 7</xref>).</p>
      <fig id="fig07-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf07-en.jpg"/></fig>
      <p>5. It can be identified by the digital subtraction of the QRS at the surface ECG and spectral analysis of the tracing of the fast Fourier transform (FFT), before the ablation. </p>
      <p><italic>Association between background tachycardia and atrial fibrillation - </italic>In the present study it was possible to visualize the background tachycardia after the ablation of the AF nests. It was observed that the AF starts to organize and becomes background tachycardia with the progressive elimination of the AF nests. These data suggest that this tachycardia is a key element in the physiopathology of AF. It is a regular tachycardia (originated by reentry), which, apparently exists at a second plane (background) during the AF. Its very high frequency stimulates the AF nests, promoting its disorganization, its resonance and refeeding. The presence of an entry blockage protects the background tachycardia focus, so that it is not reversed by the stimuli that originate from the activation of the AF nests. The larger the entry blockage is (more difficult to reverse with atrial stimulation), the more prolonged the AF. The combination of background tachycardia with very high and disorganized frequency of AF nests constitutes the apparently chaotic electrical activity that characterizes the classical morphology of f waves at the ECG of frank AF. Many times there is a periodical alternateness of resonance of the AF nests, making the background tachycardia to appear more or less cyclically organized. This constitutes a condition that is frequently known as "fibrillo-flutter". From an electrical point of view, this tachycardia is the main oscillator of the AF<sup>2</sup>.</p>
      <p><italic>Ablation of the background tachycardia - </italic>After the ablation of the AF nests, the focus of the background tachycardia induced by atrial stimulation was sought and its ablation was attempted (<xref ref-type="fig" rid="fig08-body2">Fig. 8</xref>). Eventually, the focus of this tachycardia might have been eliminated indirectly during the ablation of the AF nests. In this study, the evolution of the patients who had the background tachycardia treated or those in whom it was impossible to induce it when compared to the group who remained untreated was very different. In the first group, the success rate was 88.9%; in the second group, however, the AF was eliminated in only 73% (p=0.008). Nevertheless, due to mechanisms of protection, many times the background tachycardia could not be induced. Additionally, its mapping is hindered by the high frequency. </p>
      <fig id="fig08-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gf08-en.jpg"/></fig>
      <p><italic>Physiopathology of atrial fibrillation based on AF nests - </italic>This study suggests that the AF results from the fusion of arrhythmias constituted essentially by a protected atrial tachycardia (background tachycardia), which stimulates the nests and maintain them under a constant state of repetitive responses (<xref ref-type="fig" rid="fig08-body2">Fig. 8</xref>). The observation of this group of patients, of the respective ablations and the clinical history of each case allows us to establish a specific physiopathology for AF based on the following components:</p>
      <p>1. Modulator: autonomic nervous system (extensively modified by the ablation of the "AF nests"<sup>20</sup>).</p>
      <p>2. Trigger: extra-systoles and non-sustained tachycardias of the pulmonary veins<sup>9,19,22-24</sup>.</p>
      <p>3. Substrate (multiplier element): AF nests that respond with high frequency to the rapid atrial stimulation, due to the resonant properties (microreentry and/or triggered activity). The capacity to multiply the stimuli is one of the factors that sustain the AF.</p>
      <p>4. Maintainer: <italic>background</italic> tachycardia, which works as an asynchronic atrial pacemaker with a very high frequency, capable of activating the AF nests, maintaining them within the range of repetitive responses. It is the analogue of the artificial pacemaker used by Wijffels et al<sup>25</sup> and Moreira et al<sup>26</sup> to produce AF, stimulating with very high frequencies. </p>
      <p>This physiopathology explains the several classically known clinical pictures (<xref ref-type="table" rid="tab03-body2">Table 3</xref>).</p>
      <table-wrap id="tab03-body2">
        <graphic xlink:href="1678-4170-abc-89-03-0140-00001-gt03-en.jpg"/></table-wrap>
      <p><italic>Comparison with other ablation methods of atrial fibrillation - </italic>The cure of AF is a great challenge for all the available technique<sup>27</sup>. Although it was published in 2004<sup>1</sup>, the ablation of AF nests was developed in the end of the 90&#146;s, without being based on previous techniques. The initial proposal of the authors of the present study was to use spectral mapping to search for the AF substrate even in an apparently normal heart, and including patients who had presented a history of AF and, certainly, without atrial fibrosis. The AF nests are frequent in the antrum of pulmonary veins. During their elimination, the electrical isolation of these structures can occur. However, as the spectrum-oriented isolation searches for the frequencies &gt; 80 Hz, most of the times the pulmonary veins are not completely isolated by the ablation of the AF nests, resulting in the electrical conduction of potentials &lt; 80 Hz. This fact differentiates this technique from the methods developed by Haissaguerre et al<sup>11</sup>, Natale et al<sup>28</sup>, Pappone et al<sup>19,29</sup> and Oral et al<sup>30,31</sup>, among others, which are characterized by the complete isolation of the pulmonary veins with the use of extensive ablations and large amounts of energy. The exclusive elimination of the high frequencies of the spectrum allows the preservation of the more compact myocardium of the atrial wall, preventing deep lesions and reducing the risk of perforation, of atrioesophageal fistulas<sup>29,32</sup> and of stenosis of the pulmonary veins<sup>33,34</sup>, a fact that also differentiates the technique from other methods based on extensive and deep lines of blockage<sup>19</sup>.</p>
