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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">J695CQmw3BxJM94s78tgGZQ</article-id>
      <article-id pub-id-type="other">00012</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2009000900012</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(09)09300312</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2009000900012</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Artigos Originais</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>MAPA em portadores de DPOC com dessatura&#231;&#227;o no sono</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Aidar</surname>
            <given-names>Neila Anders</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Silva</surname>
            <given-names>M&#225;rcio Alberto Carvalho da</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Silva</surname>
            <given-names>C&#233;sar Augusto Melo e</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Ferreira J&#250;nior</surname>
            <given-names>Pedro Nery</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Tavares</surname>
            <given-names>Paulo</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">Bras&#237;lia</named-content>
          <named-content content-type="state">Distrito Federal</named-content>
        </addr-line>
        <institution content-type="orgname">Universidade de Bras&#237;lia</institution>
        <institution content-type="orgdiv1">Hospital Universit&#225;rio de Bras&#237;lia </institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>09</month>
        <year>2009</year>
      </pub-date>
      <volume>93</volume>
      <issue>3</issue>
      <fpage>275</fpage>
      <lpage>282</lpage>
      <history>
        <date date-type="accepted">
          <day>31</day>
          <month>10</month>
          <year>2008</year>
        </date>
        <date date-type="rev-recd">
          <day>28</day>
          <month>10</month>
          <year>2008</year>
        </date>
        <date date-type="received">
          <day>26</day>
          <month>06</month>
          <year>2008</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: A hipoxemia no per&#237;odo de sono pode, por mecanismo de ativa&#231;&#227;o simp&#225;tica, alterar a press&#227;o arterial. Poucos estudos demonstram os par&#226;metros press&#243;ricos em portadores de DPOC, que n&#227;o t&#234;m apn&#233;ia do sono, mas que dessaturam nesse per&#237;odo. OBJETIVOS: Analisar os par&#226;metros press&#243;ricos em pacientes com DPOC e dessatura&#231;&#227;o no sono, n&#227;o causada por apn&#233;ia. M&#201;TODOS: Treze pacientes com DPOC foram submetidos &#224; espirometria, gasometria arterial, polissonografia e MAPA para avalia&#231;&#227;o press&#243;rica. Quatorze pacientes sem DPOC foram submetidos &#224; espirometria, oximetria e MAPA. As an&#225;lises press&#243;ricas foram feitas tanto na vig&#237;lia quanto no sono. Os dois grupos foram constitu&#237;dos por pacientes sem antecedentes hipertensivos. RESULTADOS: Os dois grupos eram semelhantes em rela&#231;&#227;o &#224; idade, altura, peso e &#237;ndice de massa corporal. Houve diferen&#231;a significativa (p &lt; 0,05) entre os par&#226;metros press&#243;ricos nos per&#237;odos de vig&#237;lia, sono, 24 horas e descenso do sono. Observou-se valores press&#243;ricos maiores nos portadores de DPOC, exceto em n&#237;veis diast&#243;licos em vig&#237;lia, m&#225;ximos valores ao sono e nas 24 horas. O descenso do sono no grupo DPOC foi atenuado, enquanto no grupo controle foi fisiol&#243;gico, com menores valores press&#243;ricos. CONCLUS&#213;ES: Os resultados da press&#227;o arterial sist&#243;lica e diast&#243;lica se mostraram maiores no grupo DPOC do que no grupo controle. A signific&#226;ncia dessa afirma&#231;&#227;o ocorreu em todos os per&#237;odos aferidos, exceto em vig&#237;lia e nas 24 horas para n&#237;veis de press&#227;o diast&#243;lica. Pode-se concluir que, o grupo portador de DPOC com dessatura&#231;&#227;o no sono possui n&#237;veis de press&#227;o arterial significativamente maiores do que o grupo controle.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>Monitoriza&#231;&#227;o ambulatorial da press&#227;o arterial</kwd>
        <kwd>sono</kwd>
        <kwd>doen&#231;a pulmonar obstrutiva cr&#244;nica</kwd>
        <kwd>polissonografia</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>22</day>
        <month>10</month>
        <year>2009</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>ARTIGO ORIGINAL </p>
    <p> MAPEAMENTO AMBULATORIA DA PA (MAPA)</p>
    <p>MAPA em portadores de DPOC com dessatura&#231;&#227;o no sono</p>
    <p>
      <bold>Neila Anders Aidar; M&#225;rcio Alberto Carvalho da Silva; C&#233;sar Augusto Melo e Silva; Pedro Nery Ferreira J&#250;nior; Paulo Tavares</bold>
    </p>
    <p>Hospital Universit&#225;rio de Bras&#237;lia (HUB), da Universidade de Bras&#237;lia (UnB), Bras&#237;lia, DF, Brasil</p>
    <p>
      <xref ref-type="corresp" rid="end">Correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p><bold>FUNDAMENTO:</bold> A hipoxemia no per&#237;odo de sono pode, por mecanismo de ativa&#231;&#227;o simp&#225;tica, alterar a press&#227;o arterial. Poucos estudos demonstram os par&#226;metros press&#243;ricos em portadores de DPOC, que n&#227;o t&#234;m apn&#233;ia do sono, mas que dessaturam nesse per&#237;odo. </p>
    <p><bold>OBJETIVOS:</bold> Analisar os par&#226;metros press&#243;ricos em pacientes com DPOC e dessatura&#231;&#227;o no sono, n&#227;o causada por apn&#233;ia. </p>
    <p><bold>M&#201;TODOS:</bold> Treze pacientes com DPOC foram submetidos &#224; espirometria, gasometria arterial, polissonografia e MAPA para avalia&#231;&#227;o press&#243;rica. Quatorze pacientes sem DPOC foram submetidos &#224; espirometria, oximetria e MAPA. As an&#225;lises press&#243;ricas foram feitas tanto na vig&#237;lia quanto no sono. Os dois grupos foram constitu&#237;dos por pacientes sem antecedentes hipertensivos. </p>
    <p><bold>RESULTADOS:</bold> Os dois grupos eram semelhantes em rela&#231;&#227;o &#224; idade, altura, peso e &#237;ndice de massa corporal. Houve diferen&#231;a significativa (p &lt; 0,05) entre os par&#226;metros press&#243;ricos nos per&#237;odos de vig&#237;lia, sono, 24 horas e descenso do sono. Observou-se valores press&#243;ricos maiores nos portadores de DPOC, exceto em n&#237;veis diast&#243;licos em vig&#237;lia, m&#225;ximos valores ao sono e nas 24 horas. O descenso do sono no grupo DPOC foi atenuado, enquanto no grupo controle foi fisiol&#243;gico, com menores valores press&#243;ricos. </p>
    <p><bold>CONCLUS&#213;ES:</bold> Os resultados da press&#227;o arterial sist&#243;lica e diast&#243;lica se mostraram maiores no grupo DPOC do que no grupo controle. A signific&#226;ncia dessa afirma&#231;&#227;o ocorreu em todos os per&#237;odos aferidos, exceto em vig&#237;lia e nas 24 horas para n&#237;veis de press&#227;o diast&#243;lica. Pode-se concluir que, o grupo portador de DPOC com dessatura&#231;&#227;o no sono possui n&#237;veis de press&#227;o arterial significativamente maiores do que o grupo controle.</p>
    <p><bold>Palavras-chave:</bold> Monitoriza&#231;&#227;o ambulatorial da press&#227;o arterial, sono, doen&#231;a pulmonar obstrutiva cr&#244;nica, polissonografia.</p>
    <p>
      <bold>Introdu&#231;&#227;o</bold>
    </p>
    <p>A doen&#231;a pulmonar obstrutiva cr&#244;nica (DPOC) &#233; atualmente a quarta causa de mortalidade, cuja principal complica&#231;&#227;o correlaciona-se a eventos cardiovasculares<sup>1-3</sup>. A literatura demonstra que, no per&#237;odo de cinco anos, 48% das interna&#231;&#245;es de pacientes com DPOC ocorreram por complica&#231;&#245;es cardiovasculares e que, independente do g&#234;nero, idade e presen&#231;a do tabagismo, a DPOC duplica o risco cardiovascular<sup>1,2 </sup>. Os fatores que relacionam a DPOC aos eventos cardiovasculares ainda n&#227;o est&#227;o totalmente esclarecidos. Estudos demonstram que a inflama&#231;&#227;o sist&#234;mica cr&#244;nica e os dist&#250;rbios da regula&#231;&#227;o neuro-humoral podem estar envolvidos<sup>3-7</sup> e sugerem que pacientes portadores de DPOC cursam com hiperatividade simp&#225;tica, redu&#231;&#227;o do t&#244;nus vagal e disautonomia.</p>
    <p>A hipertens&#227;o arterial sist&#234;mica (HAS) &#233; uma doen&#231;a de alta preval&#234;ncia na popula&#231;&#227;o mundial<sup>8,9</sup>. A preval&#234;ncia de HAS aumenta com a eleva&#231;&#227;o na faixa et&#225;ria<sup>9</sup> na faixa et&#225;ria entre 60 e 69 anos, mais de 50% dessa popula&#231;&#227;o &#233; acometida por HAS. J&#225; na faixa et&#225;ria acima de 70 anos, a preval&#234;ncia de HAS aumenta para 75%. A mortalidade por doen&#231;a cardiovascular aumenta com a eleva&#231;&#227;o da press&#227;o arterial (PA)<sup>9,10</sup>. </p>
    <p>A literatura que correlaciona n&#237;veis press&#243;ricos em indiv&#237;duos portadores de DPOC com dados escassos e conflitantes, evidencia a necessidade de novos estudos para a elucida&#231;&#227;o do comportamento da press&#227;o arterial na vig&#234;ncia de dessatura&#231;&#227;o no sono e, sobretudo, as repercuss&#245;es em &#243;rg&#227;os-alvo. A monitoriza&#231;&#227;o ambulatorial da press&#227;o arterial (MAPA) &#233; o m&#233;todo diagn&#243;stico que permite essa an&#225;lise, possibilitando o conhecimento do perfil de varia&#231;&#227;o da press&#227;o arterial em vig&#237;lia e no sono<sup>11,12</sup>.</p>
    <p>O objetivo deste estudo &#233; avaliar o comportamento da press&#227;o arterial &#224;s 24 horas, mediante an&#225;lise dos par&#226;metros da MAPA, nos pacientes com DPOC e dessatura&#231;&#227;o no sono, n&#227;o causada por apn&#233;ia.</p>
    <p>
      <bold>Metodologia</bold>
    </p>
    <p>Trata-se de um estudo descritivo, do tipo transversal, com pacientes portadores de DPOC referenciados ao programa de reabilita&#231;&#227;o pulmonar do ambulat&#243;rio de pneumologia do Hospital Universit&#225;rio de Bras&#237;lia (HUB).</p>
    <p>
      <bold>Crit&#233;rios de inclus&#227;o</bold>
    </p>
    <p>Foram inclu&#237;dos 13 pacientes encaminhados ao referido programa, com diagn&#243;stico cl&#237;nico e funcional (espirom&#233;trico: VEF1/CVF abaixo de 0,70, p&#243;s-broncodilatador) de DPOC. O grupo controle foi constitu&#237;do de 14 volunt&#225;rios, n&#227;o portadores de DPOC (diagn&#243;stico cl&#237;nico e espirom&#233;trico). Os pacientes dos dois grupos n&#227;o tinham antecedentes de hipertens&#227;o arterial sist&#234;mica, n&#227;o faziam uso de medica&#231;&#227;o anti-hipertensiva, nem eram portadores de hipertens&#227;o de consult&#243;rio. Com a concord&#226;ncia em participar do estudo, assinaram o termo de consentimento livre e esclarecido.</p>
    <p>
      <bold>Crit&#233;rios de exclus&#227;o</bold>
    </p>
    <p>Ap&#243;s hist&#243;ria cl&#237;nica detalhada, exame f&#237;sico e eletrocardiograma de 12 deriva&#231;&#245;es, foram adotados os seguintes crit&#233;rios: Presen&#231;a de outra enfermidade pulmonar detect&#225;vel clinicamente; presen&#231;a de s&#237;ndrome da apn&#233;ia obstrutiva do sono (detectada pela polissonografia); presen&#231;a de insufici&#234;ncia em outro &#243;rg&#227;o ou sistema (insufici&#234;ncia renal, insufici&#234;ncia card&#237;aca e insufici&#234;ncia hep&#225;tica); presen&#231;a de hipertens&#227;o arterial sist&#234;mica; impossibilidade t&#233;cnica de realizar a MAPA de 24h; e presen&#231;a de condi&#231;&#245;es que afetem a fun&#231;&#227;o neuroauton&#244;mica (neuropatias, doen&#231;as psiqui&#225;tricas, diabetes mellitus, doen&#231;a autoimune, doen&#231;a de Parkinson). </p>
