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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">7THxLV7FzKDBCmbwNzFxgYf</article-id>
      <article-id pub-id-type="other">00011</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2011000200011</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(11)09600211</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2011005000013</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Artigos Originais</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Efeitos agudos do tabagismo sobre a modula&#231;&#227;o auton&#244;mica: an&#225;lise por meio do plot de poincar&#233;</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Manzano</surname>
            <given-names>Beatriz Martins</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Vanderlei</surname>
            <given-names>Luiz Carlos Marques</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Ramos</surname>
            <given-names>Ercy Mara</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Ramos</surname>
            <given-names>Dionei</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">Presidente Prudente</named-content>
          <named-content content-type="state">S&#227;o Paulo</named-content>
        </addr-line>
        <institution content-type="orgname">Universidade Estadual Paulista</institution>
        <institution content-type="orgdiv1">Faculdade de Ci&#234;ncias e Tecnologia </institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>02</month>
        <year>2011</year>
      </pub-date>
      <volume>96</volume>
      <issue>2</issue>
      <fpage>154</fpage>
      <lpage>160</lpage>
      <history>
        <date date-type="received">
          <day>11</day>
          <month>01</month>
          <year>2010</year>
        </date>
        <date date-type="rev-recd">
          <day>23</day>
          <month>05</month>
          <year>2010</year>
        </date>
        <date date-type="accepted">
          <day>06</day>
          <month>08</month>
          <year>2010</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: O tabagismo altera a fun&#231;&#227;o auton&#244;mica. OBJETIVO: Investigar os efeitos agudos do tabagismo sobre a modula&#231;&#227;o auton&#244;mica e a recupera&#231;&#227;o dos &#237;ndices de variabilidade de frequ&#234;ncia card&#237;aca (VFC) p&#243;s-fumo, por meio do plot de Poincar&#233; e &#237;ndices lineares. M&#201;TODOS: Foram avaliados 25 fumantes jovens, os quais tiveram a frequ&#234;ncia card&#237;aca analisada, batimento a batimento, na posi&#231;&#227;o sentada, ap&#243;s 8 horas de abstin&#234;ncia, por 30 minutos em repouso, 20 minutos durante o fumo e 30 minutos p&#243;s-fumo. An&#225;lise de vari&#226;ncia para medidas repetidas, seguido do teste de Tukey, ou teste de Friedman seguido do teste de Dunn foram aplicados dependendo da normalidade dos dados, com p &lt; 0,05. RESULTADOS: Durante o fumo, houve redu&#231;&#227;o dos &#237;ndices SD1 (23,4 &#177; 9,2 vs 13,8 &#177; 4,8), raz&#227;o SD1/SD2 (0,31 &#177; 0,08 vs 0,2 &#177; 0,04), RMSSD (32,7 &#177; 13 vs 19,1 &#177; 6,8), SDNN (47,6 &#177; 14,8 vs 35,5 &#177; 8,4), HFnu (32,5 &#177; 11,6 vs 19 &#177; 8,1) e do intervalo RR (816,8 &#177; 89 vs 696,5 &#177; 76,3) em rela&#231;&#227;o ao repouso, enquanto que aumentos do &#237;ndice LFnu (67,5 &#177; 11,6 vs 81 &#177; 8,1) e da raz&#227;o LF/HF (2,6 &#177; 1,7 vs 5,4 &#177; 3,1) foram observados. A an&#225;lise visual do plot mostrou menor dispers&#227;o dos intervalos RR durante o fumo. Com exce&#231;&#227;o da raz&#227;o SD1/SD2, os demais &#237;ndices apresentaram recupera&#231;&#227;o dos valores, 30 minutos ap&#243;s o tabagismo. CONCLUS&#195;O: O tabagismo produziu agudamente modifica&#231;&#245;es no controle auton&#244;mico, caracterizadas por ativa&#231;&#227;o simp&#225;tica e retirada vagal, com recupera&#231;&#227;o 30 minutos ap&#243;s o fumo.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>Tabagismo</kwd>
        <kwd>sistema nervoso aut&#244;nomo</kwd>
        <kwd>frequ&#234;ncia card&#237;aca</kwd>
        <kwd>din&#226;mica n&#227;o linear</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>28</day>
        <month>01</month>
        <year>2011</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>Efeitos agudos do tabagismo sobre a modula&#231;&#227;o auton&#244;mica: an&#225;lise por meio do <italic>plot</italic> de poincar&#233;</bold>
    </p>
    <p>
      <bold>Beatriz Martins Manzano; Luiz Carlos Marques Vanderlei; Ercy Mara Ramos; Dionei Ramos</bold>
    </p>
    <p>Faculdade de Ci&#234;ncias e Tecnologia - FCT - UNESP - Presidente Prudente, S&#227;o Paulo, SP - Brasil</p>
    <p>
      <xref ref-type="corresp" rid="ntb">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p><bold>FUNDAMENTO:</bold> O tabagismo altera a fun&#231;&#227;o auton&#244;mica. </p>
    <p><bold>OBJETIVO:</bold> Investigar os efeitos agudos do tabagismo sobre a modula&#231;&#227;o auton&#244;mica e a recupera&#231;&#227;o dos &#237;ndices de variabilidade de frequ&#234;ncia card&#237;aca (VFC) p&#243;s-fumo, por meio do <italic>plot</italic> de Poincar&#233; e &#237;ndices lineares. </p>
    <p><bold>M&#201;TODOS:</bold> Foram avaliados 25 fumantes jovens, os quais tiveram a frequ&#234;ncia card&#237;aca analisada, batimento a batimento, na posi&#231;&#227;o sentada, ap&#243;s 8 horas de abstin&#234;ncia, por 30 minutos em repouso, 20 minutos durante o fumo e 30 minutos p&#243;s-fumo. An&#225;lise de vari&#226;ncia para medidas repetidas, seguido do teste de Tukey, ou teste de Friedman seguido do teste de Dunn foram aplicados dependendo da normalidade dos dados, com p &lt; 0,05. </p>
    <p><bold>RESULTADOS:</bold> Durante o fumo, houve redu&#231;&#227;o dos &#237;ndices SD1 (23,4 &#177; 9,2 <italic>vs</italic> 13,8 &#177; 4,8), raz&#227;o SD1/SD2 (0,31 &#177; 0,08 <italic>vs</italic> 0,2 &#177; 0,04), RMSSD (32,7 &#177; 13 <italic>vs</italic> 19,1 &#177; 6,8), SDNN (47,6 &#177; 14,8 <italic>vs</italic> 35,5 &#177; 8,4), HFnu (32,5 &#177; 11,6 <italic>vs</italic> 19 &#177; 8,1) e do intervalo RR (816,8 &#177; 89 <italic>vs</italic> 696,5 &#177; 76,3) em rela&#231;&#227;o ao repouso, enquanto que aumentos do &#237;ndice LFnu (67,5 &#177; 11,6 <italic>vs</italic> 81 &#177; 8,1) e da raz&#227;o LF/HF (2,6 &#177; 1,7 <italic>vs</italic> 5,4 &#177; 3,1) foram observados. A an&#225;lise visual do <italic>plot</italic> mostrou menor dispers&#227;o dos intervalos RR durante o fumo. Com exce&#231;&#227;o da raz&#227;o SD1/SD2, os demais &#237;ndices apresentaram recupera&#231;&#227;o dos valores, 30 minutos ap&#243;s o tabagismo. </p>
    <p><bold>CONCLUS&#195;O:</bold> O tabagismo produziu agudamente modifica&#231;&#245;es no controle auton&#244;mico, caracterizadas por ativa&#231;&#227;o simp&#225;tica e retirada vagal, com recupera&#231;&#227;o 30 minutos ap&#243;s o fumo. </p>
    <p><bold>Palavras-chave:</bold> Tabagismo, sistema nervoso aut&#244;nomo/efeitos de drogas, frequ&#234;ncia card&#237;aca, din&#226;mica n&#227;o linear.</p>
    <p>
      <bold>Introdu&#231;&#227;o</bold>
    </p>
    <p>Os efeitos cr&#244;nicos do fumo sobre a variabilidade da frequ&#234;ncia card&#237;aca (VFC), uma medida n&#227;o invasiva dos impulsos auton&#244;micos que indica a habilidade do cora&#231;&#227;o em responder aos m&#250;ltiplos est&#237;mulos fisiol&#243;gicos e ambientais, bem como compensar desordens induzidas por doen&#231;as<sup>1-3</sup>, est&#227;o bem estabelecidos na literatura que aponta para sua redu&#231;&#227;o em fumantes<sup>4,5</sup>. Tal condi&#231;&#227;o est&#225; associada &#224; eleva&#231;&#227;o do risco de mortalidade e susceptibilidade para arritmias com risco de vida<sup>6-8</sup> e para, neste sentido, estudar condi&#231;&#245;es que favorecem a redu&#231;&#227;o da VFC &#233; fundamental.</p>
    <p>Agudamente, sabe-se que o fumo de cigarro resulta em aumento da press&#227;o arterial, frequ&#234;ncia card&#237;aca (FC), resist&#234;ncia vascular, descarga simp&#225;tica e diminui&#231;&#227;o da atividade barorreflexa<sup>6,9,10</sup>, o que pode alterar os &#237;ndices de VFC. Entretanto, ap&#243;s busca na literatura t&#233;cnica pertinente para elabora&#231;&#227;o desta pesquisa, os efeitos agudos do fumo de cigarro sobre &#237;ndices de VFC, principalmente o per&#237;odo imediatamente ap&#243;s o ato de fumar, n&#227;o t&#234;m sido exaustivamente estudados e os trabalhos que abordam o tema<sup>11,12</sup> fazem-no por meio de &#237;ndices lineares.</p>
    <p>Para avalia&#231;&#227;o da VFC, m&#233;todos lineares, analisados tanto no dom&#237;nio do tempo (DT) quanto no dom&#237;nio da frequ&#234;ncia (DF), e n&#227;o lineares podem ser utilizados<sup>2,13</sup>. A an&#225;lise linear &#233; amplamente utilizada para estudo do controle auton&#244;mico em diversas condi&#231;&#245;es, inclusive o tabagismo, no entanto, recentemente, os m&#233;todos n&#227;o lineares t&#234;m despertado grande interesse, uma vez que descrevem as flutua&#231;&#245;es complexas do ritmo e conseguem separar, nas s&#233;ries temporais de batimentos card&#237;acos, estruturas de comportamento n&#227;o linear mais adequadamente do que os m&#233;todos lineares<sup>14</sup>. Isso tem mostrado uma nova vis&#227;o sobre as anormalidades do comportamento da FC em v&#225;rias condi&#231;&#245;es, fornecendo informa&#231;&#245;es progn&#243;sticas adicionais quando comparada com os m&#233;todos tradicionais<sup>15,16</sup>.</p>
    <p>Um dos m&#233;todos considerado por alguns autores como baseado na din&#226;mica n&#227;o linear &#233; o <italic>plot</italic> de Poincar&#233;<sup>17,18</sup>, uma t&#233;cnica quantitativa-visual, na qual cada intervalo RR &#233; correlacionado com o intervalo antecedente e define um ponto no <italic>plot</italic><sup>19</sup>, sendo considerada uma das mais importantes t&#233;cnicas utilizadas para representar visualmente a VFC e de grande import&#226;ncia por sua capacidade de evidenciar aspectos n&#227;o lineares em uma sequ&#234;ncia de dados<sup>20</sup>.</p>
    <p>Assim, com intuito de acrescentar &#224; literatura elementos relacionados ao tema exposto, pretende-se, com este estudo, avaliar os efeitos agudos do tabagismo sobre o controle auton&#244;mico card&#237;aco e a recupera&#231;&#227;o dos &#237;ndices de VFC p&#243;s-fumo, por meio do <italic>plot</italic> de Poincar&#233;, juntamente com &#237;ndices de VFC no DT e DF.</p>
    <p>
      <bold>M&#233;todos</bold>
    </p>
    <p>Para a realiza&#231;&#227;o deste estudo, foram analisados dados de 25 volunt&#225;rios jovens (16 homens e 9 mulheres), selecionados dentre os participantes do Programa de Cessa&#231;&#227;o do Tabagismo da Faculdade de Ci&#234;ncias e Tecnologia - FCT/UNESP. Os volunt&#225;rios apresentaram como caracter&#237;sticas idade m&#233;dia de 22,9 &#177; 3,2 anos, IMC de 23,7 &#177; 4,1 kg/m<sup>2</sup>, consumo de 10 cigarros/dia (mediana), tempo de tabagismo m&#233;dio de 5,7 &#177; 4 anos, teste de Fargerstr&#246;m predominante (52,0%) de zero a dois pontos, o que corresponde a grau de depend&#234;ncia muito baixo e n&#237;veis de mon&#243;xido de carbono (CO) expirado de 4,9 &#177; 2,4 ppm.</p>