      <p>As well as in the techniques that directly eliminate the paracardiac ganglia<sup>35,36</sup>, the ablation of the AF nests, in a simplified form, promotes a significant parasympathetic denervation through the direct elimination of intramural neurons and the indirect elimination of the paracardiac ganglia. Therefore, in addition to acting directly on the autonomous nervous system, it eliminates a large part of the neuromyocardial interface, which has resonant properties (due to its microstructure) and specific spectral characteristics<sup>20</sup> (interpolation of fibers). The elimination of the intramural neuron and the fibrosis of the neuromyocardial junction significantly reduces the extension of the reinnervation. </p>
      <p>The method developed by Nademanee et al<sup>37</sup>, also published in 2004, describes the ablation during the AF oriented by complex fractionated electrograms (CFAEs), which are areas of highly fractioned electrical activity and directly identified by the time domain. It is known, however, that during the AF, due to the large number of wavefront collisions, many virtual areas of complex potentials are formed, a problem that does not exist during the sinus rhythm and, therefore, during the ablation of AF nests. </p>
      <p>Likely due to this fact, it is well-known the difficulty to reverse a persistent or chronic AF with the ablation of CFAES. Only the paroxysmal AF can be reversed more easily and the reversion, in this case, can be occasional and not necessarily electrophysiological. </p>
      <p>In fact, most of the methods have developed in the sense of causing progressively more extensive intramural lesions on the atrial wall. Clearly, the larger the area destroyed, the larger the number of eliminated AF nests, which can influence the results<sup>38</sup>, regardless of the method. Additionally, it has been observed that the origin of the background tachycardia can inadvertently eliminated during these extensive ablations, favoring the long-term outcome. This aspect is highly desirable; however, considering the spectral mapping as the basis, it is understood that it is preferable to direct the ablations rationally into the substrate, eliminate only the resonant frequencies (fibrillar myocardium), preserve the compact muscle, apply the least amount of energy possible to prevent complications and try to induce the background tachycardia with the subsequent ablation of its focus of origin. </p>
      <p>
        <bold>Conclusions</bold>
      </p>
      <p>The AF nests were easily found in sinus rhythm through the spectral mapping, allowing them to be treated by ablation with conventional radiofrequency, regardless of the isolation of the pulmonary veins. During the AF, this type of myocardium (fibrillar type) presents a reactive-resonant high-frequency pattern, which refeeds the arrhythmia. Differently, the compact myocardium responds in an organized form and with low frequency. After the ablation of the AF nests, it became progressively more difficult the reinduction of the AF, showing that they are directly associated with the physiopathology of arrhythmia. Additionally, the removal of the AF nests allowed the visualization of a residual tachycardia with entry blockage and high frequency, the background tachycardia. The treatment of this condition was followed by significant outcome improvement. These observations, in addition to contributing to the better understanding of the AF physiopathology, allow us to conclude that the ablation of the AF nests followed by the treatment of the background tachycardia is a safe, feasible and highly efficient method to cure or clinically control the AF. </p>
      <p>
        <bold>Potential Conflict of Interest</bold>
      </p>
      <p>No potential conflict of interest relevant to this article was reported.</p>
      <p>
        <bold>Sources of Funding</bold>
      </p>
      <p>There were no external funding sources for this study.</p>
      <p>
        <bold>Study Association</bold>
      </p>
      <p>This article is part of the thesis associate professor submitted by Jos&#233; Carlos Pach&#243;n Mateos, from Universidade de S&#227;o Paulo.</p>
      <p>
        <bold>References</bold>
      </p>
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      <p>
        <fn id="end-body2" fn-type="corresp">
          <p>Mailing address:</p>
          <p> Jos&#233; Carlos Pach&#243;n Mateos </p>
          <p> Av. A&#231;oc&#234;, 515/31 </p>
          <p> 04075-000</p>
          <p> S&#227;o Paulo, SP - Brazil</p>
          <p> E-mail: </p>
          <p>
            <email xlink:href="jcpachon@hotmail.com">jcpachon@hotmail.com</email>
          </p>
        </fn>
      </p>
      <p>Manuscript received February 25, 2007; revised manuscript received March 1, 2007; accepted March 7, 2007.</p>
    </body>
  </sub-article>
</article>