    <p>Os crit&#233;rios para defini&#231;&#227;o de Hipertens&#227;o arterial foram seguidos em conformidade &#224;s IV Diretrizes de MAPA<sup>11</sup>. S&#227;o considerados par&#226;metros de normalidade da MAPA: PA em 24 horas &lt; 130/ 80 mmHg; PA diurna &lt; 135/85 mmHg; e PA noturna &lt;120/70 mmHg. </p>
    <p>Os pacientes portadores de DPOC participantes do estudo foram submetidos &#224; avalia&#231;&#227;o cl&#237;nica detalhada. Em seguida, foram realizadas espirometria, gasometria arterial, polissonografia (PSG) e MAPA 24horas. Os pacientes do grupo controle tamb&#233;m foram submetidos &#224; avalia&#231;&#227;o cl&#237;nica detalhada, sendo em seguida, submetidos &#224; espirometria, oximetria de pulso em per&#237;odo correspondente a sono e MAPA 24 horas.</p>
    <p>
      <bold>Avalia&#231;&#227;o cl&#237;nica</bold>
    </p>
    <p>No grupo DPOC, com 13 pacientes, sendo oito (61%) masculinos, todos foram fumantes<sup>12</sup> e encontravam-se em uso de agonistas de receptores beta2-adren&#233;rgicos - seletivos para esses receptores, em formula&#231;&#227;o inalat&#243;ria com libera&#231;&#227;o direta no ponto de a&#231;&#227;o em vias a&#233;reas, fatores que levam &#224; diminui&#231;&#227;o dos efeitos colaterais extrapulmonares, especialmente os card&#237;acos, com menor possibilidade de influ&#234;ncia nas medi&#231;&#245;es de press&#227;o arterial -. No grupo controle, com 14 pacientes, seis (42%) eram masculinos, sem antecedentes de tabagismo. </p>
    <p>O &#237;ndice de massa corporal (IMC)<sup>13</sup> foi calculado pela divis&#227;o do peso (kg) pelo quadrado da altura (m). Os valores foram classificados em: &lt; 18,5 kg/m<sup>2</sup> (baixo peso); 18,5 a 24,9 kg/m<sup>2 </sup>(normal); 25 a 29,9 kg/m<sup>2 </sup>(sobrepeso) e <underline>&gt;</underline> 30 kg/m<sup>2</sup> (obesidade total).</p>
    <p>Para comparar os grupos DPOC e controle, testaram-se as m&#233;dias das medidas antropom&#233;tricas, a fim de controlar fatores que poderiam causar interfer&#234;ncias nos resultados das medidas da press&#227;o arterial e oxim&#233;tricas.</p>
    <p><italic>Espirometria</italic> &#150; Realizada nos dois grupos, com os pacientes sentados, sob uso de adaptador que obstru&#237;a a ventila&#231;&#227;o pelas narinas. A ventila&#231;&#227;o foi totalmente bucal, com o sistema fechado e o adaptador anat&#244;mico conectado &#224; cavidade oral e o sistema acoplado ao aparelho, seguindo as normas da <italic>American Thoracic Society</italic>. Para o procedimento, foi utilizado o aparelho Vmax<sup>&#174;</sup>-22 (s&#233;rie spirometer Sensor Medics Yorba Linda, Calif&#243;rnia, EUA, 2004).</p>
    <p><italic>Gasometria arterial</italic> &#150; Coleta de sangue da art&#233;ria radial, realizada apenas no grupo DPOC, para compara&#231;&#227;o com n&#237;veis de dessatura&#231;&#227;o no sono. Gas&#244;metro Ciba Corning 278 Gas System<sup>&#174;</sup> (Ciba Corning, Diagnostics Corp.; Medfield, USA, 2004).</p>
    <p><italic>Polissonografia</italic> - Realizada em apenas uma noite de sono, somente no grupo portador de DPOC, exame de noite inteira, no Laborat&#243;rio do Sono do Hospital Universit&#225;rio de Bras&#237;lia. A PSG foi realizada nesse grupo para afastar outras desordens do sono<sup>14</sup>, dentre as quais a s&#237;ndrome de apn&#233;ia do sono (SAOS), entidade nosol&#243;gica distinta de DPOC, tamb&#233;m causadora de hipoxemia noturna. A polissonografia foi realizada conforme crit&#233;rios estabelecidos por Rechtschaffen e Kales<sup>15 </sup>e revisados por Carskadon e cols.<sup>16</sup>. O aparelho usado para a realiza&#231;&#227;o da polissonografia foi o Alice 3<sup>&#174;</sup> (Infant and Adult Computadorized Polyssomnographyc System, Ge&#243;rgia, EUA).</p>
    <p><italic>An&#225;lise Oxim&#233;trica no per&#237;odo de sono real do grupo controle</italic> &#150; O aparelho usado foi o Nonin 3100 WristOx. Os par&#226;metros de an&#225;lise &#224; oximetria noturna foram: epis&#243;dios de dessatura&#231;&#227;o (considerando queda da SpO<sub>2</sub> de pelo menos 4% em per&#237;odo m&#237;nimo de 10 segundos) e epis&#243;dios de altera&#231;&#227;o da frequ&#234;ncia de pulso (pelo menos 4 bpm durante um per&#237;odo m&#237;nimo de 10 segundos). A an&#225;lise oxim&#233;trica foi escolhida como m&#233;todo de avalia&#231;&#227;o no grupo controle, pelo embasamento na literatura de possibilidade de compara&#231;&#227;o entre os dois grupos, n&#227;o submetidos aos mesmos procedimentos de avalia&#231;&#227;o. O que justifica tal afirma&#231;&#227;o baseia-se no fato da oximetria ser uma t&#233;cnica comprovadamente eficaz para esse fim, com v&#225;rios estudos<sup>17-19</sup>, que demonstraram a efetividade do m&#233;todo para diagn&#243;stico de outras desordens do sono, incluindo SAOS. Esse fato foi importante neste estudo no tocante &#224; redu&#231;&#227;o de custo. &#201; importante frisar que o controle oxim&#233;trico na polissonografia (grupo DPOC) foi realizado com o mesmo aparelho de oximetria utilizado no grupo controle. Os pacientes do grupo DPOC n&#227;o tinham &#237;ndice de hipopn&#233;ia-apn&#233;ia (AIH) &gt; 5, portanto n&#227;o tinham SAOS. Por outro lado, nenhum dos indiv&#237;duos do grupo controle apresentava queixas sugestivas de SAOS (roncos, paradas respirat&#243;rias testemunhadas em sono e sonol&#234;ncia diurna). Foram consideradas desnecess&#225;rias as polissonografias no grupo controle e substitu&#237;das pela oximetria de noite inteira, para afastar a possibilidade remota de hipoxemia em sono. </p>
    <p><italic>MAPA de 24h</italic> &#150; Foi utilizada para avaliar as vari&#225;veis da press&#227;o arterial nos dois grupos estudados, pelo m&#233;todo oscilom&#233;trico, com ABP-Monitor port&#225;til da Dyna-MAPA (Cardio Sistemas Comercial e Industrial Ltda, S&#227;o Paulo, Brasil) validado pela Associa&#231;&#227;o para o Avan&#231;o de Instrumentos M&#233;dicos dos Estados Unidos (AAMI)<sup>20</sup> e pela Sociedade Brit&#226;nica de Hipertens&#227;o (BHS)<sup>21</sup>. Considerou-se como sono, o per&#237;odo real e n&#227;o o hor&#225;rio fixo. As vari&#225;veis foram descritas por valores m&#237;nimo, m&#225;ximo, m&#233;dia e desvio-padr&#227;o. </p>
    <p><italic>Aspectos &#201;ticos</italic> &#150; Este estudo foi aprovado pela Diretoria Adjunta de Ensino e Pesquisa do Hospital Universit&#225;rio de Bras&#237;lia (HUB). </p>
    <p><italic>An&#225;lise estat&#237;stica</italic> &#150; Os dados coletados passaram pelo testes de Shapiro-Wilk para testar a normalidade das vari&#225;veis quantitativas, visando a compara&#231;&#227;o das m&#233;dias das vari&#225;veis nos grupos DPOC e controle. Foi utilizado o teste t de Student para amostras independentes onde a distribui&#231;&#227;o era param&#233;trica. O teste de Mann-Whitney foi utilizado para as vari&#225;veis que apresentaram distribui&#231;&#227;o n&#227;o-param&#233;trica. A an&#225;lise estat&#237;stica foi realizada com o aux&#237;lio do programa Statistical Package for the Social Sciences (SPSS) 11.0.4 vers&#227;o para Mac OSX (Chicago, Illinois, EUA). Todas as an&#225;lises foram feitas separadamente para cada grupo de pacientes e o n&#237;vel de signific&#226;ncia adotado foi de 5%.</p>
    <p><italic>Financiamento</italic> &#150;N&#227;o houve financiamento externo deste estudo por nenhum &#243;rg&#227;o.</p>
    <p>
      <bold>Resultados</bold>
    </p>
    <p>Os principais resultados deste estudo foram:</p>
    <p>A m&#233;dia de idade do grupo DPOC era de 70 &#177; 11 anos, enquanto no grupo controle era de 70 &#177; 8 anos, sem diferen&#231;a entre os grupos em rela&#231;&#227;o &#224; faixa et&#225;ria.</p>
    <p>A m&#233;dia do IMC no grupo DPOC foi de 24 &#177; 4 kg/m<sup>2</sup> e no grupo controle foi de 24 &#177; 2 kg/m<sup>2</sup>, ambos com &#237;ndices dentro da normalidade<sup>13</sup>. </p>
    <p>A <xref ref-type="table" rid="tab01">tabela 1</xref> mostra que n&#227;o houve diferen&#231;a entre os dois grupos, em rela&#231;&#227;o &#224;s medidas antropom&#233;tricas.</p>
    <table-wrap id="tab01">
      <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gt01.jpg"/></table-wrap>
    <p>Na espirometria, a m&#233;dia do &#237;ndice VEF<sub>1 </sub>/CVF% foi de 44 &#177; 5% no grupo DPOC, e de 74 &#177; 2% no grupo controle. Considerando a classifica&#231;&#227;o de GOLD<sup>22</sup>, pelos crit&#233;rios espirom&#233;tricos o grupo DPOC foi caracterizado como grave (est&#225;gio III) e o grupo controle apresentou par&#226;metros de normalidade. </p>
    <p>Na gasometria, no grupo DPOC, a PaO<sub>2 </sub>m&#233;dia foi de 60,6 &#177; 6,1 mmHg e a PaCO<sub>2</sub> m&#233;dia foi de 36,7 &#177; 6,9 mmHg, compat&#237;veis com a literatura em portadores de DPOC com gravidade est&#225;gio III<sup>22</sup>. </p>
    <p>Na polissonografia do grupo DPOC foi observado o tempo total de sono de 326,7 &#177; 70 minutos, inferior ao desejado, mas concordante com a revis&#227;o liter&#225;ria<sup>16</sup>. A m&#233;dia da efici&#234;ncia do sono foi de 74,8%, pouco abaixo do valor preconizado como ideal para indiv&#237;duos dessa faixa et&#225;ria, em torno de 80%. A m&#233;dia da lat&#234;ncia do sono foi de 29,7 &#177; 30 minutos, pouco acima do esperado. A m&#233;dia de lat&#234;ncia do sono REM (LatREM) de 151 &#177; 84 minutos, foi aumentada al&#233;m do tempo esperado de 150 minutos. Nenhum paciente apresentou priva&#231;&#227;o do sono REM. A aus&#234;ncia de &#237;ndice de apn&#233;ia-hipopn&#233;ia foi <underline>&gt;</underline> 5. </p>
    <p>Os par&#226;metros de press&#227;o arterial e oxim&#233;tricos est&#227;o demonstrados na <xref ref-type="table" rid="tab02">tabela 2</xref> e s&#227;o descritos a seguir. </p>
    <table-wrap id="tab02">
      <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gt02.jpg"/></table-wrap>
    <p>Em rela&#231;&#227;o ao descenso do sono, foram observadas diferen&#231;as significativas, tanto na medida sist&#243;lica quanto na diast&#243;lica, com descenso atenuado no grupo DPOC e fisiol&#243;gico no grupo controle, conforme o <xref ref-type="fig" rid="grf01">gr&#225;fico 1</xref>.</p>
    <fig id="grf01">
      <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf01.jpg"/></fig>
    <p>Quanto aos par&#226;metros da press&#227;o arterial sist&#243;lica em vig&#237;lia (mmHg), observa-se que tanto o valor m&#233;dio, quanto o m&#237;nimo e o m&#225;ximo, se apresentaram estatisticamente maiores no grupo DPOC do que no grupo controle, com p-valores 0,009, 0,018 e 0,032, respectivamente. J&#225; os par&#226;metros da press&#227;o arterial diast&#243;lica em vig&#237;lia n&#227;o apresentaram diferen&#231;as significativas entre grupos.</p>
    <p>As medidas da press&#227;o arterial durante o sono (mmHg) mostraram-se estatisticamente maiores entre os indiv&#237;duos do grupo DPOC do que no grupo controle, com exce&#231;&#227;o ao valor m&#225;ximo da press&#227;o diast&#243;lica, que n&#227;o demonstra diferen&#231;a significativa entre os grupos. </p>
    <p>Quanto ao par&#226;metro da m&#233;dia press&#243;rica nas 24 horas, observaram-se valores estatisticamente maiores no grupo DPOC para a press&#227;o arterial sist&#243;lica (p=0,002). A medida diast&#243;lica n&#227;o apresentou diferen&#231;a significativa entre os grupos. Os valores m&#233;dios das medidas da press&#227;o arterial no per&#237;odo matutino, tanto a sist&#243;lica quanto a diast&#243;lica, mostraram-se estatisticamente maiores no grupo DPOC. </p>