    <p>N&#227;o foram inclu&#237;dos no estudo indiv&#237;duos que apresentaram pelo menos uma das seguintes caracter&#237;sticas: uso de medicamentos que alterassem a atividade auton&#244;mica do cora&#231;&#227;o, como por exemplo, propranolol e atropina, etilistas e indiv&#237;duos com infec&#231;&#245;es, doen&#231;as metab&#243;licas ou do sistema cardiorrespirat&#243;rio conhecidas, as quais pudessem interferir no controle auton&#244;mico card&#237;aco.</p>
    <p>Os volunt&#225;rios foram devidamente informados sobre os procedimentos e objetivos do estudo, e um termo de consentimento livre e esclarecido foi assinado ap&#243;s a concord&#226;ncia em fazer parte do estudo. Todos os procedimentos utilizados foram aprovados pelo Comit&#234; de &#201;tica em Pesquisa da Faculdade de Ci&#234;ncias e Tecnologia - FCT/UNESP (protocolo 258/08) e seguiram a Resolu&#231;&#227;o 196/96 do Conselho Nacional de Sa&#250;de.</p>
    <p>
      <bold>Procedimentos</bold>
    </p>
    <p>O protocolo experimental foi realizado em uma sala com temperatura entre 22&#186; e 24&#186; Celsius, umidade entre 40-60,0%, no mesmo per&#237;odo do dia (entre 8 e 12 h), para amenizar poss&#237;veis influ&#234;ncias do ciclo circadiano. Previamente, todos os volunt&#225;rios foram orientados a abster-se de cafe&#237;na, atividade f&#237;sica e cigarro, por pelo menos 8 horas antes do estudo. A confirma&#231;&#227;o do per&#237;odo de abstin&#234;ncia do fumo foi realizada por meio da capta&#231;&#227;o dos n&#237;veis de CO utilizando o aparelho monox&#237;metro Micro CO (Micro Medical Limited, Rochester, Inglaterra). Indiv&#237;duos com valores iguais ou menores do que 10 ppm<sup>21</sup> foram aceitos como abstinentes.</p>
    <p>A coleta dos dados antropom&#233;tricos (peso e altura), hist&#243;ria tabag&#237;stica, antecedentes de sa&#250;de e medica&#231;&#227;o em uso, al&#233;m do grau de depend&#234;ncia e consumo tabag&#237;stico, atrav&#233;s do question&#225;rio de Fagerstr&#246;m, tamb&#233;m antecedeu o protocolo experimental.</p>
    <p>Ap&#243;s tais procedimentos, foi colocada no t&#243;rax dos volunt&#225;rios, no ter&#231;o distal do esterno, a cinta de capta&#231;&#227;o e, no punho dos mesmos, o receptor de frequ&#234;ncia card&#237;aca Polar S810i (Polar Electro, Finl&#226;ndia), equipamento previamente validado para capta&#231;&#227;o da FC, batimento a batimento, e utiliza&#231;&#227;o dos seus dados para c&#225;lculos dos &#237;ndices de VFC<sup>22,23</sup>. Os volunt&#225;rios foram posicionados sentados e orientados a permanecerem em repouso, sem movimentos de grande amplitude e sem conversarem durante a coleta que foi realizada de forma individual.</p>
    <p>A coleta teve dura&#231;&#227;o de 80 minutos cont&#237;nuos e constituiu-se de tr&#234;s momentos: 1) Repouso - os volunt&#225;rios permaneceram em repouso com respira&#231;&#227;o espont&#226;nea por 30 minutos; 2) Fumo - foi solicitado o fumo de dois cigarros rotineiramente consumidos pelos indiv&#237;duos, em um tempo de aproximadamente 20 minutos; e 3) P&#243;s-fumo - ao terminar de fumar, os volunt&#225;rios permaneceram novamente em repouso, com respira&#231;&#227;o espont&#226;nea por mais 30 minutos.</p>
    <p>Para an&#225;lise da VFC, o padr&#227;o de seu comportamento foi registrado batimento a batimento, durante todo o protocolo, com uma taxa de amostragem de 1.000 Hz. A an&#225;lise dos dados foi realizada utilizando os primeiros 1.000 intervalos RR consecutivos, ap&#243;s a filtragem digital pelo <italic>software Polar Precision Performance SW</italic> (vers&#227;o 4.01.029) complementada por manual, para elimina&#231;&#227;o de batimentos ect&#243;picos prematuros e artefatos, e somente s&#233;ries com mais de 95,0% de batimentos sinusais foram inclu&#237;das no estudo<sup>24</sup>. </p>
    <p>O per&#237;odo de repouso foi avaliado utilizando-se os 10 primeiros minutos para estabiliza&#231;&#227;o dos par&#226;metros hemodin&#226;micos e a FC registrada neste per&#237;odo foi descartada para an&#225;lise. O momento p&#243;s-fumo foi dividido em dois per&#237;odos de 15 minutos cada e denominados P&#243;s 1 e P&#243;s 2.</p>
    <p>
      <bold>An&#225;lise do <italic>plot</italic> de Poincar&#233;</bold>
    </p>
    <p>Para an&#225;lise n&#227;o linear, foi utilizado o <italic>plot</italic> de Poincar&#233;, gr&#225;fico em que cada intervalo RR &#233; registrado em fun&#231;&#227;o do intervalo RR pr&#233;vio, isto &#233;, a dura&#231;&#227;o de um intervalo (RR<sub>n</sub>) &#233; representada no eixo "x" e a dura&#231;&#227;o do intervalo seguinte (RR<sub>n+1</sub>) no eixo "y", de forma que cada ponto (RR<sub>n</sub>, RR<sub>n+1</sub>) no gr&#225;fico corresponde a dois batimentos sucessivos<sup>25</sup>.</p>
    <p>Para an&#225;lise quantitativa do <italic>plot, </italic>pelo ajuste da elipse da figura formada pelo atrator, foram calculados os seguintes &#237;ndices: SD1 (desvio-padr&#227;o da variabilidade instant&#226;nea batimento a batimento), SD2 (desvio-padr&#227;o em longo prazo dos intervalos RR cont&#237;nuos) e a raz&#227;o SD1/SD2<sup>1,15</sup>.</p>
    <p>A an&#225;lise qualitativa do <italic>plot </italic>foi feita por meio da an&#225;lise das figuras formadas pelo seu atrator, as quais foram descritas por Tulppo e cols.<sup>26</sup>. Foram considerados os seguintes padr&#245;es: figuras com aumento na dispers&#227;o dos intervalos RR foram consideradas caracter&#237;sticas de um <italic>plot</italic> normal, e figuras com pequena dispers&#227;o global, batimento a batimento e sem aumento da dispers&#227;o dos intervalos RR, a longo prazo. </p>
    <p>
      <bold>An&#225;lise linear da VFC</bold>
    </p>
    <p>A VFC foi tamb&#233;m analisada por meio de m&#233;todos lineares, no DT e no DF. No DT, foram utilizados os &#237;ndices RMSSD que correspondem &#224; raiz quadrada da m&#233;dia do quadrado das diferen&#231;as entre os intervalos RR normais adjacentes, expresso em milissegundos (ms)<sup>27</sup> e o SDNN que representa o desvio-padr&#227;o da m&#233;dia de todos os intervalos RR normais, expresso em ms<sup>16</sup>.</p>
    <p>Para an&#225;lise da VFC no DF, foram utilizados os componentes espectrais de baixa frequ&#234;ncia (LF, 0,04-015 Hz) e alta frequ&#234;ncia (HF, 0,15-0,40 Hz), em unidades normalizadas e em ms<sup>2</sup>, e a raz&#227;o entre estes componentes (LF/HF), que representa o valor relativo de cada componente espectral em rela&#231;&#227;o &#224; pot&#234;ncia total, menos os componentes de muito baixa frequ&#234;ncia (VLF). A an&#225;lise espectral foi calculada usando o algoritmo da Transformada R&#225;pida de Fourier<sup> 2</sup>. </p>
    <p>Dados da dura&#231;&#227;o dos intervalos RR foram tamb&#233;m analisados e para c&#225;lculo dos &#237;ndices de VFC foi utilizado o <italic>software HRV analysis</italic><sup>28</sup>. </p>
    <p>
      <bold>An&#225;lise dos dados</bold>
    </p>
    <p>Para caracteriza&#231;&#227;o do perfil da amostra, foi utilizada estat&#237;stica descritiva, com os seguintes dados sendo representados: valores de m&#233;dia, desvio-padr&#227;o, mediana e intervalos de confian&#231;a a 95,0%. A normalidade dos dados foi determinada por meio do teste Shapiro-Wilk.</p>
    <p>Para an&#225;lise dos momentos de repouso, fumo e p&#243;s-fumo, quando os dados apresentaram distribui&#231;&#227;o normal, foi aplicada an&#225;lise de vari&#226;ncia para medidas repetidas, seguido da aplica&#231;&#227;o do teste de Tukey (vari&#225;vel SDNN). Nos dados que n&#227;o apresentaram normalidade, foi aplicado o teste de Friedman para medidas repetidas seguido da aplica&#231;&#227;o do teste de Dunn (vari&#225;veis: intervalo RR, RMSSD, LFnu, HFnu, LFms<sup>2</sup>, HFms<sup>2</sup>, LF/HF, SD1, SD2, SD1/SD2). As diferen&#231;as nesses testes foram consideradas estatisticamente significantes quando o valor de "(p"( foi menor do que 0,05.</p>
    <p>O c&#225;lculo do poder do estudo (<italic>Software GraphPad StatMate version 2.00 for Windows, GraphPad Software</italic>, San Diego California USA), com o n&#250;mero de volunt&#225;rios analisados e n&#237;vel de signific&#226;ncia de 5,0% (teste bi-caudal), garantiu um poder do teste superior a 80,0% para detectar diferen&#231;as entre as vari&#225;veis.</p>
    <p>
      <bold>Resultados</bold>
    </p>
    <p>Os valores dos &#237;ndices obtidos do <italic>plot</italic> de Poincar&#233; para os volunt&#225;rios, antes, durante e ap&#243;s o fumo, s&#227;o apresentados na <xref ref-type="table" rid="aop00111tab01m">Tabela 1</xref>. Observaram-se valores de SD1 significantemente menores nos momentos Fumo e P&#243;s 1, em rela&#231;&#227;o ao Repouso e P&#243;s 2. O &#237;ndice SD2 mostrou-se significantemente menor em Fumo e P&#243;s 1 quando comparado a P&#243;s 2. A raz&#227;o SD1/SD2 apresentou valor significantemente menor em todos os momentos em rela&#231;&#227;o ao Repouso. Al&#233;m disso, o valor em Fumo foi tamb&#233;m significantemente menor do que em P&#243;s 2.</p>
    <p content-type="asset">
      <table-wrap id="aop00111tab01m">
        <graphic xlink:href="1678-4170-abc-96-02-0154-00013-gt01.jpg"/></table-wrap>
    </p>
    <p>Os valores do intervalo RR e dos &#237;ndices no DT e DF antes, durante e ap&#243;s o fumo podem ser visibilizados na <xref ref-type="table" rid="aop00111tab02m">Tabela 2</xref>. Observaram-se valores de intervalo RR, SDNN, RMSSD, LFms<sup>2</sup> e HFms<sup>2</sup> significantemente menores nos momentos Fumo e P&#243;s 1 em rela&#231;&#227;o ao Repouso e P&#243;s 2. Os valores de LFnu e raz&#227;o LF/HF apresentaram-se significantemente maiores, enquanto que HFnu mostrou-se significantemente menor no momento Fumo em rela&#231;&#227;o ao Repouso.</p>
    <p content-type="asset">
      <table-wrap id="aop00111tab02m">
        <graphic xlink:href="1678-4170-abc-96-02-0154-00013-gt02.jpg"/></table-wrap>
    </p>
    <p>A <xref ref-type="fig" rid="aop00111fig01">Figura 1</xref> mostra um exemplo da an&#225;lise qualitativa do <italic>plot</italic> de Poincar&#233; antes, durante e nos per&#237;odos analisados ap&#243;s o fumo. </p>
    <p><fig id="aop00111fig01"/>&#13;
&#160;&#13;
</p>
    <p>
      <fig id="aop00111fig01a">
        <graphic xlink:href="1678-4170-abc-96-02-0154-00013-gf01.jpg"/></fig>
    </p>
    <p>&#13;
  <fig id="aop00111fig01xfig1b"/><fig id="aop00111fig01b"><graphic xlink:href="1678-4170-abc-96-02-0154-00013-gf02.jpg"/></fig></p>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>Os resultados obtidos por meio dos &#237;ndices de VFC neste estudo mostraram que o fumo produziu modifica&#231;&#245;es nos &#237;ndices de VFC de forma aguda, caracterizada por diminui&#231;&#227;o da atividade parassimp&#225;tica e aumento da simp&#225;tica, e recupera&#231;&#227;o destes &#237;ndices, 30 minutos ap&#243;s o fumo. </p>
    <p>An&#225;lises dos &#237;ndices do <italic>plot</italic> de Poincar&#233; mostraram que a modula&#231;&#227;o vagal, representada pelo &#237;ndice SD1<sup>29</sup>, e a raz&#227;o SD1/SD2 apresentaram redu&#231;&#227;o significante durante o fumo em compara&#231;&#227;o com o repouso, indicando redu&#231;&#227;o da VFC nesses indiv&#237;duos (<xref ref-type="table" rid="aop00111tab01m">Tabela 01</xref>). Redu&#231;&#245;es nos &#237;ndices lineares RMSSD e HF, em unidades normalizadas e ms<sup>2</sup>, tamb&#233;m ocorreram durante o per&#237;odo de fumo, al&#233;m do aumento da rela&#231;&#227;o LF/HF, confirmando a redu&#231;&#227;o na atividade parassimp&#225;tica observada pelos &#237;ndices extra&#237;dos do <italic>plot</italic> (<xref ref-type="table" rid="aop00111tab02m">Tabela 02</xref>).</p>
    <p>Redu&#231;&#227;o na modula&#231;&#227;o vagal durante o tabagismo foi tamb&#233;m observada por Karakaya e cols.<sup>11</sup>, os quais avaliaram os efeitos agudos do fumo em 15 volunt&#225;rios n&#227;o fumantes sobre &#237;ndices de VFC e observaram mudan&#231;as dos &#237;ndices no DT e DF, particularmente nos 5-10 minutos imediatamente ap&#243;s o ato de fumar, caracterizadas por redu&#231;&#227;o dos &#237;ndices SDNN, RMSSD e HF e aumento do &#237;ndice LF. Nabors-Oberg e cols.<sup>30</sup> igualmente verificaram redu&#231;&#227;o de HF durante o tabagismo. Essas altera&#231;&#245;es parassimp&#225;ticas parecem estar relacionadas aos efeitos do fumo sobre a automaticidade do n&#243; sinusal<sup>31</sup>.</p>
    <p>Os intervalos RR apresentaram-se reduzidos durante o fumo em compara&#231;&#227;o ao per&#237;odo de repouso, al&#233;m disso, houve aumento dos &#237;ndices LFnu e da raz&#227;o LF/HF (<xref ref-type="table" rid="aop00111tab02m">Tabela 02</xref>), sugerindo que durante o fumo, associado &#224; redu&#231;&#227;o da atividade parassimp&#225;tica, ocorreu aumento da atividade simp&#225;tica. Kobayashi e cols.<sup>32</sup> observaram aumento da raz&#227;o LF/HF dentro de 5 minutos ap&#243;s fumar. Esses achados tamb&#233;m est&#227;o em concord&#226;ncia com os estudos de Narkiewikz e cols.<sup>9</sup> e Gerhardt e cols.<sup>10</sup>, que observaram aumento da modula&#231;&#227;o simp&#225;tica durante o fumo.</p>
    <p>O &#237;ndice SD2, caracter&#237;stico de modula&#231;&#227;o auton&#244;mica global, apresentou, durante o fumo, valores inferiores aos encontrados em repouso (<xref ref-type="table" rid="aop00111tab01m">Tabela 01</xref>), o mesmo ocorreu com o &#237;ndice SDNN e LF em ms<sup>2</sup> (<xref ref-type="table" rid="aop00111tab02m">Tabela 02</xref>). </p>
    <p>A an&#225;lise qualitativa (visual) do <italic>plot</italic> tamb&#233;m evidenciou o efeito agudo do fumo e aponta redu&#231;&#227;o da VFC nos fumantes. O gr&#225;fico do <italic>plot</italic> de Poincar&#233; mostra uma diminui&#231;&#227;o na dispers&#227;o dos pontos nos momentos Fumo e P&#243;s 1 (<xref ref-type="fig" rid="aop00111fig01">Figuras 1B</xref> e <xref ref-type="fig" rid="aop00111fig01">1C</xref>) em rela&#231;&#227;o aos momentos Repouso e P&#243;s 2 (<xref ref-type="fig" rid="aop00111fig01">Figuras 1A</xref> e <xref ref-type="fig" rid="aop00111fig01">1D</xref>). Esse padr&#227;o gr&#225;fico, segundo a literatura, demonstra um aumento da atividade simp&#225;tica e, consequente, redu&#231;&#227;o de VFC<sup>5,33</sup>.</p>
    <p>Os efeitos agudos do tabagismo s&#227;o atribu&#237;dos principalmente &#224; a&#231;&#227;o da nicotina que se liga a receptores colin&#233;rgicos nicot&#237;nicos presentes nos g&#226;nglios auton&#244;micos, jun&#231;&#245;es neuromusculares e sistema nervoso central, os quais, quando estimulados, aumentam a libera&#231;&#227;o de v&#225;rios neurotransmissores<sup>34,35</sup>. A nicotina e outras subst&#226;ncias do cigarro estimulam tamb&#233;m a libera&#231;&#227;o de adrenalina e noradrenalina no sistema nervoso simp&#225;tico (SNS). Adicionalmente, a estimula&#231;&#227;o de receptores nicot&#237;nicos no SNA foi relacionada aos efeitos excitat&#243;rios simp&#225;ticos do tabagismo<sup>36</sup>.</p>
    <p>Existem tr&#234;s poss&#237;veis mecanismos que explicam essa ativa&#231;&#227;o simp&#225;tica. A primeira seria um efeito direto no sistema nervoso central; a segunda, um efeito estimulat&#243;rio na transmiss&#227;o simp&#225;tica ganglionar que leva a um subsequente aumento na atividade simp&#225;tica eferente p&#243;s-ganglionar; e a terceira, um efeito sobre as termina&#231;&#245;es nervosas simp&#225;ticas perif&#233;ricas<sup>34,37</sup>. Para Grassi e cols.<sup>38</sup>, al&#233;m da estimula&#231;&#227;o adren&#233;rgica perif&#233;rica, h&#225; uma perda parcial da habilidade barorreflexa em cont&#234;-la.</p>
    <p>No per&#237;odo de recupera&#231;&#227;o, a an&#225;lise dos &#237;ndices obtidos pelo <italic>plot</italic> de Poincar&#233; evidenciou aumento da modula&#231;&#227;o vagal avaliada pelo &#237;ndice SD1, atingindo, no per&#237;odo P&#243;s 2, valores pr&#243;ximos aos de repouso. O &#237;ndice SD2 retornou aos valores basais ao final do per&#237;odo estudado, enquanto que a raz&#227;o SD1/SD2 permaneceu reduzida no decorrer dos 30 minutos p&#243;s-fumo (<xref ref-type="table" rid="aop00111tab01m">Tabela 01</xref>). A redu&#231;&#227;o da raz&#227;o SD1/SD2 deve-se ao aumento pronunciado do &#237;ndice SD2.</p>
    <p>Quanto &#224; an&#225;lise qualitativa do <italic>plot,</italic> as altera&#231;&#245;es observadas durante o fumo persistiram durante o per&#237;odo imediatamente ap&#243;s (P&#243;s 1), com recupera&#231;&#227;o e padr&#227;o bastante semelhante ao repouso no per&#237;odo P&#243;s 2 (<xref ref-type="fig" rid="aop00111fig01">Figura 1 D</xref>).</p>
    <p>Essa recupera&#231;&#227;o tamb&#233;m foi observada em todos os &#237;ndices lineares de VFC no decorrer dos 30 minutos que sucederam o fumo (<xref ref-type="table" rid="aop00111tab02m">Tabelas 02</xref>), o que vem corroborar com os achados de Hayano e cols.<sup>12</sup>, que estudaram fumantes jovens e observaram um aumento na FC, um decr&#233;scimo no &#237;ndice HF, tr&#234;s minutos ap&#243;s o fumo, e um aumento no &#237;ndice LF, 10 a 17 minutos ap&#243;s o fumo, com retorno aos valores iniciais ao fim de 24 minutos.</p>
    <p>A recupera&#231;&#227;o dos &#237;ndices de VFC pode estar relacionada ao fato de que, ap&#243;s fumar, ocorre um pico de concentra&#231;&#227;o de nicotina circulante, que declina rapidamente nos 20 minutos subsequentes, devido &#224; distribui&#231;&#227;o tecidual<sup>39</sup>, o que indica que as altera&#231;&#245;es induzidas pela nicotina no SNA podem ser amenizadas no decorrer desse tempo.</p>
    <p>Outros fatores podem tamb&#233;m ser citados para explicar a r&#225;pida recupera&#231;&#227;o p&#243;s-fumo e, neste sentido, a idade e as caracter&#237;sticas tabag&#237;sticas dos indiv&#237;duos estudados devem ser consideradas. Por se tratarem de jovens saud&#225;veis, supomos que o SNA est&#225; &#237;ntegro, o que garante o balan&#231;o simpato-vagal necess&#225;rio para manter a normalidade do controle auton&#244;mico card&#237;aco. Em rela&#231;&#227;o &#224;s caracter&#237;sticas tabag&#237;sticas, o baixo consumo de cigarros e tempo de tabagismo podem tamb&#233;m ter influenciado nestes resultados.</p>
    <p>O <italic>plot </italic>de Poincar&#233; &#233; uma t&#233;cnica que permite a visualiza&#231;&#227;o de todos os pontos descritos em uma s&#233;rie de intervalo RR consecutivos, bem como facilita a identifica&#231;&#227;o dos pontos anormais correspondentes a batimentos prematuros, pausas compensat&#243;rias ou artefatos t&#233;cnicos, o que permite f&#225;cil corre&#231;&#227;o da s&#233;rie RR para an&#225;lise da VFC. Essa visualiza&#231;&#227;o n&#227;o &#233; poss&#237;vel pela an&#225;lise espectral ou por m&#233;todos no DT, o que representa uma boa vantagem do <italic>plot</italic> de Poincar&#233; em rela&#231;&#227;o a estes m&#233;todos. O <italic>plot</italic> de Poincar&#233; permite a an&#225;lise de s&#233;ries de intervalos RR n&#227;o estacion&#225;rias<sup>25</sup> e fornece tanto informa&#231;&#245;es resumidas quanto detalhadas, batimento a batimento, do comportamento card&#237;aco<sup>40</sup>. Tais aspectos representam vantagens importantes da sua utiliza&#231;&#227;o em rela&#231;&#227;o aos m&#233;todos lineares de an&#225;lise, contudo, &#233; importante salientar que a medida direta da atividade auton&#244;mica poderia determinar se o <italic>plot </italic>de Poincar&#233; pode ser considerado um m&#233;todo mais sens&#237;vel para detectar altera&#231;&#245;es auton&#244;micas em compara&#231;&#227;o a tais m&#233;todos.</p>
    <p>Em resumo, os resultados deste trabalho mostraram que o tabagismo agudamente produziu modifica&#231;&#245;es nos &#237;ndices de VFC, caracterizadas por diminui&#231;&#227;o da atividade parassimp&#225;tica e aumento da simp&#225;tica, e recupera&#231;&#227;o destes &#237;ndices, 30 minutos ap&#243;s o fumo, as quais puderam ser avaliadas quantitativamente e qualitativamente pelo <italic>plot</italic> de Poincar&#233;.</p>
    <p>
      <bold>Conclus&#227;o</bold>
    </p>
    <p>As an&#225;lises dos &#237;ndices extra&#237;dos do <italic>plot</italic> de Poincar&#233; e dos &#237;ndices lineares nos DT e DF mostraram que o tabagismo produziu agudamente modifica&#231;&#245;es no controle auton&#244;mico card&#237;aco, caracterizadas pela diminui&#231;&#227;o da atividade parassimp&#225;tica e aumento da atividade simp&#225;tica, e recupera&#231;&#227;o destes &#237;ndices, 30 minutos ap&#243;s o fumo. Adicionalmente, o <italic>plot </italic>de Poincar&#233; mostrou-se um m&#233;todo sens&#237;vel e simples para detectar altera&#231;&#245;es agudas da VFC provocadas pelo tabagismo. </p>
    <p>
      <bold>Potencial Conflito de Interesses</bold>
    </p>
    <p>Declaro n&#227;o haver conflito 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>Este artigo &#233; parte de disserta&#231;&#227;o de Mestrado de Beatriz Martins Manzano pela Faculdade de Ci&#234;ncias e Tecnologia - FCT - UNESP.</p>
    <p>
      <fn id="ntb" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Beatriz Martins Manzano </p>
        <p> Rua Jos&#233; Bonif&#225;cio Mori, 239 - Centro </p>
        <p> 19200-000 - Pirapozinho, SP - Brasil </p>
        <p> E-mail: </p>
        <p><email xlink:href="biamanzano@hotmail.com">biamanzano@hotmail.com</email>, </p>
        <p>
          <email xlink:href="bia_mmanzano@yahoo.com.br">bia_mmanzano@yahoo.com.br</email>
        </p>
      </fn>
    </p>
    <p> Artigo recebido em 11/01/10;revisado recebido em 23/05/10; aceito em 06/08/10.</p>
  </body>
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  <sub-article article-type="translation" id="TRes" xml:lang="es">
    <front-stub>
      <article-categories/>
      <title-group>
        <article-title xml:lang="es">Efectos agudos del tabaquismo sobre la modulaci&#243;n auton&#243;mica: an&#225;lisis por medio del plot de Poincar&#233;</article-title>
      </title-group>
      <abstract xml:lang="es">