    <p>A medida da satura&#231;&#227;o m&#237;nima atingida no per&#237;odo de sono (SpO<sub>2</sub> m&#237;nima %) n&#227;o demonstrou diferen&#231;a significativa entre os dois grupos, conforme o <xref ref-type="fig" rid="grf02">gr&#225;fico 2</xref>. O par&#226;metro que demonstrou relevante diferen&#231;a foi o tempo de dessatura&#231;&#227;o do grupo DPOC (T90 &gt; 30%), enquanto no grupo controle foi pr&#243;xima a zero, conforme mostra o <xref ref-type="fig" rid="grf03">gr&#225;fico 3</xref>. </p>
    <fig id="grf02">
      <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf02.jpg"/></fig>
    <fig id="grf03">
      <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf03.jpg"/></fig>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>A DPOC caracteriza-se por ser uma doen&#231;a complexa, com limita&#231;&#227;o ao fluxo a&#233;reo, parcialmente revers&#237;vel com o uso de drogas broncodilatadoras<sup>3,5-7</sup>, apresentando comorbidades cardiovasculares<sup>1-7</sup>.</p>
    <p>Na presente pesquisa, foram estudadas vari&#225;veis da press&#227;o arterial e oxim&#233;tricas em portadores de DPOC. Os resultados foram comparados ao grupo controle, com caracter&#237;sticas antropom&#233;tricas semelhantes. </p>
    <p>No grupo DPOC, todos eram hipox&#234;micos ao sono (T90 m&#233;dio de 42 &#177;36) e apresentavam comprometimento na qualidade do sono<sup>14</sup>, com efici&#234;ncia do sono pouco abaixo do ideal em compara&#231;&#227;o a indiv&#237;duos saud&#225;veis dessa faixa et&#225;ria (80%), e par&#226;metros de lat&#234;ncia do sono e LatREM acima do esperado. Nenhum paciente apresentava quadro de apn&#233;ia do sono. </p>
    <p><italic>Descenso da PA no sono -</italic> Os pacientes portadores de DPOC apresentaram m&#233;dia de descenso do sono atenuado (sist&#243;lico e diast&#243;lico), enquanto pacientes sem DPOC apresentaram m&#233;dia de descenso do sono fisiol&#243;gico (sist&#243;lico e diast&#243;lico)<sup>23</sup>. Trabalhos de Tanigawa e cols.<sup>24</sup> correlacionaram a gravidade dos dist&#250;rbios respirat&#243;rios &#224; eleva&#231;&#227;o em n&#237;veis diast&#243;licos no sono, prejudicando o descenso fisiol&#243;gico nesse per&#237;odo. Nossos dados est&#227;o em concord&#226;ncia com a literatura<sup>24</sup>, quando se menciona a redu&#231;&#227;o m&#233;dia da satura&#231;&#227;o de oxig&#234;nio no per&#237;odo de sono e descenso do sono. Isso pode decorrer por causa do acionamento do gatilho simp&#225;tico pela hip&#243;xia noturna, liberando catecolaminas na circula&#231;&#227;o sangu&#237;nea e elevando, assim, os n&#237;veis press&#243;ricos<sup>25</sup>. </p>
    <p>O papel do sistema nervoso aut&#244;nomo sobre o descenso do sono ainda &#233; um assunto controverso, mas evid&#234;ncias da participa&#231;&#227;o simp&#225;tica na regula&#231;&#227;o da press&#227;o arterial encontram-se presentes em portadores de SAOS<sup>25</sup>, nos quais pela hip&#243;xia e hipercapnia, quimiorreceptores acionam o aumento da atividade simp&#225;tica.A resposta vasoconstritora simp&#225;tica aos eventos apn&#233;icos ocasiona eleva&#231;&#245;es da press&#227;o arterial durante o sono, principalmente &#224; finaliza&#231;&#227;o do evento apn&#233;ico. Oliveira e cols.<sup>26</sup> relatam que a aus&#234;ncia de descenso press&#243;rico no sono tem sido atribu&#237;da &#224; disfun&#231;&#227;o nervosa auton&#244;mica, relacionando-se a aumento do risco cardiovascular e les&#245;es em &#243;rg&#227;os-alvo, principalmente em massa ventricular esquerda, doen&#231;a cerebrovascular silenciosa e microalbumin&#250;ria. </p>
    <p><italic>Em vig&#237;lia -</italic> Foram observados n&#237;veis sist&#243;licos mais elevados no grupo DPOC em valores m&#233;dio, m&#237;nimo e m&#225;ximo. Em concord&#226;ncia com a literatura, o subestudo <italic>Syst-Eur</italic><sup>27</sup>, demonstrou que a hipertens&#227;o sist&#243;lica isolada em pacientes idosos est&#225; associada ao descenso do sono atenuado, com associa&#231;&#227;o inversa entre o descenso da press&#227;o arterial e o risco cardiovascular. No per&#237;odo da vig&#237;lia n&#227;o foram observadas diferen&#231;as significativas em n&#237;veis diast&#243;licos (valores m&#233;dio, m&#237;nimo e m&#225;ximo) entre os grupos. </p>
    <p><italic>No sono</italic><bold> - </bold>A press&#227;o arterial durante o sono foi mais elevada no grupo DPOC em press&#227;o arterial sist&#243;lica (PAS) - valores m&#233;dio, m&#237;nimo e m&#225;ximo -, e press&#227;o arterial diast&#243;lica (PAD) - valores m&#233;dio e m&#237;nimo -. O valor m&#225;ximo da PAD durante o sono n&#227;o demonstrou diferen&#231;a entre os grupos DPOC e controle. No sono, embora os mediadores da press&#227;o arterial n&#227;o estejam completamente elucidados, a press&#227;o arterial e a frequ&#234;ncia card&#237;aca correlacionam-se &#224; atividade do sistema nervoso simp&#225;tico<sup>28</sup>.</p>
    <p><italic>M&#233;dia nas 24 horas</italic> - A m&#233;dia dos valores de PAS &#224;s 24 horas foi maior no grupo DPOC, sem diferen&#231;a significativa em rela&#231;&#227;o &#224; m&#233;dia da PAD no per&#237;odo. Conforme dados da literatura, as m&#233;dias press&#243;ricas obtidas nas 24 horas constituem-se no "padr&#227;o-ouro" dentre os par&#226;metros obtidos pelo m&#233;todo, por apresentarem correla&#231;&#245;es mais precisas com les&#245;es em &#243;rg&#227;os-alvo, morbidade e mortalidade<sup>28</sup>. </p>
    <p><italic>No per&#237;odo matutino</italic><bold><italic> -</italic></bold> Os valores m&#233;dios de PAS e PAD foram estatisticamente maiores no grupo DPOC, em compara&#231;&#227;o ao grupo controle. Em concord&#226;ncia com esses resultados, estudos demonstram que o descenso do sono atenuado ou inexistente predisp&#245;e &#224; manuten&#231;&#227;o de press&#227;o arterial elevada &#224;s primeiras horas da manh&#227;. Eguchi e cols.<sup>18</sup>, Kario e cols.<sup>29,30</sup> definiram que o aumento de n&#237;veis press&#243;ricos, &#224;s duas primeiras horas ap&#243;s o despertar, se correlacionou de modo significativo &#224; maior preval&#234;ncia de infartos cerebrais. A eleva&#231;&#227;o de n&#237;veis press&#243;ricos em per&#237;odo matutino correlaciona-se a maior risco de les&#245;es de &#243;rg&#227;os-alvo e eventos cardiovasculares, bem como aumento no risco de isquemia coronariana e acidentes vasculares cerebrais<sup>27,31-34</sup>. Concordante com nossos resultados, Kishimoto e cols.<sup>35</sup> descreveram que a redu&#231;&#227;o na satura&#231;&#227;o de oxig&#234;nio no sono, se correlacionou significativamente &#224; eleva&#231;&#227;o press&#243;rica matinal. Elliot<sup>33</sup> e Cohen e cols.<sup>34</sup> correlacionaram a hipertens&#227;o matutina &#224; maior mortalidade cardiovascular. </p>
    <p><italic>Quanto aos par&#226;metros da satura&#231;&#227;o de oxig&#234;nio (SpO</italic><sub>2</sub><italic> m&#237;nima %) e T90 (%) -</italic> O grupo DPOC demonstrou dessatura&#231;&#227;o mais prolongada no per&#237;odo de sono. No grupo controle, a avalia&#231;&#227;o foi realizada pela oximetria digital, cuja acur&#225;cia diagn&#243;stica tem comprova&#231;&#227;o na literatura em diversos estudos<sup>17-19</sup>. O grupo controle, pela oximetria, demonstrou epis&#243;dios de dessatura&#231;&#227;o m&#237;nima sem diferen&#231;a significativa em rela&#231;&#227;o ao grupo DPOC, por&#233;m de dura&#231;&#227;o insignificante (pr&#243;ximo a zero / epis&#243;dios pontuais), enquanto o grupo DPOC apresentou dessatura&#231;&#227;o mais prolongada. Em concord&#226;ncia com a literatura, estudos de Tanigawa e cols.<sup>24</sup> correlacionaram o &#237;ndice de dessatura&#231;&#227;o de oxig&#234;nio pela oximetria de pulso com n&#237;veis press&#243;ricos. O &#237;ndice de dessatura&#231;&#227;o de oxig&#234;nio (3%) foi associado &#224; eleva&#231;&#227;o em PAS de 0,8 mmHg (p= 0,05) e aumento de PAD de 0,7 mmHg (p= 0,05). </p>
    <p><italic>Limita&#231;&#245;es do estudo</italic> &#150; Se correlaciona ao tamanho da amostra, fato que decorreu da gravidade da patologia nos indiv&#237;duos do grupo DPOC com dessatura&#231;&#227;o noturna, idosos em sua maioria, que apresentaram dificuldade f&#237;sica &#224; realiza&#231;&#227;o de exames complementares. Nota-se, em hospitais p&#250;blicos e privados, uma demanda reprimida de leitos para o estudo do sono, fato que justifica a oximetria como m&#233;todo de an&#225;lise de pacientes sem DPOC e sem queixas sugestivas de dist&#250;rbios de sono, diante dos estudos j&#225; citados<sup>17-19</sup>, que demonstram comparabilidade entre os m&#233;todos. A oximetria &#233; o exame mais facilmente realiz&#225;vel, pelo seu menor custo em rela&#231;&#227;o &#224; polissonografia. As polissonografias s&#227;o muito trabalhosas e dispendiosas, fato que limita sua indica&#231;&#227;o em pacientes n&#227;o portadores de queixas relacionadas &#224; sono.</p>
    <p>Neste trabalho, a polissonografia foi usada para diferenciar as vari&#225;veis do sono e, em particular, identificar indiv&#237;duos portadores ou n&#227;o de s&#237;ndrome de apn&#233;ia obstrutiva do sono. O Exame foi realizado em apenas uma noite de sono.</p>
    <p>Apesar das limita&#231;&#245;es, consideramos que o estudo tem validade na correla&#231;&#227;o de doen&#231;a pulmonar cr&#244;nica grave, senilidade, press&#227;o arterial e n&#237;veis oxim&#233;tricos.</p>
    <p>
      <bold>Conclus&#245;es</bold>
    </p>
    <p>Nosso estudo sugere que o descenso do sono encontra-se atenuado ou ausente em pacientes com DPOC dessaturados no sono. Os resultados da press&#227;o arterial sist&#243;lica e diast&#243;lica mostraram-se maiores no grupo DPOC do que no grupo controle. A signific&#226;ncia dessa afirma&#231;&#227;o ocorreu em todos os per&#237;odos aferidos, exceto em vig&#237;lia, nas 24 horas e valores m&#225;ximos ao sono para n&#237;veis de press&#227;o diast&#243;lica. Pode-se concluir ent&#227;o, neste estudo, que o grupo portador de DPOC possui n&#237;veis de press&#227;o arterial maiores que o grupo controle, fato que pode decorrer da ativa&#231;&#227;o simp&#225;tica aumentada, pela dessatura&#231;&#227;o no sono. </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 tese de mestrado de Neila Anders Aidar pela Universidade de Bras&#237;lia &#150; UnB.</p>
    <p>
      <fn id="end" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Neila Anders Aidar </p>
        <p> SMPW quadra 07, conjunto 3, casa 3 </p>
        <p> 71740-703 &#150; Bras&#237;lia, DF, Brasil </p>
        <p> E-mail: </p>
        <p><email xlink:href="naaidar@cardiol.br">naaidar@cardiol.br</email>, </p>
        <p>
          <email xlink:href="naaidar@brturbo.com.br">naaidar@brturbo.com.br</email>
        </p>
      </fn>
    </p>
    <p>Artigo recebido em 26/06/08; revisado recebido em 28/10/08; aceito em 31/10/08.</p>
  </body>
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  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Original Articles</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">ABPM in COPD patients with sleep desaturation</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>BACKGROUND: Sleep hypoxemia may change blood pressure by sympathetic activation. Few studies have analyzed blood pressure parameters in COPD patients who do not present sleep apnea, but do present sleep desaturation. OBJECTIVES: To analyze blood pressure parameters in COPD patients with sleep desaturation not caused by apnea. METHODS: Thirteen patients with COPD underwent spirometry, blood gas, polysomnography and ABPM for blood pressure evaluation. Fourteen patients without COPD underwent spirometry, oximetry and ABPM. Blood pressure analyses were carried out both during wakefulness and sleep. Both groups were comprised of patients with no history of hypertension. RESULTS: The two groups were similar as regards age, height, weight, and body mass index. A significant difference (p&lt;0.05) was found between blood pressure levels during the wakefulness, sleep, 24-hour and sleep dip periods. Higher blood pressure levels were observed in patients with COPD, except for diastolic levels during wakefulness and maximum values during sleep and in the 24 hours. Sleep dip in the COPD group was attenuated, whereas physiological dip was observed in the control group, with lower blood pressure levels. CONCLUSIONS: Systolic and diastolic blood pressure levels in the COPD group were higher than those of the control group, with a significant difference found for all periods studied, except for diastolic levels during wakefulness and in the 24 hours. We can conclude that the group of COPD patients with sleep desaturation has significantly higher blood pressure levels than the control group.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>Blood Pressure Monitoring</kwd>
        <kwd>Ambulatory</kwd>
        <kwd>Sleep</kwd>
        <kwd>Pulmonary Disease</kwd>
        <kwd>Chronic Obstructive</kwd>
        <kwd>Polysomnography</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ORIGINAL ARTICLE</bold>
      </p>
      <p><undefined id="tx-body2"/>ABPM in COPD patients with sleep desaturation</p>
      <p>
        <bold>Neila Anders Aidar; M&#225;rcio Alberto Carvalho da Silva; C&#233;sar Augusto Melo e Silva; Pedro Nery Ferreira J&#250;nior; Paulo Tavares</bold>
      </p>
      <p>Hospital Universit&#225;rio de Bras&#237;lia (HUB), da Universidade de Bras&#237;lia (UnB), Bras&#237;lia, DF, Brasil</p>
      <p>Mailing address</p>
      <p>
        <bold>SUMMARY</bold>
      </p>
      <p><bold>BACKGROUND:</bold> Sleep hypoxemia may change blood pressure by sympathetic activation. Few studies have analyzed blood pressure parameters in COPD patients who do not present sleep apnea, but do present sleep desaturation.</p>
      <p><bold>OBJECTIVES:</bold> To analyze blood pressure parameters in COPD patients with sleep desaturation not caused by apnea.</p>
      <p><bold>METHODS:</bold> Thirteen patients with COPD underwent spirometry, blood gas, polysomnography and ABPM for blood pressure evaluation. Fourteen patients without COPD underwent spirometry, oximetry and ABPM. Blood pressure analyses were carried out both during wakefulness and sleep. Both groups were comprised of patients with no history of hypertension.</p>
      <p><bold>RESULTS:</bold> The two groups were similar as regards age, height, weight, and body mass index. A significant difference (p&lt;0.05) was found between blood pressure levels during the wakefulness, sleep, 24-hour and sleep dip periods. Higher blood pressure levels were observed in patients with COPD, except for diastolic levels during wakefulness and maximum values during sleep and in the 24 hours. Sleep dip in the COPD group was attenuated, whereas physiological dip was observed in the control group, with lower blood pressure levels.</p>
      <p><bold>CONCLUSIONS: </bold>Systolic and diastolic blood pressure levels in the COPD group were higher than those of the control group, with a significant difference found for all periods studied, except for diastolic levels during wakefulness and in the 24 hours. We can conclude that the group of COPD patients with sleep desaturation has significantly higher blood pressure levels than the control group. </p>
      <p><bold>Key words:</bold> Blood Pressure Monitoring, Ambulatory; Sleep; Pulmonary Disease, Chronic Obstructive; Polysomnography.</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of death, and its main complication is related to cardiovascular events<sup>1-3</sup>. The literature shows that in a five-year period 48% of all hospitalizations of patients with COPD were due to cardiovascular complications and that, independent of gender, age, and smoking, COPD increases the cardiovascular risk twofold<sup>1,2</sup>. The factors that correlate COPD with cardiovascular events are not fully understood. Studies demonstrate that chronic systemic inflammation and disorders of the neurohumoral regulation may be involved<sup>3-7</sup>, and suggest that patients with COPD develop sympathetic hyperactivity, decreased vagal tonus and dysautonomia.</p>
      <p>The prevalence of hypertension is high among the world population<sup>8,9</sup>, and increases with the age range<sup>9</sup>; between 60 and 69 years of age, more than 50% of the individuals are affected by hypertension. Above 70 years of age, in turn, the prevalence of hypertension reaches 75%. Mortality for cardiovascular diseases increases with blood pressure (BP) elevation<sup>9,10</sup>.</p>
      <p>In addition to showing scarce and conflicting data on blood pressure in patients with COPD, the literature also points out the need for further studies to explain the behavior of blood pressure during sleep desaturation and, most importantly, its effects on target organs. Ambulatory blood pressure monitoring (ABPM) is the diagnostic tool that provides this analysis, thus permitting the knowledge of the pattern of blood pressure variations during wakefulness and sleep<sup>11,12</sup>.</p>
      <p>The objective of this study was to evaluate the behavior of blood pressure in the 24 hours, in COPD patients with sleep desaturation not caused by apnea, using ABPM parameters. </p>
      <p>
        <bold>Methodology</bold>
      </p>
      <p>This is a descriptive, cross-sectional study of patients with COPD referred to the pulmonary rehabilitation program of the Pneumology outpatient clinic of <italic>Hospital Universit&#225;rio de Bras&#237;lia </italic>(HUB).</p>
      <p>
        <bold>Inclusion criteria </bold>
      </p>
      <p>A total of 13 patients clinically and functionally (spirometry: FEV1/FVC lower than 0.70 post bronchodilator) diagnosed with COPD and enrolled in the previously mentioned program were included. The control group was comprised of 14 volunteers without COPD (clinical and spirometric diagnosis). The patients of both groups had a negative history of hypertension, did not use any antihypertensive medication and did not present white-coat hypertension. Those who agreed to participate in the study gave their written informed consent.</p>
      <p>
        <bold>Exclusion criteria</bold>
      </p>
      <p>After thorough history taking, physical examination and 12-lead echocardiogram, the presence of the following conditions was used as the exclusion criterium: other clinically detectable pulmonary disorder; obstructive sleep apnea syndrome (as detected by polysomnography); other system or organ failure (renal failure, heart failure and hepatic failure); systemic hypertension; technically unfeasible 24-h ABPM; and conditions affecting the autonomic nervous function (neuropathies, psychiatric disorders, diabetes mellitus, autoimmune diseases, Parkinson's disease).</p>
      <p>Criteria from the IV ABPM Guidelines<sup>11</sup> were used for the definition of hypertension. The following ABPM parameters are considered normal: 24-hour BP &lt; 130/80 mmHg; daytime BP &lt; 135/85 mmHg; and night-time BP &lt; 120/70 mmHg.</p>
      <p>Patients with COPD who participated in the study underwent thorough clinical assessment. Next, spirometry, blood gas, polysomnography (PSG) and 24-hour ABPM were performed. Control group patients also underwent thorough clinical assessment, followed by spirometry, pulse oximetry during sleep and 24-hour ABPM.</p>
      <p>
        <bold>Clinical assessment</bold>
      </p>
      <p>The COPD group comprised 13 patients, of whom eight (61%) were males. All had been smokers<sup>12</sup> and were receiving inhaled beta 2-adrenergic receptor agonists, selective for these receptors, with direct delivery at the site of action in the airways; these features provide a reduction of extrapulmonary side effects, particularly of cardiac effects, and thus blood pressure readings were less likely to be influenced. In the control group, with 14 patients, six (42%) were males with no history of smoking. </p>
      <p>Body mass index (BMI)<sup>13</sup> was calculated by dividing weight (kg) by the square height (m). Values were classified as: &lt; 18.5 kg/m<sup>2</sup> (underweight); 18.5 to 24.9 kg/m<sup>2 </sup>(normal weight); 25 to 29.9 kg/m<sup>2 </sup>(overweight) and <underline>&gt;</underline> 30 kg/m<sup>2</sup> (overall obesity).</p>
      <p>In order to compare the COPD and control groups, the mean anthropometric measurements were tested to control the factors that could interfere with blood pressure and oximetry parameters.</p>
      <p><italic>Spirometry</italic> &#150; Both groups underwent spirometry with the patients in the sitting position and using an adaptor to prevent breathing through the nares. Ventilation was fully oral, with the circuit closed and the anatomical adaptor connected to the oral cavity; the circuit was coupled to the device, according to the guidelines of the American Thoracic Society. The Vmax<sup>&#174;</sup>-22 device (spirometer series, SensorMedics, Yorba Linda, California, USA, 2004) was used for the procedure.</p>
      <p><italic>Blood gas &#150; </italic>Blood was drawn from the radial artery only in the COPD group, for comparison with sleep desaturation levels. The Ciba Corning 278 Gas System<sup>&#174;</sup> blood gas analyzer (Ciba Corning, Diagnostics Corp, Medfield, USA, 2004) was used. </p>
      <p><italic>Polysomnography &#150; </italic>Polysomnography (PSG) was performed over only one night's sleep, exclusively in the COPD group, during the whole night, at the Sleep Laboratory of <italic>Hospital Universit&#225;rio de Bras&#237;lia</italic>. PSG was performed in this group to rule out other sleep disorders<sup>14</sup>, among which is the obstructive sleep apnea syndrome (OSAS), a condition that is distinct from COPD, but also causes nocturnal hypoxemia. Polysomnography was performed according to criteria established by Rechtschaffen and Kales<sup>15</sup> and revised by Carskadon et al<sup>16</sup>. The Alice 3<sup>&#174;</sup> device (Infant and Adult Computerized Polysomnographic System, Georgia, USA) was used.</p>
      <p><italic>Oximetry analysis in the real sleep time of the control group</italic> &#150; The Nonin 3100 WristOx device was used. The parameters analyzed on nocturnal oximetry were: episodes of desaturation (considering a SpO<sub>2</sub> fall of at least 4% for at least 10 seconds) and episodes of pulse rate change (at least 4 bpm for at least 10 seconds). Oximetry analysis was chosen as the assessment method in the control group, based on data from the literature showing that it is possible to compare these two groups even if they had not undergone the same assessment procedures. This statement is supported by the fact that oximetry is proven to be an efficient technique for this purpose, and several studies<sup>17-19</sup> have demonstrated its effectiveness for the diagnosis of other sleep disorders, including OSAS. This was important in our study in relation to cost reduction. It is important to underscore that the oximetric control in polysomnography (COPD group) was made with the same oximeter used in the control group. The apnea-hypopnea indexes (AHI) in COPD patients were not &gt; 5, therefore they did not present OSAS. On the other hand, no individuals in the control group had complaints suggestive of OSAS (snoring, respiratory arrests witnessed during sleep, and daily sleepiness). Polysomnography was considered unnecessary for the control group and was replaced by overnight oximetry to rule out the remote possibility of sleep hypoxemia. </p>