        <p>FUNDAMENTO: El tabaquismo altera la funci&#243;n auton&#243;mica. OBJETIVO: Investigar los efectos agudos del tabaquismo sobre la modulaci&#243;n auton&#243;mica y la recuperaci&#243;n de los &#237;ndices de variabilidad de frecuencia card&#237;aca (VFC) post tabaco, por medio del plot de Poincar&#233; e &#237;ndices lineales. M&#201;TODOS: Fueron evaluados 25 fumantes j&#243;venes, los cuales tuvieron la frecuencia card&#237;aca analizada, latido a latido, en la posici&#243;n sentada, despu&#233;s de 8 horas de abstinencia, por 30 minutos en reposo, 20 minutos durante el tabaco y 30 minutos post tabaco. An&#225;lisis de varianza para medidas repetidas, seguido del test de Tukey, o test de Friedman seguido del test de Dunn fueron aplicados dependiendo de la normalidad de los datos, con p &lt; 0,05. RESULTADOS:: Durante el tabaco, hubo reducci&#243;n de los &#237;ndices SD1 (23,4 &#177; 9,2 vs 13,8 &#177; 4,8), raz&#243;n SD1/SD2 (0,31 &#177; 0,08 vs 0,2 &#177; 0,04), RMSSD (32,7 &#177; 13 vs 19,1 &#177; 6,8), SDNN (47,6 &#177; 14,8 vs 35,5 &#177; 8,4), HFnu (32,5 &#177; 11,6 vs 19 &#177; 8,1) y del intervalo RR (816,8 &#177; 89 vs 696,5 &#177; 76,3) en relaci&#243;n al reposo, mientras que aumentos del &#237;ndice LFnu (67,5 &#177; 11,6 vs 81 &#177; 8,1) y de la raz&#243;n LF/HF (2,6 &#177; 1,7 vs 5,4 &#177; 3,1) fueron observados. El an&#225;lisis visual del plot mostr&#243; menor dispersi&#243;n de los intervalos RR durante el tabaco. Con excepci&#243;n de la raz&#243;n SD1/SD2, los dem&#225;s &#237;ndices presentaron recuperaci&#243;n de los valores, 30 minutos despu&#233;s del tabaquismo. CONCLUSI&#211;N: El tabaquismo produjo agudamente modificaciones en el control auton&#243;mico, caracterizadas por activaci&#243;n simp&#225;tica y retirada vagal, con recuperaci&#243;n 30 minutos despu&#233;s del tabaco.</p>
      </abstract>
      <kwd-group xml:lang="es">
        <kwd>Tabaquismo</kwd>
        <kwd>sistema nervioso aut&#243;nomo</kwd>
        <kwd>frecuencia card&#237;aca</kwd>
        <kwd>din&#225;mica no lineal</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ART&#205;CULO ORIGINAL</bold>
      </p>
      <p>
        <fn id="enda-body2">
          <label>
            <bold>Efectos agudos del tabaquismo sobre la modulaci&#243;n auton&#243;mica: an&#225;lisis por medio del <italic>plot</italic> de Poincar&#233;</bold>
          </label>
          <p>
            <bold>Beatriz Martins Manzano; Luiz Carlos Marques Vanderlei; Ercy Mara Ramos; Dionei Ramos</bold>
          </p>
        </fn>
      </p>
      <p> Faculdade de Ci&#234;ncias e Tecnologia - FCT- UNESP - Presidente Prudente, S&#227;o Paulo, SP - Brasil</p>
      <p>Correspondencia</p>
      <p>
        <bold>RESUMEN</bold>
      </p>
      <p><bold>FUNDAMENTO:</bold> El tabaquismo altera la funci&#243;n auton&#243;mica. </p>
      <p><bold>OBJETIVO:</bold> Investigar los efectos agudos del tabaquismo sobre la modulaci&#243;n auton&#243;mica y la recuperaci&#243;n de los &#237;ndices de variabilidad de frecuencia card&#237;aca (VFC) post tabaco, por medio del <italic>plot</italic> de Poincar&#233; e &#237;ndices lineales. </p>
      <p><bold>M&#201;TODOS:</bold> Fueron evaluados 25 fumantes j&#243;venes, los cuales tuvieron la frecuencia card&#237;aca analizada, latido a latido, en la posici&#243;n sentada, despu&#233;s de 8 horas de abstinencia, por 30 minutos en reposo, 20 minutos durante el tabaco y 30 minutos post tabaco. An&#225;lisis de varianza para medidas repetidas, seguido del test de Tukey, o test de Friedman seguido del test de Dunn fueron aplicados dependiendo de la normalidad de los datos, con p &lt; 0,05. </p>
      <p><bold>RESULTADOS:: </bold> Durante el tabaco, hubo reducci&#243;n de los &#237;ndices SD1 (23,4 &#177; 9,2 vs 13,8 &#177; 4,8), raz&#243;n SD1/SD2 (0,31 &#177; 0,08 vs 0,2 &#177; 0,04), RMSSD (32,7 &#177; 13 vs 19,1 &#177; 6,8), SDNN (47,6 &#177; 14,8 vs 35,5 &#177; 8,4), HFnu (32,5 &#177; 11,6 vs 19 &#177; 8,1) y del intervalo RR (816,8 &#177; 89 vs 696,5 &#177; 76,3) en relaci&#243;n al reposo, mientras que aumentos del &#237;ndice LFnu (67,5 &#177; 11,6 vs 81 &#177; 8,1) y de la raz&#243;n LF/HF (2,6 &#177; 1,7 vs 5,4 &#177; 3,1) fueron observados. El an&#225;lisis visual del plot mostr&#243; menor dispersi&#243;n de los intervalos RR durante el tabaco. Con excepci&#243;n de la raz&#243;n SD1/SD2, los dem&#225;s &#237;ndices presentaron recuperaci&#243;n de los valores, 30 minutos despu&#233;s del tabaquismo.</p>
      <p><bold>CONCLUSI&#211;N:</bold> El tabaquismo produjo agudamente modificaciones en el control auton&#243;mico, caracterizadas por activaci&#243;n simp&#225;tica y retirada vagal, con recuperaci&#243;n 30 minutos despu&#233;s del tabaco. (Arq Bras Cardiol 2010;96(2):154-160)</p>
      <p><bold>Palabras-clave:</bold> Tabaquismo, sistema nervioso aut&#243;nomo/efectos de drogas, frecuencia card&#237;aca, din&#225;mica no lineal. </p>
      <p>
        <bold>Introducci&#243;n</bold>
      </p>
      <p>Los efectos cr&#243;nicos del tabaco sobre la variabilidad de la frecuencia card&#237;aca (VFC), una medida no invasiva de los impulsos auton&#243;micos que indica la habilidad del coraz&#243;n para responder a los m&#250;ltiples est&#237;mulos fisiol&#243;gicos y ambientales, as&#237; como compensar des&#243;rdenes inducidos por enfermedades<sup>1-3</sup>, est&#225;n bien establecidos en la literatura que se&#241;ala hacia su reducci&#243;n en fumantes<sup>4,5</sup>. Tal condici&#243;n est&#225; asociada a la elevaci&#243;n del riesgo de mortalidad y susceptibilidad para arritmias con riesgo de vida<sup>6-8</sup> y para, en este sentido, estudiar condiciones que favorecen la reducci&#243;n de la VFC, es fundamental. </p>
      <p>Agudamente, se sabe que el humo de cigarrillo resulta en aumento de la presi&#243;n arterial, frecuencia card&#237;aca (FC), resistencia vascular, descarga simp&#225;tica y disminuci&#243;n de la actividad barorreflexa<sup>6,9,10</sup>, lo que puede alterar los &#237;ndices de VFC. Entre tanto, despu&#233;s de b&#250;squeda en la literatura t&#233;cnica pertinente para elaboraci&#243;n de esta investigaci&#243;n, los efectos agudos del tabaco de cigarrillo sobre &#237;ndices de VFC, principalmente el per&#237;odo inmediatamente posterior al acto de fumar, no han sido exhaustivamente estudiados y los trabajos que abordan el tema<sup>11,12</sup> lo hacen por medio de &#237;ndices lineales. </p>
      <p>Para evaluaci&#243;n de la VFC, m&#233;todos lineales, analizados tanto en el dominio del tiempo (DT) como en el dominio de la frecuencia (DF), y no lineales pueden ser utilizados<sup>2,13</sup>. El an&#225;lisis lineal es ampliamente utilizado para estudio del control auton&#243;mico en diversas condiciones, inclusive el tabaquismo, mientras tanto, recientemente, los m&#233;todos no lineales han despertado gran inter&#233;s, ya que describen las fluctuaciones complexas del ritmo y consiguen separar, en las series temporales de latidos card&#237;acos, estructuras de comportamiento no lineal m&#225;s adecuadamente que los m&#233;todos lineales<sup>14</sup>. Eso ha mostrado una nueva visi&#243;n sobre las anormalidades del comportamiento de la FC en varias condiciones, proveyendo informaciones pron&#243;sticas adicionales cuando fue comparada con los m&#233;todos tradicionales<sup>15,16</sup>. </p>
      <p>Uno de los m&#233;todos considerado por algunos autores como basado en la din&#225;mica no lineal es el <italic>plot</italic> de Poincar&#233;<sup>17,18</sup>, una t&#233;cnica cuantitativa visual, en la cual cada intervalo RR es correlacionado con el intervalo antecedente y define un punto en el <italic>plot</italic><sup>19</sup>, siendo considerada una de las m&#225;s importantes t&#233;cnicas utilizadas para representar visualmente la VFC y de gran importancia por su capacidad de evidenciar aspectos no lineales en una secuencia de datos<sup>20</sup>. </p>
      <p>As&#237;, con el prop&#243;sito de acrecentar a la literatura elementos relacionados al tema expuesto, se pretende, con este estudio, evaluar los efectos agudos del tabaquismo sobre el control auton&#243;mico card&#237;aco y la recuperaci&#243;n de los &#237;ndices de VFC post tabaco, por medio del <italic>plot</italic> de Poincar&#233;, juntamente con &#237;ndices de VFC en el DT y DF. </p>
      <p>
        <bold>M&#233;todos</bold>
      </p>
      <p>Para la realizaci&#243;n de este estudio, fueron analizados datos de 25 voluntarios j&#243;venes (16 hombres y 9 mujeres), seleccionados entre los participantes del Programa de Cesaci&#243;n del Tabaquismo de la Facultad de Ciencias y Tecnolog&#237;a - FCT/UNESP. Los voluntarios presentaron como caracter&#237;sticas edad media de 22,9 &#177; 3,2 a&#241;os, IMC de 23,7 &#177; 4,1 kg/m<sup>2</sup>, consumo de 10 cigarrillos/d&#237;a (mediana), tiempo de tabaquismo medio de 5,7 &#177; 4 a&#241;os, test de Fargerstr&#246;m predominante (52,0%) de cero a dos puntos, lo que corresponde a grado de dependencia muy bajo y niveles de mon&#243;xido de carbono (CO) expirado de 4,9 &#177; 2,4 ppm. </p>
      <p>No fueron incluidos en el estudio individuos que presentaron por lo menos una de las siguientes caracter&#237;sticas: uso de medicamentos que alterasen la actividad auton&#243;mica del coraz&#243;n, como por ejemplo, propranolol y atropina, etilistas e individuos con infecciones, enfermedades metab&#243;licas o del sistema cardiorrespiratorio conocidas, las cuales pudiesen interferir en el control auton&#243;mico card&#237;aco. </p>
      <p>Los voluntarios fueron debidamente informados sobre los procedimientos y objetivos del estudio, y un t&#233;rmino de consentimiento libre y aclarado fue firmado despu&#233;s de la concordancia en hacer parte del estudio. Todos los procedimientos utilizados fueron aprobados por el Comit&#233; de &#201;tica en Investigaci&#243;n de la Facultad de Ciencias y Tecnolog&#237;a - FCT/UNESP (protocolo 258/08) y siguieron la Resoluci&#243;n 196/96 del Consejo Nacional de Salud. </p>
      <p>
        <bold>Procedimientos</bold>
      </p>
      <p>El protocolo experimental fue realizado en una sala con temperatura entre 22&#186; y 24&#186; Celsius, humedad entre 40-60,0%, en el mismo per&#237;odo del d&#237;a (entre 8 y 12 h), para amenizar posibles influencias del ciclo circadiano. Previamente, todos los voluntarios fueron orientados a abstenerse de cafe&#237;na, actividad f&#237;sica y cigarrillo, por al menos 8 horas antes del estudio. La confirmaci&#243;n del per&#237;odo de abstinencia del tabaco fue realizada por medio de la captaci&#243;n de los niveles de CO utilizando el aparato monox&#237;metro Micro CO (<italic>Micro Medical Limited</italic>, Rochester, Inglaterra). Individuos con valores iguales o menores a 10 ppm<sup>21 </sup>fueron aceptados como abstinentes. </p>
      <p>La colecta de los datos antropom&#233;tricos (peso y altura), historia tab&#225;quica, antecedentes de salud y medicaci&#243;n en uso, adem&#225;s del grado de dependencia y consumo tab&#225;quico, a trav&#233;s del cuestionario de Fagerstr&#246;m, tambi&#233;n antecedi&#243; el protocolo experimental. </p>
      <p>Despu&#233;s de tales procedimientos, fue colocada en el t&#243;rax de los voluntarios, en el tercio distal del estern&#243;n, la cinta de captaci&#243;n y, en la mu&#241;eca de los mismos, el receptor de frecuencia card&#237;aca Polar S810i (Polar Electro, Finlandia), equipamiento previamente validado para captaci&#243;n de la FC, latido a latido, y utilizaci&#243;n de sus datos para c&#225;lculos de los &#237;ndices de VFC<sup>22,23</sup>. Los voluntarios fueron posicionados sentados y orientados a permanecer en reposo, sin movimientos de gran amplitud y sin conversar durante la colecta que fue realizada de forma individual. </p>
      <p>La colecta tuvo una duraci&#243;n de 80 minutos continuos y estuvo constituida por tres momentos: 1) Reposo - los voluntarios permanecieron en reposo con respiraci&#243;n espont&#225;nea por 30 minutos; 2) Tabaco - fue solicitado que fumaran dos cigarrillos rutinariamente consumidos por los individuos, en un tiempo de aproximadamente 20 minutos; y 3) Post tabaco - al terminar de fumar, los voluntarios permanecieron nuevamente en reposo, con respiraci&#243;n espont&#225;nea 30 minutos m&#225;s. </p>
      <p>Para an&#225;lisis de la VFC, el est&#225;ndar de su comportamiento fue registrado latido a latido, durante todo el protocolo, con una tasa de muestreo de 1.000 Hz. El an&#225;lisis de los datos fue realizado utilizando los primeros 1.000 intervalos RR consecutivos, despu&#233;s del filtrado digital por el <italic>software Polar Precision Performance SW</italic> (versi&#243;n 4.01.029) complementada por manual, para eliminaci&#243;n de latidos ect&#243;picos prematuros y artefactos, y solamente las series con m&#225;s de 95,0% de latidos sinusales fueron incluidas en el estudio<sup>24</sup>. </p>
      <p>El per&#237;odo de reposo fue evaluado utilizando los 10 primeros minutos para estabilizaci&#243;n de los par&#225;metros hemodin&#225;micos y la FC registrada en este per&#237;odo fue descartada para an&#225;lisis. El momento post tabaco fue dividido en dos per&#237;odos de 15 minutos denominados Post 1 y Post 2. </p>
      <p>
        <bold>An&#225;lisis del <italic>plot</italic> de Poincar&#233;</bold>
      </p>
      <p>Para an&#225;lisis no lineal, fue utilizado el <italic>plot</italic> de Poincar&#233;, gr&#225;fico en que cada intervalo RR es registrado en funci&#243;n del intervalo RR previo, o sea, la duraci&#243;n de un intervalo (RR<sub>n</sub>) es representada en el eje "x" y la duraci&#243;n del intervalo siguiente (RR<sub>n+1</sub>) en el eje "y", de forma de que cada punto (RR<sub>n</sub>, RR<sub>n+1</sub>) en el gr&#225;fico corresponde a dos latidos sucesivos<sup>25</sup>. </p>
      <p>Para an&#225;lisis cuantitativo del <italic>plot, </italic>por el ajuste de la elipse de la figura formada por el atractor, fueron calculados los siguientes &#237;ndices: SD1 (desviaci&#243;n est&#225;ndar de la variabilidad instant&#225;nea latido a latido), SD2 (desviaci&#243;n est&#225;ndar a largo plazo de los intervalos RR continuos) y la raz&#243;n SD1/SD2<sup>1,15</sup>. </p>
      <p>El an&#225;lisis cualitativo del <italic>plot </italic>fue hecho por medio del an&#225;lisis de las figuras formadas por su atractor, las cuales fueron descriptas por Tulppo et al<sup>26</sup>. Fueron considerados los siguientes est&#225;ndares: figuras con aumento en la dispersi&#243;n de los intervalos RR fueron consideradas caracter&#237;sticas de un <italic>plot</italic> normal, y figuras con peque&#241;a dispersi&#243;n global, latido a latido y sin aumento de la dispersi&#243;n de los intervalos RR, a largo plazo. </p>
      <p>
        <bold>An&#225;lisis lineal de la VFC</bold>
      </p>
      <p>La VFC fue tambi&#233;n analizada por medio de m&#233;todos lineales, en el DT y en el DF. En el DT, fueron utilizados los &#237;ndices RMSSD que corresponden a la ra&#237;z cuadrada de la media del cuadrado de las diferencias entre los intervalos RR normales adyacentes, expresado en milisegundos (ms)<sup>27</sup> y el SDNN que representa la desviaci&#243;n est&#225;ndar de la media de todos los intervalos RR normales, expresado en ms<sup>16</sup>. </p>
      <p>Para an&#225;lisis de la VFC en el DF, fueron utilizados los componentes espectrales de baja frecuencia (LF, 0,04-015 Hz) y alta frecuencia (HF, 0,15-0,40 Hz), en unidades normalizadas y en ms<sup>2</sup>, y la raz&#243;n entre estos componentes (LF/HF), que representa el valor relativo de cada componente espectral en relaci&#243;n a la potencia total, menos los componentes de muy baja frecuencia (VLF). El an&#225;lisis espectral fue calculado usando el algoritmo de la Transformada R&#225;pida de Fourier<sup> 2</sup>. </p>
      <p>Datos de la duraci&#243;n de los intervalos RR fueron tambi&#233;n analizados y para c&#225;lculo de los &#237;ndices de VFC fue utilizado el <italic>software HRV analysis </italic><sup>28</sup>. </p>
      <p>
        <bold>An&#225;lisis de los datos</bold>
      </p>
      <p>Para caracterizaci&#243;n del perfil de la muestra, fue utilizada estad&#237;stica descriptiva, siendo representados los siguientes datos: valores de media, desviaci&#243;n est&#225;ndar, mediana e intervalos de confianza a 95,0%. La normalidad de los datos fue determinada por medio del test Shapiro-Wilk. </p>
      <p>Para an&#225;lisis de los momentos de reposo, tabaco y post tabaco, cuando los datos presentaron distribuci&#243;n normal, fue aplicado an&#225;lisis de varianza para medidas repetidas, seguido de la aplicaci&#243;n del test de Tukey (variable SDNN). En los datos que no presentaron normalidad, fue aplicado el test de Friedman para medidas repetidas seguido de la aplicaci&#243;n del test de Dunn (variables: intervalo RR, RMSSD, LFnu, HFnu, LFms<sup>2</sup>, HFms<sup>2</sup>, LF/HF, SD<sup>1</sup>, SD<sup>2</sup>, SD<sup>1</sup>/SD<sup>2</sup>). Las diferencias en esos tests fueron consideradas estad&#237;sticamente significativas cuando el valor de "(p"( fue menor que 0,05. </p>
      <p>El c&#225;lculo del poder del estudio (<italic>Software GraphPad StatMate version 2.00 for Windows, GraphPad Software</italic>, San Diego California USA), con el n&#250;mero de voluntarios analizados y nivel de significaci&#243;n de 5,0% (test bicaudal), garantiz&#243; un poder del test superior a 80,0% para detectar diferencias entre las variables. </p>
      <p>
        <bold>Resultados</bold>
      </p>
      <p>Los valores de los &#237;ndices obtenidos del <italic>plot</italic> de Poincar&#233; para los voluntarios, antes, durante y despu&#233;s del tabaco, son presentados en la <xref ref-type="table" rid="es_a11tab01m-body2">Tabla 1</xref>. Se observaron valores de SD1 significativamente menores en los momentos Tabaco y Post 1, en relaci&#243;n al Reposo y Post 2. El &#237;ndice SD2 se mostr&#243; significativamente menor en Tabaco y Post 1 cuando fue comparado a Post 2. La raz&#243;n SD1/SD2 present&#243; valor significativamente menor en todos los momentos en relaci&#243;n al Reposo. Adem&#225;s de eso, el valor en Tabaco fue tambi&#233;n significativamente menor que en Post 2. </p>
      <p content-type="asset">
        <table-wrap id="es_a11tab01m-body2">
          <graphic xlink:href="1678-4170-abc-96-02-0154-00013-gt01-es.jpg"/></table-wrap>
      </p>
      <p>Los valores del intervalo RR y de los &#237;ndices en el DT y DF antes, durante y despu&#233;s del tabaco pueden ser visibilizados en la <xref ref-type="table" rid="es_a11tab02m-body2">Tabla 2</xref>. Se observaron valores de intervalo RR, SDNN, RMSSD, LFms<sup>2</sup> y HFms<sup>2</sup> significativamente menores en los momentos Tabaco y Post 1 en relaci&#243;n al Reposo y Post 2. Los valores de LFnu y raz&#243;n LF/HF se presentaron significativamente mayores, mientras que HFnu se mostr&#243; significativamente menor en el momento Tabaco en relaci&#243;n al Reposo. </p>
      <p content-type="asset">
        <table-wrap id="es_a11tab02m-body2">
          <graphic xlink:href="1678-4170-abc-96-02-0154-00013-gt02-es.jpg"/></table-wrap>
      </p>
      <p>La <xref ref-type="fig" rid="es_a11fig01-body2">Figura 1</xref> muestra un ejemplo del an&#225;lisis cualitativo del <italic>Plot</italic> de Poincar&#233; antes, durante y en los per&#237;odos analizados despu&#233;s del tabaco. </p>
      <p content-type="html"><fig id="es_a11fig01-body2"><graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/7THxLV7FzKDBCmbwNzFxgYf/2e8864dae423578b0097d14a28be26f1907990f3.jpg"/><graphic xlink:href="1678-4170-abc-96-02-0154-00013-gf01-es.jpg"/></fig>&#13;
&#160;&#13;
</p>
      <p>
        <bold>Discusi&#243;n</bold>
      </p>
      <p>Los resultados obtenidos por medio de los &#237;ndices de VFC en este estudio mostraron que el tabaco produjo modificaciones en los &#237;ndices de VFC de forma aguda, caracterizada por disminuci&#243;n de la actividad parasimp&#225;tica y aumento de la simp&#225;tica, y recuperaci&#243;n de estos &#237;ndices, 30 minutos despu&#233;s del tabaco. </p>
      <p>An&#225;lisis de los &#237;ndices del <italic>plot</italic> de Poincar&#233; mostraron que la modulaci&#243;n vagal, representada por el &#237;ndice SD1<sup>29</sup>, y la raz&#243;n SD1/SD2 presentaron reducci&#243;n significativa durante el tabaco en comparaci&#243;n con el reposo, indicando reducci&#243;n de la VFC en esos individuos (<xref ref-type="table" rid="es_a11tab01m-body2">Tabla 1</xref>). Reducciones en los &#237;ndices lineales RMSSD y HF, en unidades normalizadas y ms<sup>2</sup>, tambi&#233;n ocurrieron durante el per&#237;odo de tabaco, adem&#225;s de aumento de la relaci&#243;n LF/HF, confirmando la reducci&#243;n en la actividad parasimp&#225;tica observada por los &#237;ndices extra&#237;dos del <italic>plot</italic> (<xref ref-type="table" rid="es_a11tab02m-body2">Tabla 2</xref>). </p>
      <p>Reducci&#243;n en la modulaci&#243;n vagal durante el tabaquismo fue tambi&#233;n observada por Karakaya et al. <sup>11</sup>, los cuales evaluaron los efectos agudos del tabaco en 15 voluntarios no fumantes sobre &#237;ndices de VFC y observaron cambios de los &#237;ndices en el DT y DF, particularmente en los 5-10 minutos inmediatamente despu&#233;s del acto de fumar, caracterizados por reducci&#243;n de los &#237;ndices SDNN, RMSSD y HF y aumento del &#237;ndice LF. Nabors-Oberg et al. <sup>30</sup> igualmente verificaron reducci&#243;n de HF durante el tabaquismo. Esas alteraciones parasimp&#225;ticas parecen estar relacionadas a los efectos del tabaco sobre la automaticidad del nudo sinusal<sup>31</sup>. </p>
      <p>Los intervalos RR se presentaron reducidos durante el tabaco en comparaci&#243;n al per&#237;odo de reposo, adem&#225;s de eso, hubo aumento de los &#237;ndices LFnu y de la raz&#243;n LF/HF (<xref ref-type="table" rid="es_a11tab02m-body2">Tabla 02</xref>), sugiriendo que durante el tabaco, asociado a la reducci&#243;n de la actividad parasimp&#225;tica, ocurri&#243; aumento de la actividad simp&#225;tica. Kobayashi et al. <sup>32</sup> observaron aumento de la raz&#243;n LF/HF dentro de 5 minutos despu&#233;s de fumar. Esos hallazgos tambi&#233;n est&#225;n en concordancia con los estudios de Narkiewikz et al. <sup>9</sup> y Gerhardt et al. <sup>10</sup>, que observaron aumento de la modulaci&#243;n simp&#225;tica durante el tabaco. </p>
      <p>El &#237;ndice SD2, caracter&#237;stico de modulaci&#243;n auton&#243;mica global, present&#243;, durante el tabaco, valores inferiores a los encontrados en reposo (<xref ref-type="table" rid="es_a11tab01m-body2">Tabla 01</xref>), lo mismo ocurri&#243; con el &#237;ndice SDNN y LF en ms<sup>2</sup> (<xref ref-type="table" rid="es_a11tab02m-body2">Tabla 2</xref>). </p>
      <p>El an&#225;lisis cualitativo (visual) del <italic>plot</italic> tambi&#233;n evidenci&#243; el efecto agudo del tabaco y se&#241;ala reducci&#243;n de la VFC en los fumantes. El gr&#225;fico del <italic>plot</italic> de Poincar&#233; muestra una disminuci&#243;n en la dispersi&#243;n de los puntos en los momentos Tabaco y Post 1 (<xref ref-type="fig" rid="es_a11fig01-body2">Figuras 1B</xref> y <xref ref-type="fig" rid="es_a11fig01-body2">1C</xref>) en relaci&#243;n a los momentos Reposo y Post 2 (<xref ref-type="fig" rid="es_a11fig01-body2">Figuras 1A</xref> y <xref ref-type="fig" rid="es_a11fig01-body2">1D</xref>). Ese est&#225;ndar gr&#225;fico, seg&#250;n la literatura, demuestra un aumento de la actividad simp&#225;tica y, consecuente, reducci&#243;n de VFC<sup>5,33</sup>. </p>