      <p><italic>24-h ABPM</italic> &#150; 24-h ABPM was used to evaluate blood pressure variables in the two groups studied using the oscillometric method, with a portable Dyna-MAPA ABP-Monitor (<italic>Cardio Sistemas Comercial e Industrial Ltda, </italic>Sao Paulo, Brazil) validated both by the American Association for the Advancement of Medical Instrumentation (AAMI)<sup>20</sup> and by the British Hypertension Society (BHS)<sup>21</sup>. The sleep period was considered the real period and not the fixed time. Variables were described as minimum, maximum and mean values, and standard-deviation. </p>
      <p><italic>Ethical Aspects &#150; </italic>This study was approved by the Adjunct Learning and Research Board of <italic>Hospital Universit&#225;rio de Bras&#237;lia </italic>(HUB).</p>
      <p><italic>Statistical analysis &#150; </italic>The Shapiro-Wilk test was used to analyze the data collected in order to test normality of quantitative variables, aiming to compare the mean values of variables in the COPD and control groups. The Student's t test and Mann-Whitney test were used for independent samples with parametric distribution and for variables with non-parametric distribution, respectively. The Statistical</p>
      <p> Package for the Social Sciences (SPSS) version 11.0.4 for Mac OSX (Chicago, Illinois, USA) was used for the statistical analysis. All analyses were carried out for each group of patients separately and the significance level was set at 5%.</p>
      <p><italic>Sponsoring</italic> &#150; This study was not sponsored by external sources. </p>
      <p>
        <bold>Results</bold>
      </p>
      <p>The main results of this study were:</p>
      <p>The mean age was 70 &#177; 11 years and 70 &#177; 8 years for the COPD and control groups, respectively, with no difference between the groups in relation to the age range.</p>
      <p>The mean BMI was 24 &#177; 4 kg/m<sup>2</sup> and 24 &#177; 2 kg/m<sup>2</sup> for the COPD and control groups, respectively, and both were within normal limits<sup>13</sup>.</p>
      <p>No difference was found between the two groups as regards the anthropometric measurements, as shown in <xref ref-type="table" rid="tab01-body2">Table 1</xref>.</p>
      <table-wrap id="tab01-body2">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gt01-en.jpg"/></table-wrap>
      <p>On spirometry, the mean FEV<sub>1</sub>/FVC% ratio was 44 &#177; 5% and 74 &#177; 2% in the COPD and in the control group, respectively. Considering the GOLD classification<sup>22</sup>, based on spirometric criteria, in the COPD group the disease was characterized as severe (stage III) whereas the control group showed normal parameters. </p>
      <p>Blood gas showed mean PaO<sub>2 </sub>of 60.6 &#177; 6.1 mmHg and mean PaCO<sub>2</sub> of 36.7 &#177; 6.9 mmHg in the COPD group. These values are consistent with stage III COPD, according to the literature<sup>22</sup>.</p>
      <p>Polysomnography of the COPD group showed a total sleep time of 326.7 &#177; 70 minutes, which is lower than desired, but consistent with values found in the review of the literature<sup>16</sup>. The mean sleep efficacy was 74.8%, slightly lower than the value considered as ideal for individuals in this age range, which is of approximately 80%. The mean sleep latency was 29.7 &#177; 30 minutes, slightly above the expected. The mean REM sleep latency (LatREM) was 151 &#177; 84 minutes, above the expected time of 150 minutes. No patient experienced REM sleep deprivation. The absence of apnea-hypopnea index was <underline>&gt;</underline> 5.</p>
      <p>Blood pressure and oximetry parameters are shown in <xref ref-type="table" rid="tab02-body2">Table 2</xref> and are described below.</p>
      <table-wrap id="tab02-body2">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gt02-en.jpg"/></table-wrap>
      <p>In relation to sleep dip, significant differences were observed both for systolic and diastolic measurements, with attenuated dip in the COPD group and physiological dip in the control group, as shown in <xref ref-type="fig" rid="grf01-body2">Graph 1</xref>.</p>
      <fig id="grf01-body2">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf01-en.jpg"/></fig>
      <p>As regards systolic blood pressure parameters during wakefulness (mmHg), the mean, minimum and maximum values were statistically higher in the COPD group than in the control group, with p values of 0.009, 0.018 and 0.032, respectively. In turn, no significant difference was found between the groups in relation to diastolic blood pressure parameters during wakefulness.</p>
      <p>Blood pressure measurements during sleep (mmHg) were statistically higher among individuals of the COPD group than among those of the control group, except for the maximum diastolic blood pressure level, for which no significant difference was found between the groups.</p>
      <p>As regards the mean 24-hour blood pressure parameter, statistically higher values were found in the COPD group for systolic blood pressure (p=0.002). No significant difference was found between the groups for the diastolic measurements. The mean systolic and diastolic blood pressure readings taken in the morning were statistically higher in the COPD group.</p>
      <p>Minimum saturation values achieved during sleep (minimum % SpO<sub>2</sub>) were not significantly different between the two groups, as shown in <xref ref-type="fig" rid="grf02-body2">Graph 2</xref>. The parameter for which a significant difference was found was desaturation time in the COPD group (T90 &gt; 30%), whereas this value was close to zero in the control group, as shown in <xref ref-type="fig" rid="grf03-body2">Graph 3</xref>.</p>
      <fig id="grf02-body2">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf02-en.jpg"/></fig>
      <fig id="grf03-body2">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf03-en.jpg"/></fig>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>COPD is a complex disorder characterized by airflow obstruction, which is partially reversible with the use of bronchodilator drugs<sup>3,5-7</sup>, and is accompanied by cardiovascular comorbidities<sup>1-7</sup>.</p>
      <p>In the present study, blood pressure and oximetry variables were analyzed in patients with COPD. The results were compared with those of the control group, which had similar anthropometric characteristics.</p>
      <p>All individuals in the COPD group were hypoxemic during sleep (mean T90 of 42 &#177;36) and their sleep quality was affected<sup>14</sup>, with sleep efficiency slightly lower than optimum in comparison to healthy individuals of the same age range (80%), and sleep latency and LatREM above the expected. No patient presented with sleep apnea.</p>
      <p><italic>BP dip during sleep &#150; </italic>Patients with COPD showed attenuated mean sleep dip (systolic and diastolic), whereas those without COPD showed physiological mean sleep dip (systolic and diastolic)<sup>23</sup>. Tanigawa et al<sup>24</sup> studies correlated the severity of respiratory disorders with increased diastolic blood pressure levels during sleep, thus hindering the physiological dip in this period. Our data are consistent with those of the literature<sup>24</sup> with regard to the mean reduction of oxygen saturation during sleep and sleep dip. This may occur because the sympathetic activity is triggered by nocturnal hypoxia, thus releasing catecholamines in blood circulation, and consequently elevating blood pressure<sup>25</sup>. </p>
      <p>The role of the autonomous nervous system on sleep dip remains controversial, but there are evidences of sympathetic participation on blood pressure regulation in patients with OSAS<sup>25</sup>, in whom hypoxia and hypercapnia, acting via the chemoreceptors, elicit increases in sympathetic activity. The sympathetic vasoconstrictor response to apneic events leads to increases in blood pressure during sleep, especially at the end of apnea. Oliveira et al<sup>26</sup> reported that the absence of blood pressure dip during sleep has been attributed to an autonomic nervous dysfunction and is related to increased cardiovascular risk and target-organ damage, particularly in the left ventricular mass, silent cerebrovascular disease and microalbuminuria. </p>
      <p><italic>During wakefulness</italic> &#150; Higher mean, minimum and maximum systolic blood pressure levels were observed in the COPD group. In agreement with the literature, the Syst-Eur substudy<sup>27</sup> demonstrated that isolated systolic hypertension in older patients is associated with attenuated sleep dip, with an inverse association between blood pressure dip and cardiovascular risk. No significant differences in diastolic blood pressure levels (mean, minimum and maximum values) were observed between the groups during wakefulness.</p>
      <p><italic>During sleep</italic> &#150; Mean, minimum and maximum systolic blood pressure (SBP) levels, as well as mean and minimum diastolic blood pressure (DBP) levels during sleep were higher in the COPD group. No difference was found in maximum DBP levels between the COPD and control groups. During sleep, although blood pressure mediators are not fully understood, blood pressure and heart rate correlate with the sympathetic nervous system activity<sup>28</sup>.</p>
      <p><italic>24-hour means</italic> &#150; Mean 24-hour SBP values were higher in the COPD group, but with no significant difference in relation to mean DBP in this period. According to data from the literature, mean 24-hour blood pressure levels are the gold-standard parameter among those obtained by ABPM, because they are more accurately correlated with target-organ damage, morbidity and mortality<sup>28</sup>.</p>
      <p><italic>Morning period</italic> &#150; Mean SBP and DBP values were statistically higher in the COPD group in comparison to the control group. Corroborating these findings, studies have demonstrated that attenuated or absent sleep dip predisposes to sustained high blood pressure in the first few hours of the morning. Eguchi et al, Kario et al<sup>29,30</sup> showed that increased blood pressure levels in the first two hours after waking up were significantly correlated with a higher prevalence of cerebral infarcts. Morning blood pressure elevation is correlated with increased risk of target-organ damage and cardiovascular events, as well as with increased risk of coronary ischemia and stroke<sup>27,31-34</sup>. In corroboration with our findings, Kishimoto et al<sup>35</sup> demonstrated that the reduction in sleep oxygen saturation was significantly correlated with morning blood pressure elevation. Elliot<sup>33</sup> and Cohen et al<sup>34</sup> correlated morning hypertension with higher cardiovascular mortality.</p>
      <p><italic>Oxygen saturation (minimum % SpO</italic><sub>2</sub><italic>) and T90(%)</italic> - The COPD group showed more prolonged desaturation during sleep. In the control group, the assessment was made using digital oximetry, whose diagnostic accuracy has been proven in several studies of the literature<sup>17-19</sup>. Oximetry in the control group showed episodes of minimal desaturation with no statistical difference in relation to the COPD group; however, the duration of desaturation was negligible (close to zero / punctual events), whereas it lasted longer in the COPD group. Consistent with the literature, Tanigawa et al<sup>24</sup> studies correlated oxygen desaturation index on pulse oximetry with blood pressure levels. Oxygen desaturation index (3%) was associated with SBP elevation by 0.8 mmHg (p=0.05) and increased DBP by 0.7 mmHg (p=0.05).</p>