      <p>Los efectos agudos del tabaquismo son atribuidos principalmente a la acci&#243;n de la nicotina que se liga a receptores colin&#233;rgicos nicot&#237;nicos presentes en los ganglios auton&#243;micos, junciones neuromusculares y sistema nervioso central, los cuales, cuando son estimulados, aumentan la liberaci&#243;n de varios neurotransmisores<sup>34,35</sup>. La nicotina y otras substancias del cigarrillo estimulan tambi&#233;n la liberaci&#243;n de adrenalina y noradrenalina en el sistema nervioso simp&#225;tico (SNS). Adicionalmente, la estimulaci&#243;n de receptores nicot&#237;nicos en el SNA fue relacionada a los efectos excitatorios simp&#225;ticos del tabaquismo<sup>36</sup>. </p>
      <p>Existen tres posibles mecanismos que explican esa activaci&#243;n simp&#225;tica. La primera ser&#237;a un efecto directo en el sistema nervioso central; la segunda, un efecto estimulatorio en la transmisi&#243;n simp&#225;tica ganglionar que lleva a un subsecuente aumento en la actividad simp&#225;tica eferente post ganglionar; y la tercera, un efecto sobre las terminaciones nerviosas simp&#225;ticas perif&#233;ricas<sup>34,37</sup>. Para Grassi et al. <sup>38</sup>, adem&#225;s de la estimulaci&#243;n adren&#233;rgica perif&#233;rica, hay una p&#233;rdida parcial de la habilidad barorrefleja para contenerla. </p>
      <p>En el per&#237;odo de recuperaci&#243;n, el an&#225;lisis de los &#237;ndices obtenidos por el <italic>plot</italic> de Poincar&#233; evidenci&#243; aumento de la modulaci&#243;n vagal evaluada por el &#237;ndice SD1, alcanzando, en el per&#237;odo Post 2, valores pr&#243;ximos a los de reposo. El &#237;ndice SD2 retorn&#243; a los valores basales al final del per&#237;odo estudiado, mientras que la raz&#243;n SD1/SD2 permaneci&#243; reducida en el transcurso de los 30 minutos post tabaco (<xref ref-type="table" rid="es_a11tab01m-body2">Tabla 01</xref>). La reducci&#243;n de la raz&#243;n SD1/SD2 se debe al aumento pronunciado del &#237;ndice SD2. </p>
      <p>En cuanto al an&#225;lisis cualitativo del <italic>plot,</italic> las alteraciones observadas durante el tabaco persistieron durante el per&#237;odo inmediatamente posterior (Post 1), con recuperaci&#243;n y est&#225;ndar bastante semejante al reposo en el per&#237;odo Post 2 (<xref ref-type="fig" rid="es_a11fig01-body2">Figura 1 D</xref>). </p>
      <p>Esa recuperaci&#243;n tambi&#233;n fue observada en todos los &#237;ndices lineales de VFC en el transcurso de los 30 minutos que sucedieron al tabaco (<xref ref-type="table" rid="es_a11tab02m-body2">Tablas 2</xref>), lo que viene a corroborar los hallazgos de Hayano et al. <sup>12</sup>, que estudiaron fumantes j&#243;venes y observaron un aumento en la FC, una disminuci&#243;n en el &#237;ndice HF, tres minutos despu&#233;s del tabaco, y un aumento en el &#237;ndice LF, 10 a 17 minutos despu&#233;s del tabaco, con retorno a los valores iniciales a los de 24 minutos. </p>
      <p>La recuperaci&#243;n de los &#237;ndices de VFC puede estar relacionada al hecho de que, despu&#233;s de fumar, ocurre un pico de concentraci&#243;n de nicotina circulante, que declina r&#225;pidamente en los 20 minutos subsecuentes, debido a la distribuci&#243;n tisular<sup>39</sup>, lo que indica que las alteraciones inducidas por la nicotina en el SNA pueden ser amenizadas en el transcurso de ese tiempo. </p>
      <p>Otros factores pueden tambi&#233;n ser citados para explicar la r&#225;pida recuperaci&#243;n post tabaco y, en este sentido, la edad y las caracter&#237;sticas tab&#225;quicas de los individuos estudiados deben ser consideradas. Por tratarse de j&#243;venes sanos, suponemos que el SNA est&#225; &#237;ntegro, lo que garantiza el balance simp&#225;tico vagal necesario para mantener la normalidad del control auton&#243;mico card&#237;aco. En relaci&#243;n a las caracter&#237;sticas tab&#225;quicas, el bajo consumo de cigarrillos y tiempo de tabaquismo pueden tambi&#233;n haber influenciado en estos resultados. </p>
      <p>El <italic>plot </italic>de Poincar&#233; es una t&#233;cnica que permite la visualizaci&#243;n de todos los puntos descriptos en una serie de intervalo RR consecutivos, as&#237; como facilita la identificaci&#243;n de los puntos anormales correspondientes a latidos prematuros, pausas compensatorias o artefactos t&#233;cnicos, lo que permite f&#225;cil correcci&#243;n de la serie RR para an&#225;lisis de la VFC. Esa visualizaci&#243;n no es posible por el an&#225;lisis espectral o por m&#233;todos en el DT, lo que representa una buena ventaja del <italic>plot</italic> de Poincar&#233; en relaci&#243;n a estos m&#233;todos. El <italic>plot</italic> de Poincar&#233; permite el an&#225;lisis de series de intervalos RR no estacionarios<sup>25</sup> y provee tanto informaciones resumidas como detalladas, latido a latido, del comportamiento card&#237;aco<sup>40</sup>. Tales aspectos representan ventajas importantes de su utilizaci&#243;n en relaci&#243;n a los m&#233;todos lineales de an&#225;lisis, con todo, es importante destacar que la medida directa de la actividad auton&#243;mica podr&#237;a determinar si el <italic>plot </italic>de Poincar&#233; puede ser considerado un m&#233;todo m&#225;s sensible para detectar alteraciones auton&#243;micas en comparaci&#243;n a tales m&#233;todos. </p>
      <p>En resumen, los resultados de este trabajo mostraron que el tabaquismo agudamente produjo modificaciones en los &#237;ndices de VFC, caracterizadas por disminuci&#243;n de la actividad parasimp&#225;tica y aumento de la simp&#225;tica, y recuperaci&#243;n de estos &#237;ndices, 30 minutos despu&#233;s del tabaco, las cuales pudieron ser evaluadas cuantitativamente y cualitativamente por el <italic>plot</italic> de Poincar&#233;. </p>
      <p>
        <bold>Conclusi&#243;n</bold>
      </p>
      <p>Los an&#225;lisis de los &#237;ndices extra&#237;dos del <italic>plot</italic> de Poincar&#233; y de los &#237;ndices lineales en los DT y DF mostraron que el tabaquismo produjo agudamente modificaciones en el control auton&#243;mico card&#237;aco, caracterizadas por la disminuci&#243;n de la actividad parasimp&#225;tica y aumento de la actividad simp&#225;tica, y recuperaci&#243;n de estos &#237;ndices, 30 minutos despu&#233;s del tabaco. Adicionalmente, el <italic>plot </italic>de Poincar&#233; se mostr&#243; como un m&#233;todo sensible y simple para detectar alteraciones agudas de la VFC provocadas por el tabaquismo. </p>
      <p>
        <bold>Potencial Conflicto de Intereses</bold>
      </p>
      <p>Declaro no haber conflicto de intereses pertinentes. </p>
      <p>
        <bold>Fuentes de Financiamiento</bold>
      </p>
      <p>El presente estudio no tuvo fuentes de financiamiento externas. </p>
      <p>
        <bold>Vinculaci&#243;n Acad&#233;mica</bold>
      </p>
      <p>Este art&#237;culo es parte de disertaci&#243;n de Maestr&#237;a de Beatriz Martins Manzano por la Facultad de Ciencias y Tecnolog&#237;a - FCT - UNESP. </p>
      <p>
        <bold>Referencias</bold>
      </p>
    </body>
  </sub-article>
  <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">Acute effects of smoking on autonomic modulation: analysis by poincare plot</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>BACKGROUND: Smoking affects the autonomic function. OBJECTIVE:To investigate the acute effects of smoking on the autonomic modulation and the post-smoking recovery of the heart rate variability (HRV) index through Poincare plot and linear indices. METHODS: A total of 25 young smokers underwent beat-to-beat analysis of heart rate in the sitting position after 8 hours of tobacco abstinence, for 30 minutes at rest, 20 minutes while smoking and 30 minutes after smoking. The analysis of variance for repeated measures, followed by Tukey's test or Friedman's test followed by Dunn's test, were applied depending on the normality of data, with p &lt; 0.05. RESULTS: While smoking, there was a decrease in the indices: SD1 (23.4 &#177; 9.2 vs 13.8 &#177; 4.8), SD1/SD2 ratio (0.31 &#177; 0.08 vs 0.2 &#177; 0.04), RMSSD (32,7 &#177; 13 vs 19.1 &#177; 6.8), SDNN (47.6 &#177; 14.8 vs 35.5 &#177; 8.4), HFnu (32,5 &#177; 11.6 vs 19 &#177; 8.1) and the RR interval (816.8 &#177; 89 vs 696.5 &#177; 76.3) in relation to the rest period, whereas increases in the LFnu index (67.5 &#177; 11.6 vs 81 &#177; 8.1) and the LF/HF ratio (2.6 &#177; 1.7 vs 5.4 &#177; 3.1) were observed. The visual analysis of the plot showed a lower dispersion of RR intervals while smoking. Except for the SD1/SD2 ratio, the other indices presented recovery of values 30 minutes after smoking. CONCLUSION: Smoking resulted in acute modifications of the autonomic control, characterized by sympathetic activation and vagal withdrawal, presenting recovery 30 minutes after smoking.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Smoking</kwd>
        <kwd>autonomic nervous system</kwd>
        <kwd>heart failure</kwd>
        <kwd>nonlinear dynamics</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <fn id="nta-body3">
          <label>
            <bold>Acute effects of smoking on autonomic modulation: analysis by poincare plot</bold>
          </label>
          <p>
            <bold>Beatriz Martins Manzano; Luiz Carlos Marques Vanderlei; Ercy Mara Ramos; Dionei Ramos</bold>
          </p>
        </fn>
      </p>
      <p>Faculdade de Ci&#234;ncias e Tecnologia - FCT - UNESP - Presidente Prudente, S&#227;o Paulo, SP - Brasil</p>
      <p>Mailing address</p>
      <p>
        <bold>ABSTRACT</bold>
      </p>
      <p><bold>BACKGROUND:</bold> Smoking affects the autonomic function.</p>
      <p><bold>OBJECTIVE:</bold> To investigate the acute effects of smoking on the autonomic modulation and the post-smoking recovery of the heart rate variability (HRV) index through Poincare plot and linear indices.</p>
      <p><bold>METHODS: </bold>A total of 25 young smokers underwent beat-to-beat analysis of heart rate in the sitting position after 8 hours of tobacco abstinence, for 30 minutes at rest, 20 minutes while smoking and 30 minutes after smoking. The analysis of variance for repeated measures, followed by Tukey's test or Friedman's test followed by Dunn's test, were applied depending on the normality of data, with p &lt; 0.05.</p>
      <p><bold>RESULTS: </bold>While smoking, there was a decrease in the indices: SD1 (23.4 &#177; 9.2 <italic>vs</italic> 13.8 &#177; 4.8), SD1/SD2 ratio (0.31 &#177; 0.08 <italic>vs</italic> 0.2 &#177; 0.04), RMSSD (32,7 &#177; 13 <italic>vs</italic> 19.1 &#177; 6.8), SDNN (47.6 &#177; 14.8 <italic>vs</italic> 35.5 &#177; 8.4), HFnu (32,5 &#177; 11.6 <italic>vs</italic> 19 &#177; 8.1) and the RR interval (816.8 &#177; 89 <italic>vs</italic> 696.5 &#177; 76.3) in relation to the rest period, whereas increases in the LFnu index (67.5 &#177; 11.6 <italic>vs</italic> 81 &#177; 8.1) and the LF/HF ratio (2.6 &#177; 1.7 <italic>vs</italic> 5.4 &#177; 3.1) were observed. The visual analysis of the plot showed a lower dispersion of RR intervals while smoking. Except for the SD1/SD2 ratio, the other indices presented recovery of values 30 minutes after smoking.</p>
      <p><bold>CONCLUSION: </bold>Smoking resulted in acute modifications of the autonomic control, characterized by sympathetic activation and vagal withdrawal, presenting recovery 30 minutes after smoking. (Arq Bras Cardiol. 2011; [online].ahead print, PP.0-0)</p>
      <p><bold>Keywords:</bold> Smoking; autonomic nervous system/drug effects; heart failure; nonlinear dynamics.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>The chronic effects of smoking on the heart rate variability (HRV), a noninvasive measurement of the autonomic impulses that indicate the capacity of the heart to respond to multiple physiological and environmental stimuli, as well as compensate disorders induced by diseases<sup>1-3</sup>, are well-established in the literature, which indicates its decrease in smokers<sup>4,5</sup>. Such condition is associated with the increase in the risk of mortality and potentially fatal arrhythmia susceptibility<sup>6-8</sup> and, therefore, studying the conditions that favor the decrease in HRV is of utmost importance. </p>
      <p>Acutely, it is known that cigarette smoking results in the increase in blood pressure (BP), heart rate (HR), vascular resistance, sympathetic discharge and in the decrease in baroreflex activity<sup>6,9,10</sup>, which can alter the HRV index. However, after a review of the technical literature pertinent to this research, studies on the acute effects of cigarette smoking on the HVR index, mainly during the period immediately after the act of smoking, are scarce and the studies that do analyze the issue<sup>11,12</sup>, do so through the use of linear indices. </p>
      <p>To evaluate the HRV, linear methods, analyzed in both the time domain (TD) and the frequency domain (FD), as well as non-linear ones, can be used<sup>2,13</sup>. The linear analysis is broadly used to study the autonomic control in several conditions, including smoking; however, recently the non-linear methods have been considered with great interest, as they describe the complex fluctuations of rhythm and can better discriminate, in the temporal series of heartbeats, non-linear behavior structures, when compared to the linear methods<sup>14</sup>. That has provided a new insight on the abnormalities of HR behavior in several conditions, supplying additional prognostic information when compared with the traditional methods<sup>15,16</sup>. </p>
      <p>One of the methods considered by some authors as based on non-linear dynamics is the Poincare plot<sup>17,18</sup>, a quantitative-visual technique, in which each RR interval is correlated with the preceding interval and defines a point in the plot<sup>19</sup>, being considered one of the most important techniques used to visually represent HRV and one of great importance for its capacity to disclose non-linear aspects in a sequence of data<sup>20</sup>. </p>
      <p>Thus, with the objective of adding more information on the aforementioned subject to the literature, the present study aimed at evaluating the acute effects of smoking on the cardiac autonomic control and the recovery of HRV indices after smoking, using a Poincare plot, together with the HRV indices at the TD and FD.</p>
      <p>
        <bold>Methods</bold>
      </p>
      <p>The present study analyzed the data of 25 young volunteers (16 men and 9 women), selected among the participants of the Smoking Cessation Program of <italic>Faculdade de Ci&#234;ncias e Tecnologia </italic>- FCT/UNESP. The volunteers' mean age was 22.9 &#177; 3.2 years, with a mean BMI of 23.7 &#177; 4.1 kg/m<sup>2</sup>; they smoked 10 cigarettes/day (median) and had been smoking for 5.7 &#177; 4 years. Fargerstr&#246;m's test score showed a predominance (52.0%) of zero to two points, which corresponds to a very low degree of dependence and expired carbon monoxide (CO) levels of 4.9 &#177; 2.4 ppm. Individuals that presented at least one of the following characteristics were excluded from the study: use of medications that could alter the cardiac autonomic activity, such as propranolol and atropine, alcohol consumers and individuals that presented known infections, metabolic or cardiorespiratory system diseases, which could interfere with the cardiac autonomic control. </p>
      <p>The volunteers were adequately informed on the procedures and objectives of the study and signed the Free and Informed Consent Form after agreeing to participate in the study. All procedures used in the study were approved by the Ethics Committee in Research of <italic>Faculdade de Ci&#234;ncias e Tecnologia </italic>- FCT/UNESP (protocol #258/08) and followed the norms established by Resolution 196/96 of the National Council of Health. </p>
      <p>
        <bold>Procedures</bold>
      </p>
      <p>The experimental protocol was carried out in a room of which temperature varied from 22&#186; and 24&#186; Celsius, with humidity levels between 40-60.0%, at the same period of the day (between 8AM and 12PM), to attenuate possible influences on the circadian rhythm. Previously, all participants had been advised to abstain from caffeine, physical activity and cigarette smoking for at least 8 hours before the study. Smoking abstinence was confirmed through the measurement of CO concentrations using a Micro CO monoximeter device (Micro Medical Limited, Rochester, England). Individuals presenting values <underline>&lt;</underline> 10 ppm<sup>21</sup> were accepted as being abstinent. </p>
      <p>The collection of anthropometric data (weight and height), history of smoking, health history and medication use, in addition to the degree of dependence and cigarette consumption, through Fagerstr&#246;m questionnaire, also preceded the experimental protocol. </p>
      <p>After such procedure, the chest strap with heartbeat sensor was placed on the volunteers' thorax, on the distal third of the sternum and a Polar S810i (Polar Electro, Finland), heart rate receptor device was placed around the wrist. The equipment had been previously validated for beat-to-beat HR monitoring and the resulting data were used to calculate the HRV indices<sup>22,23</sup>. The volunteers remained in the sitting position and were advised to rest, without high range-of-motion movements and without talking during the collection of data, which was carried out individually. </p>
      <p>The collection of data lasted 80 minutes, continuously and consisted of three moments: 1) Rest - the volunteers remained at rest with spontaneous breathing for 30 minutes; 2) Smoking period - the volunteers were asked to smoke two cigarettes of the brand routinely smoked by them, in approximately 20 minutes; and 3) Post-smoking period - after they had finished smoking, the volunteers once again remained at rest, with spontaneous breathing, for 30 minutes. </p>
      <p>For the analysis of the HRV, the pattern of its behavior was recorded beat-to-beat, throughout the protocol, with a sampling rate of 1,000 Hz. The analysis of the data was carried out using the first 1,000 consecutive RR intervals, after digital filtration using the Polar Precision Performance SW software (release 4.01.029) complemented by manual filtration, to eliminate premature ectopic beats and artifacts and only series with more than 95% of sinus beats were included in the study<sup>24</sup>. </p>
      <p>The rest period was evaluated using the first 10 minutes to stabilize the hemodynamic parameters and the HR recorded during this period was disregarded for the analysis. The post-smoking period was divided in two periods of 15 minutes each and called Post 1 and Post 2. </p>
      <p>
        <bold>Analysis of Poincare plot </bold>
      </p>
      <p>The Poincare plot, used for the non-linear analysis, is a chart in which each RR interval is recorded as a function of the previous RR interval, that is, the duration of one RR interval (RR<sub>n</sub>) is represented in the "x" axis and the duration of the following interval (RR<sub>n+1</sub>) in the "y" axis, so that each point (RR<sub>n</sub>, RR<sub>n+1</sub>) in the chart corresponds to two successive beats<sup>25</sup>. </p>
      <p>The following indices were calculated for the quantitative analysis of the plot, through the adjustment of the ellipse of the figure formed by the attractor: SD1 (standard deviation of the instantaneous variability of the beat-to-beat heart rate), SD2 (standard deviation of long-term continuous RR interval variability) and the SD1/SD2 ratio<sup>1,15</sup>. </p>
      <p>The qualitative analysis of the plotwas carried out through the analysis of the figures formed by its attractor, which were described by Tulppo et al<sup>26</sup>. The following patterns were considered: figures with increased dispersion of RR intervals were considered characteristic of a normal plot and figures with little global dispersion, beat-to-beat and without increased dispersion of RR intervals in the long term. </p>
      <p>
        <bold>Linear analysis of HRV</bold>
      </p>
      <p>The HRV was also analyzed through linear methods, in the TD and FD. In the TD, the RMSSD index, which corresponds to the root mean square of the difference between successive normal adjacent R-R intervals, expressed in milliseconds (ms)<sup>27</sup> and the SDNN index, which corresponds to the standard deviation of all normal sinus R-R intervals, expressed in ms<sup>16</sup>, were used. </p>
      <p>For the analysis of the HRV in the FD, the spectral components of low frequency (LF, 0.04-0.15 Hz) and high frequency (HF, 0.15-0.40 Hz) were used in normalized units and in ms<sup>2</sup>, as well as the ratio between these components (LF/HF), which represents the relative value of each spectral component in relation to the total potency, minus the components of very-low frequency (VLF). The spectral analysis was calculated using the fast Fourier transform (FFT) algorithm<sup>2</sup>. </p>
      <p>Data on the duration of the RR intervals were also analyzed and the HRV indices were calculated using the HRV analysis software<sup>28</sup>. </p>
      <p>
        <bold>Data analysis</bold>
      </p>
      <p>Descriptive statistics was used to characterize the sample profile, with the following data being represented: mean values, standard deviations, medians and 95% confidence intervals. The normality of data was determined using the Shapiro-Wilks test.</p>
      <p>The analysis of the rest, smoking and post-smoking periods, when the data presented normal distribution, was carried out through analysis of variance (ANOVA) for repeated measures, followed by Tukey's test (SDNN variable). For data that did not present a normal distribution, Friedman's test for repeated measures was used, followed by Dunn's test (variables: RR interval, RMSSD, LFnu, HFnu, LFms<sup>2</sup>, HFms<sup>2</sup>, LF/HF, SD1, SD2, SD1/SD2). The differences in these tests were considered statistically significant when p value was &lt; 0.05. </p>
      <p>The calculation of the study power (GraphPad StatMate Software, release 2.00 for Windows, GraphPad Software, San Diego, California, USA), with the number of volunteers analyzed and a level of significance of 5% (two-tailed test) guaranteed a test power &gt; 80% to detect differences between the variables. </p>