      <p><italic>Study limitations &#150; </italic>The small sample size was a limitation of the present study, and resulted from the severity of the disease in COPD group patients with nocturnal desaturation; the majority of these individuals was elderly, with physical difficulties to undergo ancillary tests. In public and private hospitals there are few beds available for the study of sleep, and this justifies the use of oximetry as an assessment method in patients without COPD and with no complaints suggestive of sleep disorders, based on the studies previously mentioned<sup>17-19</sup>, which demonstrated that these methods are comparable. Oximetry is the easiest test to perform given its lower cost in relation to polysomnography. Polysomnography is costly and difficult to perform , and this limits its indication in patients without sleep complaints.</p>
      <p>Polysomnography was used in the present study to differentiate sleep variables and, particularly, to identify individuals with or without obstructive sleep apnea syndrome. The test was performed over a single night's sleep.</p>
      <p>Despite its limitation, we think that our study is valid for the correlation between severe chronic pulmonary disease and old age, blood pressure and oximetry levels.</p>
      <p>
        <bold>Conclusions </bold>
      </p>
      <p>Our study suggests that sleep dip is attenuated or absent in COPD patients with sleep desaturation. Systolic and diastolic blood pressure levels were higher in the COPD group than in the control group. A significant difference was observed in all periods studied, except for diastolic blood pressure during wakefulness, in the 24-hour period, and maximum values during sleep. Therefore we can conclude that the COPD group had higher blood pressure levels than the control group, and this can be the result of increased sympathetic activity elicited by sleep desaturation.</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 Neila Anders Aidar, from Universidade de Bras&#237;lia - UnB.</p>
      <p>
        <bold>References</bold>
      </p>
    </body>
  </sub-article>
  <sub-article article-type="translation" id="TRes" xml:lang="es">
    <front-stub>
      <article-categories/>
      <title-group>
        <article-title xml:lang="es">MAPA en portadores de EPOC con desaturaci&#243;n durante el sue&#241;o</article-title>
      </title-group>
      <abstract xml:lang="es">
        <p>FUNDAMENTO: La hipoxemia en el per&#237;odo de sue&#241;o puede, por mecanismo de activaci&#243;n simp&#225;tica, alterar la presi&#243;n arterial. Pocos estudios demuestran los par&#225;metros de presi&#243;n en portadores de EPOC, que no tiene apnea del sue&#241;o, y que desaturan en ese per&#237;odo. OBJETIVO: Analizar los par&#225;metros de presi&#243;n en pacientes con EPOC y desaturaci&#243;n en el sue&#241;o, no causada por apnea. M&#201;TODOS: Trece pacientes con EPOC se sometieron a la espirometr&#237;a, la gasometr&#237;a arterial, la polisonograf&#237;a y al MAPA para la evaluaci&#243;n de presi&#243;n. Un total de 14 pacientes sin EPOC se sometieron a la espirometr&#237;a, la oximetr&#237;a y MAPA. Los an&#225;lisis de presi&#243;n se hicieron tanto en la vigilia como en el sue&#241;o. Los dos grupos estaban conformados por pacientes sin antecedentes hipertensivos. RESULTADOS: Los dos grupos se asemejaban respecto a la edad, la altura, el peso e el &#237;ndice de masa corporal. Hubo diferencia significativa (p &lt; 0,05) entre los par&#225;metros de presi&#243;n en los per&#237;odos de vigilia, sue&#241;o, 24 horas y descenso del sue&#241;o. Se observaron valores de presi&#243;n arterial mayores en los portadores de EPOC, a excepci&#243;n de los niveles diast&#243;licos en vigilia, m&#225;ximos valores al sue&#241;o y en las 24 horas. El descenso del sue&#241;o en el grupo EPOC se hall&#243; atenuado, mientras que en el grupo control fue fisiol&#243;gico, con menores valores de presi&#243;n arterial. CONCLUSI&#211;N: Los resultados de la presi&#243;n arterial sist&#243;lica y diast&#243;lica se hallaron mayores en el grupo EPOC que en el grupo control. La significancia de esa afirmaci&#243;n ocurri&#243; en todos los per&#237;odos medidos, a excepci&#243;n de la vigilia y en las 24 horas para niveles de presi&#243;n diast&#243;lica. Se puede concluir que, el grupo portador de EPOC con desaturaci&#243;n en el sue&#241;o posee niveles de presi&#243;n arterial significativamente mayores que en el grupo control.</p>
      </abstract>
      <kwd-group xml:lang="es">
        <kwd>Monitoreo ambulatorio de la presi&#243;n arterial</kwd>
        <kwd>sue&#241;o</kwd>
        <kwd>enfermedad pulmonar obstructiva cr&#243;nica</kwd>
        <kwd>polisonograf&#237;a</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ART&#205;CULO ORIGINAL</bold>
      </p>
      <p>
        <fn id="tx-body3">
          <label>
            <bold>MAPA en portadores de EPOC con desaturaci&#243;n durante el sue&#241;o</bold>
          </label>
          <p>
            <bold>Neila Anders Aidar; M&#225;rcio Alberto Carvalho da Silva; C&#233;sar Augusto Melo e Silva; Pedro Nery Ferreira J&#250;nior; Paulo Tavares</bold>
          </p>
        </fn>
      </p>
      <p>Hospital Universit&#225;rio de Bras&#237;lia (HUB), da Universidade de Bras&#237;lia (UnB), Bras&#237;lia, DF - Brasil</p>
      <p>Correspondencia</p>
      <p>
        <bold>RESUMEN</bold>
      </p>
      <p><bold>FUNDAMENTO:</bold> La hipoxemia en el per&#237;odo de sue&#241;o puede, por mecanismo de activaci&#243;n simp&#225;tica, alterar la presi&#243;n arterial. Pocos estudios demuestran los par&#225;metros de presi&#243;n en portadores de EPOC, que no tiene apnea del sue&#241;o, y que desaturan en ese per&#237;odo.</p>
      <p><bold>OBJETIVO:</bold> Analizar los par&#225;metros de presi&#243;n en pacientes con EPOC y desaturaci&#243;n en el sue&#241;o, no causada por apnea.</p>
      <p><bold>M&#201;TODOS:</bold> Trece pacientes con EPOC se sometieron a la espirometr&#237;a, la gasometr&#237;a arterial, la polisonograf&#237;a y al MAPA para la evaluaci&#243;n de presi&#243;n. Un total de 14 pacientes sin EPOC se sometieron a la espirometr&#237;a, la oximetr&#237;a y MAPA. Los an&#225;lisis de presi&#243;n se hicieron tanto en la vigilia como en el sue&#241;o. Los dos grupos estaban conformados por pacientes sin antecedentes hipertensivos.</p>
      <p><bold>RESULTADOS:</bold> Los dos grupos se asemejaban respecto a la edad, la altura, el peso e el &#237;ndice de masa corporal. Hubo diferencia significativa (p &lt; 0,05) entre los par&#225;metros de presi&#243;n en los per&#237;odos de vigilia, sue&#241;o, 24 horas y descenso del sue&#241;o. Se observaron valores de presi&#243;n arterial mayores en los portadores de EPOC, a excepci&#243;n de los niveles diast&#243;licos en vigilia, m&#225;ximos valores al sue&#241;o y en las 24 horas. El descenso del sue&#241;o en el grupo EPOC se hall&#243; atenuado, mientras que en el grupo control fue fisiol&#243;gico, con menores valores de presi&#243;n arterial.</p>
      <p><bold>CONCLUSI&#211;N:</bold> Los resultados de la presi&#243;n arterial sist&#243;lica y diast&#243;lica se hallaron mayores en el grupo EPOC que en el grupo control. La significancia de esa afirmaci&#243;n ocurri&#243; en todos los per&#237;odos medidos, a excepci&#243;n de la vigilia y en las 24 horas para niveles de presi&#243;n diast&#243;lica. Se puede concluir que, el grupo portador de EPOC con desaturaci&#243;n en el sue&#241;o posee niveles de presi&#243;n arterial significativamente mayores que en el grupo control. </p>
      <p><bold>Palabras clave: </bold> Monitoreo ambulatorio de la presi&#243;n arterial, sue&#241;o, enfermedad pulmonar obstructiva cr&#243;nica, polisonograf&#237;a.</p>
      <p>
        <bold>Introducci&#243;n</bold>
      </p>
      <p>La enfermedad pulmonar obstructiva cr&#243;nica (EPOC) es actualmente la cuarta causa de mortalidad, cuya principal complicaci&#243;n se correlaciona a eventos cardiovasculares<sup>1-3</sup>. La literatura demuestra que, en el per&#237;odo de cinco a&#241;os, el 48% de las internaciones de pacientes con EPOC ocurrieron por complicaciones cardiovasculares y que, independientemente del g&#233;nero, edad y presencia del tabaquismo, la EPOC duplica el riesgo cardiovascular<sup>1,2</sup>. Los factores que relacionan la EPOC a los eventos cardiovasculares todav&#237;a no est&#225;n totalmente aclarados. Estudios revelan que la inflamaci&#243;n sist&#233;mica cr&#243;nica y los disturbios de la regulaci&#243;n neurohumoral pueden estar relacionados<sup>3-7</sup> y sugieren que pacientes portadores de EPOC cursen con hiperactividad simp&#225;tica, reducci&#243;n del tono vagal y disautonomia.</p>
      <p> La hipertensi&#243;n arterial sist&#233;mica (HAS) es una enfermedad de alta prevalencia en la poblaci&#243;n mundial<sup>8,9</sup>. La prevalencia de HAS aumenta con la elevaci&#243;n en el grupo de edad9 entre 60 y 69 a&#241;os, m&#225;s del 50% de esa poblaci&#243;n es afectada por HAS. Ya en el grupo con edad superior a 70 a&#241;os, la prevalencia de HAS aumenta para el 75%. La mortalidad por enfermedad cardiovascular aumenta con la elevaci&#243;n de la presi&#243;n arterial (PA)<sup>9,10</sup>. </p>
      <p> La literatura que correlaciona niveles de presi&#243;n en individuos portadores de EPOC con datos escasos y conflictivos, evidencia la necesidad de nuevos estudios para la elucidaci&#243;n del comportamiento de la presi&#243;n arterial en la vigencia de desaturaci&#243;n en el sue&#241;o y, sobre todo, las repercusiones en &#243;rganos blanco. El monitoreo ambulatorio de la presi&#243;n arterial (MAPA) es el m&#233;todo diagn&#243;stico que permite ese an&#225;lisis, posibilitando el conocimiento del perfil de variaci&#243;n de la presi&#243;n arterial en vigilia y en el sue&#241;o<sup>11,12</sup>.</p>
      <p>El objetivo de este estudio es evaluar el comportamiento de la presi&#243;n arterial a las 24 horas, mediante an&#225;lisis de los par&#225;metros de la MAPA, en los pacientes con EPOC y desaturaci&#243;n en el sue&#241;o, no causada por apnea.</p>
      <p>
        <bold>Metodolog&#237;a</bold>
      </p>
      <p>Se trata de un estudio descriptivo, de tipo transversal, con pacientes portadores de EPOC referenciados al programa de rehabilitaci&#243;n pulmonar del ambulatorio de neumolog&#237;a del Hospital Universitario de Brasilia (HUB).</p>
      <p>
        <bold>Criterios de inclusi&#243;n</bold>
      </p>
      <p>Se incluyeron a 13 pacientes referidos al programa, con diagn&#243;stico cl&#237;nico y funcional (espirom&#233;trico: VEF1/CVF abajo de 0,70, post broncodilatador) de EPOC. El grupo control estaba conformado por 14 voluntarios, no portadores de EPOC (diagn&#243;stico cl&#237;nico y espirom&#233;trico). Los pacientes de los dos grupos no ten&#237;an antecedentes de hipertensi&#243;n arterial sist&#233;mica, no estaban bajo medicaci&#243;n antihipertensiva, ni eran portadores de hipertensi&#243;n de consultorio. Al acordar participar en el estudio, firmaron el formulario de consentimiento informado.</p>
      <p>
        <bold>Criterios de exclusi&#243;n</bold>
      </p>
      <p>Tras la historia cl&#237;nica detallada, el examen f&#237;sico y el electrocardiograma de 12 derivaciones, se adoptaron los siguientes criterios: La presencia de otra enfermedad pulmonar detectable cl&#237;nicamente; presencia de s&#237;ndrome de la apnea obstructiva del sue&#241;o (detectada por la polisonograf&#237;a); presencia de insuficiencia en otro &#243;rgano o sistema (insuficiencia renal, insuficiencia cardiaca e insuficiencia hep&#225;tica); presencia de hipertensi&#243;n arterial sist&#233;mica; imposibilidad t&#233;cnica de realizar la MAPA de 24h; y presencia de condiciones que afectan la funci&#243;n neuroauton&#243;mica (neuropat&#237;as, enfermedades psiqui&#225;tricas, diabetes mellitus, enfermedad autoinmune, enfermedad de Parkinson). </p>
      <p>Los criterios para definici&#243;n de hipertensi&#243;n arterial se siguieron seg&#250;n las IV Directrices de MAPA<sup>11</sup>. Se consideran como par&#225;metros de normalidad de la MAPA los que siguen a continuaci&#243;n: PA en 24 horas &lt; 130/ 80 mmHg; PA diurna &lt; 135/85 mmHg; y PA nocturna &lt;120/70 mmHg. </p>
      <p>Se sometieron a los pacientes portadores de EPOC participantes en el estudio a evaluaci&#243;n cl&#237;nica detallada. Acto seguido, se realizaron espirometr&#237;a, gasometr&#237;a arterial, polisonograf&#237;a (PSG) y MAPA 24horas. A los pacientes del grupo control tambi&#233;n se les sometieron a la evaluaci&#243;n cl&#237;nica detallada, y seguidamente, se les sometieron a la espirometr&#237;a, la oximetr&#237;a de pulso en per&#237;odo correspondiente al sue&#241;o y MAPA 24 horas.</p>
      <p>
        <bold>Evaluaci&#243;n cl&#237;nica</bold>
      </p>
      <p>En el grupo EPOC, con 13 pacientes, 8 de ellos (61%) masculinos, todos fueron fumadores<sup>12</sup> y se encontraban en uso de agonistas de receptores beta2-adren&#233;rgicos - selectivos para esos receptores, en formula inhalatoria con liberaci&#243;n directa en el punto de acci&#243;n en v&#237;as a&#233;reas, factores que conllevan la disminuci&#243;n de los efectos colaterales extra pulmonares, espec&#237;ficamente los cardiacos, con menor posibilidad de influencia en las mediciones de presi&#243;n arterial. En el grupo control, con 14 pacientes, seis (42%) eran masculinos, sin antecedentes de tabaquismo. </p>
      <p>El &#237;ndice de masa corporal (IMC)<sup>13</sup> se calcul&#243; mediante la divisi&#243;n del peso (Kg) por el cuadrado de la altura (m). Los valores se clasificaron en: &lt; 18,5 Kg/m<sup>2</sup> (bajo peso); 18,5 a 24,9 Kg/m<sup>2 </sup>(normal); 25 a 29,9 Kg/m<sup>2 </sup>(sobrepeso) y <underline>&gt;</underline> 30 Kg/m<sup>2</sup> (obesidad total).</p>
      <p>Para comparar los grupos EPOC y control, se probaron los promedios de las medidas antropom&#233;tricas, a fin de controlar los factores que podr&#237;an causar interferencias en los resultados de las tomas de la presi&#243;n arterial y oxim&#233;tricas.</p>
      <p><italic>Espirometr&#237;a</italic> - Llevada a cabo en los dos grupos, con los pacientes sentados, bajo el uso de adaptador que obstru&#237;a la ventilaci&#243;n por las ventanas de la nariz. La ventilaci&#243;n se hizo totalmente por la boca, con el sistema cerrado y el adaptador anat&#243;mico conectado a la cavidad oral y el sistema acoplado al aparato, siguiendo las normas de la <italic>American Thoracic Society</italic>. Para el procedimiento, se utiliz&#243; el aparato Vmax<sup>&#174;</sup>-22 (serie spirometer Sensor Medics Yorba Linda, Calif&#243;rnia, EUA, 2004).</p>
      <p><italic>Gasometr&#237;a arterial</italic> - Extracci&#243;n de sangre de la arteria radial, efectuada solamente en el grupo EPOC, para la comparaci&#243;n con los niveles de desaturaci&#243;n en el sue&#241;o. Gas&#243;metro Ciba Corning 278 Gas System<sup>&#174;</sup> (Ciba Corning, Diagnostics Corp.; Medfield, USA, 2004).</p>
      <p><italic>Polisonograf&#237;a</italic> - Llevada a cabo en solamente una noche de sue&#241;o, s&#243;lo en el grupo portador de EPOC, examen de noche entera, en el Laboratorio del Sue&#241;o del Hospital Universitario de Brasilia. La PSG se efectu&#243; en ese grupo para alejar otros des&#243;rdenes del sue&#241;o<sup>14</sup>, entre los que el s&#237;ndrome de apnea del sue&#241;o (SAOS), la entidad nosol&#243;gica distinta de EPOC, la que tambi&#233;n provoca la hipoxemia nocturna. La polisonograf&#237;a se llev&#243; a cabo seg&#250;n criterios establecidos por Rechtschaffen y Kales<sup>15 </sup>y revisados por Carskadon et al<sup>16</sup>. El aparato usado para la realizaci&#243;n de la polisonograf&#237;a fue el Alice 3<sup>&#174;</sup> (<italic>Infant and Adult Computadorized Polyssomnographyc System</italic>, Ge&#243;rgia, EUA).</p>
      <p><italic>An&#225;lisis Oxim&#233;trico en el per&#237;odo de sue&#241;o real del grupo control -</italic> El aparato usado fue el Nonin 3100 WristOx. Los par&#225;metros de an&#225;lisis a la oximetr&#237;a nocturna fueron: episodios de desaturaci&#243;n (teniendo en cuenta el descenso de la SpO<sub>2</sub> del 4% como m&#237;nimo, en un per&#237;odo m&#237;nimo de 10 segundos) y episodios de alteraci&#243;n de la frecuencia de pulso (por lo menos 4 lpm durante un per&#237;odo m&#237;nimo de 10 segundos). El an&#225;lisis oxim&#233;trico se eligi&#243; como m&#233;todo de evaluaci&#243;n en el grupo control, teniendo como base la literatura de posibilidad de comparaci&#243;n entre los dos grupos, no sometidos a los mismos procedimientos de evaluaci&#243;n. Lo que justifica tal afirmaci&#243;n est&#225; basado en el hecho de la oximetr&#237;a ser una t&#233;cnica comprobadamente eficaz para ese fin, con diversos estudios<sup>17-19</sup>, que evidenciaron la efectividad del m&#233;todo para diagn&#243;stico de otros des&#243;rdenes del sue&#241;o, incluyendo SAOS. Ese hecho fue importante en este estudio en lo que toca a la reducci&#243;n de coste. Es importante resaltar que el control oxim&#233;trico en la polisonograf&#237;a (grupo EPOC) se realiz&#243; con el mismo aparato de oximetr&#237;a utilizado en el grupo control. Los pacientes del grupo EPOC no ten&#237;an &#237;ndice de hipopnea-apnea (AIH) &gt; 5, por lo tanto no ten&#237;an SAOS. Por otro lado, ninguno de los individuos del grupo control presentaba quejas sugestivas de SAOS (roncus, paradas respiratorias presenciadas en sue&#241;o y somnolencia diurna). Se consideraron como desnecesarias las polisonograf&#237;as en el grupo control y se las sustituyeron por la oximetr&#237;a de noche entera, para alejar la posibilidad remota de hipoxemia en sue&#241;o. </p>
      <p><italic>MAPA de 24h</italic> - Se utiliz&#243; para evaluar las variables de la presi&#243;n arterial en los dos grupos estudiados, por el m&#233;todo oscilom&#233;trico, con ABP-Monitor port&#225;til de la Dyna-MAPA (Cardio Sistemas Comercial e Industrial Ltda, S&#227;o Paulo, Brasil) validado por la Asociaci&#243;n para el Avance de Instrumentos M&#233;dicos de los Estados Unidos (AAMI)<sup>20</sup> y por la Sociedad Brit&#225;nica de Hipertensi&#243;n (BHS)<sup>21</sup>. Se consider&#243; como sue&#241;o, el per&#237;odo real y no el horario fijo. Las variables se describieron por valores m&#237;nimo, m&#225;ximo, promedio y desviaci&#243;n est&#225;ndar. </p>
      <p><italic>Aspectos &#233;ticos</italic> - El Directorio Adjunto de Ense&#241;anza e Investigaci&#243;n del Hospital Universitario de Brasilia (HUB) aprob&#243; este estudio. </p>
      <p><italic>An&#225;lisis estad&#237;stico</italic> - Los datos recolectados pasaron por las pruebas de Shapiro-Wilk para probar la normalidad de las variables cuantitativas, buscando la comparaci&#243;n de los promedios de las variables en los grupos EPOC y control. Se utiliz&#243; la prueba t de <italic>Student</italic> para muestras independientes donde la distribuci&#243;n era param&#233;trica. La prueba de Mann-Whitney se utiliz&#243; para las variables que presentaron distribuci&#243;n no-param&#233;trica. El an&#225;lisis estad&#237;stico se llev&#243; a cabo con la ayuda del programa <italic>Statistical Package for the Social Sciences</italic> (SPSS) 11.0.4 versi&#243;n para Mac OSX (Chicago, Illinois, EUA). Todos los an&#225;lisis se hicieron separadamente para cada grupo de pacientes y el nivel de significancia adoptado fue del 5%.</p>
      <p><italic>Financiaci&#243;n</italic> - Ning&#250;n &#243;rgano externo financi&#243; este estudio.</p>
      <p>
        <bold>Resultados</bold>
      </p>
      <p>Los principales resultados de este estudio fueron:</p>
      <p>El promedio de edad del grupo EPOC era de 70 &#177; 11 a&#241;os, mientras que en el grupo control era de 70 &#177; 8 a&#241;os, sin distinci&#243;n entre los grupos en relaci&#243;n con el grupo de edad.</p>
      <p>El promedio del IMC en el grupo EPOC fue de 24 &#177; 4 Kg/m<sup>2</sup> y en el grupo control fue de 24 &#177; 2 Kg/m<sup>2</sup>, ambos con &#237;ndices dentro de la normalidad13. </p>
      <p>La <xref ref-type="table" rid="tab01-body3">Tabla 1</xref> muestra que no hubo diferencia entre los dos grupos, respecto a las medidas antropom&#233;tricas.</p>
      <table-wrap id="tab01-body3">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gt01-es.jpg"/></table-wrap>
      <p>En la espirometr&#237;a, el promedio del &#237;ndice VEF<sub>1 </sub>/CVF% fue de 44 &#177; 5% en el grupo EPOC, y de 74 &#177; 2% en el grupo control. Teniendo en cuenta la clasificaci&#243;n de GOLD<sup>22</sup>, por los criterios espirom&#233;tricos el grupo EPOC se caracteriz&#243; como severa (estadio III) y el grupo control present&#243; par&#225;metros de normalidad. </p>
      <p>En la gasometr&#237;a, en el grupo EPOC, la PaO<sub>2 </sub>promedio fue de 60,6 &#177; 6,1 mmHg y el PaCO<sub>2</sub> promedio fue de 36,7 &#177; 6,9 mmHg, compatibles con la literatura en portadores de EPOC con severidad estadio III<sup>22</sup>. </p>
      <p>En la polisonograf&#237;a del grupo EPOC se observ&#243; el tiempo total de sue&#241;o de 326,7 &#177; 70 minutos, inferior al deseado, pero concordante con la revisi&#243;n liter&#225;ria<sup>16</sup>. El promedio de la eficiencia del sue&#241;o fue del 74,8%, poco abajo del valor preconizado como ideal para individuos de ese grupo de edad, alrededor del 80%. El promedio de latencia del sue&#241;o fue de 29,7 &#177; 30 minutos, poco arriba del esperado. El promedio de latencia del sue&#241;o REM (LatREM) de 151 &#177; 84 minutos, se increment&#243; m&#225;s all&#225; del tiempo esperado de 150 minutos. Ning&#250;n paciente present&#243; privaci&#243;n del sue&#241;o REM. La ausencia de &#237;ndice de apnea-hipopnea fue <underline>&gt;</underline> 5. </p>
      <p>Los par&#225;metros de presi&#243;n arterial y oxim&#233;tricos est&#225;n demostrados en la <xref ref-type="table" rid="tab02-body3">Tabla 2</xref> y se describen a continuaci&#243;n. </p>
      <table-wrap id="tab02-body3">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gt02-es.jpg"/></table-wrap>
      <p>Respecto al descenso del sue&#241;o, se observaron diferencias significativas, tanto en la medida sist&#243;lica como en la diast&#243;lica, con descenso atenuado en el grupo EPOC y fisiol&#243;gico en el grupo control, seg&#250;n el <xref ref-type="fig" rid="grf01-body3">Gr&#225;fico 1</xref>.</p>
      <fig id="grf01-body3">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf01-es.jpg"/></fig>
      <p>En cuanto a los par&#225;metros de la presi&#243;n arterial sist&#243;lica en vigilia (mmHg), se observa que tanto el valor promedio, como el m&#237;nimo y el m&#225;ximo, se presentaron estad&#237;sticamente mayores en el grupo EPOC que en el grupo control, con p-valores 0,009, 0,018 y 0,032, respectivamente. Sin embargo, los par&#225;metros de la presi&#243;n arterial diast&#243;lica en vigilia no presentaron diferencias significativas entre grupos.</p>