      <p>
        <bold>Results</bold>
      </p>
      <p>The values of the indices obtained through Poincare plot for the volunteers before, during and after smoking are shown in <xref ref-type="table" rid="en_aop00111tab01m-body3">Table 1</xref>. Significantly lower SD1 values were observed at the Smoking and Post 1 moments, when compared to the Rest and Post 2 moments. The SD2 index showed to be significantly lower at the Smoking and Post 1 moments when compared with the Post 2 moment. The SD1/SD2 ratio showed a significantly lower value in all moments when compared to the Rest moment. Additionally, the value in the Smoking moment was also significantly lower than in the Post 2 moment. </p>
      <p content-type="asset">
        <table-wrap id="en_aop00111tab01m-body3">
          <graphic xlink:href="1678-4170-abc-96-02-0154-00013-gt01-en.jpg"/></table-wrap>
      </p>
      <p>The RR interval values and the indices in the TD and FD before, during and after smoking are shown in <xref ref-type="table" rid="en_aop00111tab02m-body3">Table 2</xref>. Significantly lower RR interval, RR, SDNN, RMSSD, LFms<sup>2</sup> and HFms<sup>2 </sup>values are observed in the Smoking and Post 1 moments, when compared to the Rest and Post 2 moments. The LFnu and LF/HF ratio values were significantly higher, whereas the HFnu was significantly lower in the Smoking moment, when compared to the Rest moment. <xref ref-type="fig" rid="en_aop00111fig01-body3">Figure 1</xref> shows an example of qualitative analysis of the Poincare plot before, during and in the periods analyzed after smoking. </p>
      <p content-type="asset">
        <table-wrap id="en_aop00111tab02m-body3">
          <graphic xlink:href="1678-4170-abc-96-02-0154-00013-gt02-en.jpg"/></table-wrap>
      </p>
      <p content-type="html"><fig id="en_aop00111fig01-body3"><graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/7THxLV7FzKDBCmbwNzFxgYf/36b7a2aa65aae287743bef4bfc3548b107ed2f1c.jpg"/><graphic xlink:href="1678-4170-abc-96-02-0154-00013-gf01-en.jpg"/></fig>&#13;
&#160;&#13;
</p>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>The results obtained through the HRV indices in the present study showed that smoking resulted in acute modifications in the HRV indices, characterized by a decrease in the parasympathetic activity and increase in the sympathetic activity, as well as the recovery of these indices 30 minutes after smoking cessation. </p>
      <p>The analyses of the Poincare plot indices showed that the vagal modulation, represented by the index SD1<sup>29</sup> and the SD1/SD2 ratio presented a significant decrease during smoking, indicating a decrease in the HRV in these individuals (<xref ref-type="table" rid="en_aop00111tab01m-body3">Table 01</xref>). Decreases in the linear indices RMSSD and HF, in normalized units and ms<sup>2</sup>, also occurred during the smoking period, in addition to the increase in the LF/HF ratio, confirming the decrease in the parasympathetic activity demonstrated by the indices extracted from the plot (<xref ref-type="table" rid="en_aop00111tab02m-body3">Table 02</xref>). </p>
      <p>Decrease in the vagal modulation during smoking was also observed by Karakaya et al<sup>11</sup>, who evaluated the acute effects of smoking in 15 nonsmoker volunteers on HRV indices and observed changes in the TD and FD, particularly in the 5-10 minutes immediately after the act of smoking, characterized by a decrease in the SDNN, RMSSD and HF indices, as well as an increase in the LF index. Nabors-Oberg et al<sup>30</sup> equally verified a decrease in the HF index during smoking. These parasympathetic alterations seem to be related to the effects of smoking on the automaticity of the sinus node<sup>31</sup>.</p>
      <p>The RR intervals showed to be decreased during smoking in comparison with the rest period; moreover, there was an increase in the LFnu index and the LF/HF ratio (<xref ref-type="table" rid="en_aop00111tab02m-body3">Table 02</xref>), suggesting that during smoking, associated with the decrease in the parasympathetic activity, there was an increase in the sympathetic activity. Kobayashi et al<sup>32</sup> observed an increase in the LF/HF ratio within 5 minutes after smoking. These findings are also in agreement with the studies by Narkiewikz et al<sup>9</sup> and Gerhardt et al<sup>10</sup>, who observed an increase in the sympathetic modulation during smoking. </p>
      <p>The SD2 index, characteristic of global autonomic modulation, presented lower values during smoking when compared to those observed in the rest period (<xref ref-type="table" rid="en_aop00111tab01m-body3">Table 01</xref>) and the same occurred with the SDNN and LF indices in ms<sup>2</sup> (<xref ref-type="table" rid="en_aop00111tab02m-body3">Table 02</xref>). </p>
      <p>The qualitative analysis (visual) of the plot also demonstrated the acute effect of smoking and showed the decrease in the HRV in smokers. The Poincare plot chart shows a decrease in the dispersion of points at the Smoking and Post1 moments (<xref ref-type="fig" rid="en_aop00111fig01-body3">Figures 1B</xref> and <xref ref-type="fig" rid="en_aop00111fig01-body3">1C</xref>) when compared with the Rest and Post 2 moments (<xref ref-type="fig" rid="en_aop00111fig01-body3">Figures 1A</xref> and <xref ref-type="fig" rid="en_aop00111fig01-body3">1D</xref>). This chart pattern, according to the literature, demonstrates an increase in the sympathetic activity and, consequently, a decrease in the HRV<sup>5,33</sup>.</p>
      <p>The acute effects of smoking are attributed mainly to the action of nicotine that binds to nicotinic cholinergic receptors present in the autonomic ganglia, neuromuscular junctions and central nervous system, which, when stimulated, increase the release of several neurotransmitters<sup>34,35</sup>. The nicotine and others substances found in cigarettes also stimulate the release of adrenalin into the sympathetic nervous system (SNS). Additionally, the stimulation of the nicotinic receptors in the autonomic nervous system (ANS) has been associated with the sympathetic excitatory effects of smoking<sup>36</sup>. </p>
      <p>There are three possible mechanisms to explain this sympathetic activation. The first is a direct effect on the central nervous system; and the second is a stimulatory effect on the ganglionic sympathetic transmission that leads to a subsequent increase in the postganglionic efferent sympathetic activity; and the third, is an effect on the sympathetic peripheral nervous terminations<sup>34,37</sup>. For Grassi et al<sup>38</sup>, in addition to the peripheral adrenergic stimulation, there is a partial loss by baroreflex capacity to contain it. </p>
      <p>During the recovery period, the analysis of the indices obtained through the Poincare plot showed an increase in the vagal modulation evaluated through the SD1 index, reaching levels close to those observed in the Rest period at the Post 2 period. The SD2 index returned to basal levels at the end of the studied period, whereas the SD1/SD2 ratio remained decreased throughout the 30-minute period post-smoking (<xref ref-type="table" rid="en_aop00111tab01m-body3">Table 01</xref>). The decrease in the SD1/SD2 ratio is due to the marked increase in the SD2 index.</p>
      <p>As for the qualitative analysis of the plot, the alterations observed during smoking persisted throughout the period immediately after smoking (Post 1), with recovery and a pattern very similar to that observed in the Rest period in the Post 2 moment (<xref ref-type="fig" rid="en_aop00111fig01-body3">Figure 1D</xref>).</p>
      <p>This recovery was also observed in all linear indices of HRV throughout the 30-minute period that followed the act of smoking (<xref ref-type="table" rid="en_aop00111tab02m-body3">Table 02</xref>), which corroborates the findings by Hayano et al<sup>12</sup>, who studied young smokers and observed an increase in HR, a decrease in the HF index three minutes after smoking and an increase in the LF index 10 to 17 minutes after smoking, with values retuning to initial levels after 24 minutes. </p>
      <p>The recovery of the HRV indices might be related to the fact that, after smoking, there is a peak of circulating nicotine concentration, which rapidly declines during the subsequent 20 minutes due to tissue distribution<sup>39</sup>, indicating that the nicotine-induced effects on the ANS might be attenuated throughout time. </p>
      <p>Other factors can also be mentioned to explain the rapid post-smoking recovery and, in this sense, age and the smoking characteristics of the studied individuals must be taken into account. As the individuals are young and healthy, we suppose that the ANS is intact, which guarantees the sympathetic-vagal balance necessary to maintain the normality of the autonomic cardiac control. Regarding the smoking characteristics, the low consumption of cigarettes and time of smoking might also have influenced these results. </p>
      <p>The Poincare plot is a technique that allows the visualization of all points described in a series of consecutive RR intervals and also facilitates the identification of the abnormal points corresponding to premature beats, compensatory pauses or technical artifacts, which allows the easy correction of the RR series for the analysis of the HRV. This visualization is not possible through the spectral analysis or by the TD, which represents a good advantage of the Poincare plot in relation to these methods. </p>
      <p>The Poincare plot allows the analysis of series of non-stationary RR intervals<sup>25</sup> and provides both summarized and detailed information, beat-to-beat, of the cardiac behavior<sup>40</sup>. </p>
      <p>Such aspects represent important advantages of its use in relation to linear analysis methods; however, it is worth mentioning that the direct measurement of the autonomic activity can determine whether the Poincare plot can be considered a more sensitive method to detect autonomic alterations in comparison to such methods. </p>
      <p>In brief, the results of the present study show that smoking resulted in acute modifications in HRV indices, characterized by the decrease in the parasympathetic activity and increase in the sympathetic activity, as well as the recovery of these indices 30 minutes after smoking, which were evaluated quantitatively and qualitatively by Poincare plot. </p>
      <p>
        <bold>Conclusion</bold>
      </p>
      <p>The analyses of the indices extracted from the Poincare plot and the linear indices in the TD and FD showed that smoking resulted in acute modifications in the autonomic cardiac control, characterized by the decrease in the parasympathetic activity and increase in the sympathetic activity, as well as in the recovery of these indices 30 minutes after smoking. Additionally, the Poincare plot showed to be a sensitive and simple method to detect acute alterations in HRV caused by smoking. </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 of master submitted by Beatriz Martins Manzano, from <italic>Faculdade de Ci&#234;ncias e Tecnologia </italic>- FCT - UNESP.</p>
      <p>
        <bold>References</bold>
      </p>
    </body>
  </sub-article>
</article>