      <p>Las tomas de la presi&#243;n arterial durante el sue&#241;o (mmHg) se mostraron estad&#237;sticamente mayores entre los individuos del grupo EPOC que en el grupo control, a excepci&#243;n del valor m&#225;ximo de la presi&#243;n diast&#243;lica, que no demuestra diferencia significativa entre los grupos. </p>
      <p>En cuanto al par&#225;metro del promedio de presi&#243;n en las 24 horas, se observaron valores estad&#237;sticamente mayores en el grupo EPOC para la presi&#243;n arterial sist&#243;lica (p=0,002). La medici&#243;n diast&#243;lica no present&#243; diferencia significativa entre los grupos. Los valores promedios de las mediciones de la presi&#243;n arterial en el per&#237;odo matutino, tanto la sist&#243;lica como la diast&#243;lica, se hallaron estad&#237;sticamente mayores en el grupo EPOC. </p>
      <p>La medici&#243;n de la saturaci&#243;n m&#237;nima alcanzada en el per&#237;odo de sue&#241;o (SpO<sub>2</sub> m&#237;nima %) no revel&#243; diferencia significativa entre los dos grupos, seg&#250;n el <xref ref-type="fig" rid="grf02-body3">Gr&#225;fico 2</xref>. El par&#225;metro que evidenci&#243; relevante diferencia fue el tiempo de desaturaci&#243;n del grupo EPOC (T90 &gt; 30%), mientras que en el grupo control fue cercano a cero, seg&#250;n detalla el <xref ref-type="fig" rid="grf03-body3">Gr&#225;fico 3</xref>. </p>
      <fig id="grf02-body3">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf02-es.jpg"/></fig>
      <fig id="grf03-body3">
        <graphic xlink:href="1678-4170-abc-93-03-0275-00012-gf03-es.jpg"/></fig>
      <p>
        <bold>Discusi&#243;n</bold>
      </p>
      <p>La EPOC se caracteriza por ser una enfermedad compleja, con limitaci&#243;n al flujo a&#233;reo, parcialmente reversible con el uso de f&#225;rmacos broncodilatadores<sup>3,5-7</sup>, presentando comorbilidades cardiovasculares<sup>1-7</sup>.</p>
      <p>En la presente investigaci&#243;n, se estudiaron variables de la presi&#243;n arterial y oxim&#233;tricas en portadores de EPOC. Los resultados se compararon al grupo control, con caracter&#237;sticas antropom&#233;tricas semejantes. </p>
      <p>En el grupo EPOC, todos eran hipox&#233;micos al sue&#241;o (T90 promedio de 42 &#177;36) y presentaban compromiso en la calidad del sue&#241;o<sup>14</sup>, con eficiencia del sue&#241;o poco abajo del ideal en comparaci&#243;n a individuos sanos de ese grupo de edad (80%), y par&#225;metros de latencia del sue&#241;o y LatREM arriba de lo esperado. Ning&#250;n paciente presentaba cuadro de apnea del sue&#241;o.</p>
      <p><italic>Descenso de la PA en el sue&#241;o -</italic> Los pacientes portadores de EPOC presentaron promedio de descenso del sue&#241;o atenuado (sist&#243;lico y diast&#243;lico), mientras que pacientes sin EPOC presentaron promedio de descenso del sue&#241;o fisiol&#243;gico (sist&#243;lico y diast&#243;lico)<sup>23</sup>. Trabajos de Tanigawa et al<sup>24</sup> correlacionaron la severidad de los disturbios respiratorios a la elevaci&#243;n en niveles diast&#243;licos en el sue&#241;o, lo que perjudic&#243; el descenso fisiol&#243;gico en ese per&#237;odo. Nuestros datos est&#225;n de acuerdo con la literatura<sup>24</sup>, cuando se menciona la reducci&#243;n promedio de la saturaci&#243;n de ox&#237;geno en el per&#237;odo de sue&#241;o y descenso del sue&#241;o. Ello puede ocurrir a causa del accionamiento del gatillo simp&#225;tico por la hip&#243;xia nocturna, liberando catecolaminas en la circulaci&#243;n sangu&#237;nea y elevando, as&#237;, los niveles de presi&#243;n<sup>25</sup>. </p>
      <p> El rol del sistema nervioso aut&#243;nomo sobre el descenso del sue&#241;o todav&#237;a es un asunto controvertido. Sin embargo, evidencias de la participaci&#243;n simp&#225;tica en la regulaci&#243;n de la presi&#243;n arterial se hallan presentes en portadores de SAOS<sup>25</sup>, en los que por la hipoxia y la hipercapnia, los quimiorreceptores accionan el aumento de actividad simp&#225;tica<bold>. </bold>La respuesta vasoconstrictora simp&#225;tica a los eventos apneicos ocasiona elevaciones de la presi&#243;n arterial durante el sue&#241;o, principalmente a la finalizaci&#243;n del evento apneico. Oliveira et cols.<sup>26</sup> relatan que la ausencia de descenso de presi&#243;n en el sue&#241;o ha sido atribuida a la disfunci&#243;n nerviosa auton&#243;mica, relacion&#225;ndose al aumento del riesgo cardiovascular y lesiones en &#243;rganos blanco, principalmente en masa ventricular izquierda, enfermedad cerebrovascular silenciosa y microalbuminuria. </p>
      <p><italic>En vigilia -</italic> Se observaron niveles sist&#243;licos m&#225;s elevados en el grupo EPOC en valores promedio, m&#237;nimo y m&#225;ximo. Seg&#250;n la literatura, el subestudio <italic>Syst-Eur</italic><sup>27</sup>, evidenci&#243; que la hipertensi&#243;n sist&#243;lica aislada en pacientes adultos mayores est&#225; asociada al descenso del sue&#241;o atenuado, con asociaci&#243;n inversa entre el descenso de la presi&#243;n arterial y el riesgo cardiovascular. En el per&#237;odo de la vigilia no se observaron diferencias significativas en niveles diast&#243;licos (valores promedio, m&#237;nimo y m&#225;ximo) entre los grupos. </p>
      <p><italic>En el sue&#241;o - </italic>La presi&#243;n arterial durante el sue&#241;o fue m&#225;s elevada en el grupo EPOC en presi&#243;n arterial sist&#243;lica (PAS) - valores promedio, m&#237;nimo y m&#225;ximo -, y presi&#243;n arterial diast&#243;lica (PAD) - valores promedio y m&#237;nimo. El valor m&#225;ximo de la PAD durante el sue&#241;o no revel&#243; diferencia entre los grupos EPOC y control. En el sue&#241;o, aunque los mediadores de la presi&#243;n arterial no est&#233;n completamente elucidados, la presi&#243;n arterial y la frecuencia cardiaca se correlacionan a la actividad del sistema nervioso simp&#225;tico<sup>28</sup>.</p>
      <p><italic>Promedio en las 24 horas</italic> - El promedio de los valores de PAS a las 24 horas fue mayor en el grupo EPOC, sin diferencia con relaci&#243;n al promedio de la PAD en el periodo. Seg&#250;n datos de la literatura, los promedios de presi&#243;n obtenidos en las 24 horas se constituyen en el "patr&#243;n oro" entre los par&#225;metros obtenidos por el m&#233;todo, por presentar correlaciones m&#225;s precisas con lesiones en &#243;rganos blanco, morbilidad y mortalidad<sup>28</sup>. </p>
      <p><italic>En el per&#237;odo matutino -</italic> Los valores promedios de PAS y PAD fueron estad&#237;sticamente mayores en el grupo EPOC, en comparaci&#243;n con el grupo control. Seg&#250;n estos resultados, estudios evidencian que el descenso del sue&#241;o atenuado o inexistente predispone al mantenimiento de presi&#243;n arterial elevada a las primeras horas de la ma&#241;ana. Eguchi et al<sup>18</sup> y Kario et al<sup>29,30</sup> definieron que el incremento de los niveles de presi&#243;n, en las dos primeras horas tras el despertar, se correlacion&#243; de modo significativo a la mayor prevalencia de infartos cerebrales. La elevaci&#243;n de niveles de presi&#243;n en per&#237;odo matutino se correlaciona a un mayor riesgo de lesiones de &#243;rganos blanco y eventos cardiovasculares, as&#237; como el incremento en el riesgo de isquemia coronaria y accidentes cerebrovasculares<sup>27,31-34</sup>. Concordante con nuestros resultados, Kishimoto et al<sup>35</sup> describieron que la reducci&#243;n en la saturaci&#243;n de ox&#237;geno en el sue&#241;o, se correlacion&#243; significativamente a la elevaci&#243;n de presi&#243;n matinal. Elliot<sup>33</sup> y Cohen et al<sup>34</sup> correlacionaron la hipertensi&#243;n matutina a la mayor mortalidad cardiovascular. </p>
      <p><italic>En cuanto a los par&#225;metros de la saturaci&#243;n de ox&#237;geno (SpO<sub>2</sub> m&#237;nima %) y T90 (%) -</italic> El grupo EPOC revel&#243; desaturaci&#243;n m&#225;s prolongada en el per&#237;odo de sue&#241;o. En el grupo control, la evaluaci&#243;n se llev&#243; a cabo por la oximetr&#237;a digital, cuya exactitud diagn&#243;stica tiene comprobaci&#243;n en la literatura en diversos estudios<sup>17-19</sup>. El grupo control, por la oximetr&#237;a, evidenci&#243; episodios de desaturaci&#243;n m&#237;nima sin diferencia significativa en relaci&#243;n con el grupo EPOC, aunque de duraci&#243;n insignificante (cercana a cero / episodios puntuales), mientras que el grupo EPOC present&#243; desaturaci&#243;n m&#225;s prolongada. Seg&#250;n la literatura, estudios de Tanigawa et al<sup>24</sup> correlacionaron el &#237;ndice de desaturaci&#243;n de ox&#237;geno por la oximetr&#237;a de pulso con niveles de presi&#243;n. El &#237;ndice de desaturaci&#243;n de ox&#237;geno (3%) estaba asociado a la elevaci&#243;n en PAS de 0,8 mmHg (P= 0,05) y incremento de PAD de 0,7 mmHg (P= 0,05). </p>
      <p><italic>Limitaciones del estudio</italic> - Se correlaciona al tama&#241;o de la muestra, hecho que result&#243; de la severidad de la patolog&#237;a en los individuos del grupo EPOC con desaturaci&#243;n nocturna, adultos mayores en su gran parte, que presentaron dificultad f&#237;sica a la realizaci&#243;n de ex&#225;menes complementarios. Se puede notar que en hospitales p&#250;blicos y privados, hubo una demanda reprimida de camas para el estudio del sue&#241;o, hecho que justifica la oximetr&#237;a como m&#233;todo de an&#225;lisis de pacientes sin EPOC y sin quejas sugestivas de disturbios de sue&#241;o, ante de los estudios ya citados<sup>17-19</sup>, que evidenciaron comparabilidad entre los m&#233;todos. La oximetr&#237;a es el examen m&#225;s f&#225;cilmente realizable, por su menor coste con respecto a la polisonograf&#237;a. Las polisonograf&#237;as son muy costosas y dispendiosas, hecho que limita su indicaci&#243;n en pacientes no portadores de quejas relacionadas a sue&#241;o.</p>
      <p>En este trabajo, se utiliz&#243; la polisonograf&#237;a para diferenciar las variables del sue&#241;o y, en particular, identificar a individuos portadores o no de s&#237;ndrome de apnea obstructiva del sue&#241;o. El examen se realiz&#243; en solamente una noche de sue&#241;o.</p>
      <p>Pese a la limitaciones, consideramos que el estudio tiene validez en la correlaci&#243;n de enfermedad pulmonar cr&#243;nica severa, senilidad, presi&#243;n arterial y niveles oxim&#233;tricos.</p>
      <p>
        <bold>Conclusiones</bold>
      </p>
      <p>Nuestro estudio sugiere que el descenso del sue&#241;o se halla atenuado o ausente en pacientes con EPOC desaturados en el sue&#241;o. Los resultados de la presi&#243;n arterial sist&#243;lica y diast&#243;lica se hallaron mayores en el grupo EPOC que en el grupo control. La significancia de esa afirmaci&#243;n ocurri&#243; en todos los per&#237;odos calculados, a excepci&#243;n de la vigilia y en las 24 horas y valores m&#225;ximos al sue&#241;o para niveles de presi&#243;n diast&#243;lica. As&#237; que se puede concluir, en este estudio, que el grupo portador de EPOC posee niveles de presi&#243;n arterial mayores que el grupo control, hecho que puede resultar de la activaci&#243;n simp&#225;tica incrementada, por la desaturaci&#243;n en el sue&#241;o. </p>
      <p>
        <bold>Potencial Conflicto de Intereses</bold>
      </p>
      <p>Declaro no haber conflicto de intereses pertinentes.</p>
      <p>
        <bold>Fuentes de Financiaci&#243;n</bold>
      </p>
      <p>El presente estudio no tuvo fuentes de financiaci&#243;n externas.</p>
      <p>
        <bold>Vinculaci&#243;n Acad&#233;mica</bold>
      </p>
      <p>Este art&#237;culo forma parte de tesis de maestr&#237;a de Neila Anders Aidar por la Universidad de Brasilia - UnB.</p>
      <p>
        <bold>Referencias</bold>
      </p>
    </body>
  </sub-article>
</article>
