<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.1 20151215//EN" "https://jats.nlm.nih.gov/publishing/1.1/JATS-journalpublishing1.dtd">
<article xmlns:xlink="http://www.w3.org/1999/xlink" specific-use="sps-1.9" dtd-version="1.1" xml:lang="pt" article-type="research-article">
  <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">4QTcjwJS6NqPB8xDMZg3xnx</article-id>
      <article-id pub-id-type="other">00005</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2004000500005</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(04)08200505</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2004000500005</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Artigos Originais</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Avalia&#231;&#227;o das press&#245;es sist&#243;lica, diast&#243;lica e press&#227;o de pulso como fator de risco para doen&#231;a ateroscler&#243;tica coronariana grave em mulheres com angina inst&#225;vel ou infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Sousa</surname>
            <given-names>Jos&#233; Marconi Almeida de</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Hermann</surname>
            <given-names>Jo&#227;o L. V.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Guimar&#227;es</surname>
            <given-names>Jo&#227;o B.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Menezes</surname>
            <given-names>Pedro Paulo O.</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Carvalho</surname>
            <given-names>Antonio Carlos Camargo</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
          <xref ref-type="aff" rid="aff02"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="state">S&#227;o Paulo</named-content>
        </addr-line>
        <institution content-type="orgname">Universidade Federal de S&#227;o Paulo</institution>
        <country country="BR">Brazil</country>
      </aff>
      <aff id="aff02">
        <addr-line>
          <named-content content-type="city">S&#227;o Paulo</named-content>
          <named-content content-type="state">SP</named-content>
        </addr-line>
        <institution content-type="orgname">Hospital Santa Marcelina</institution>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>05</month>
        <year>2004</year>
      </pub-date>
      <volume>82</volume>
      <issue>5</issue>
      <fpage>426</fpage>
      <lpage>429</lpage>
      <history>
        <date date-type="accepted">
          <day>03</day>
          <month>04</month>
          <year>2003</year>
        </date>
        <date date-type="received">
          <day>07</day>
          <month>01</month>
          <year>2003</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>OBJETIVO: Avaliar se as press&#245;es, medidas na raiz da aorta, s&#227;o fatores de risco para doen&#231;a ateroscler&#243;tica coronariana grave em mulheres com angina inst&#225;vel ou infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST (AI/IAMSS). M&#201;TODO:As press&#245;es, assim como os fatores de risco para doen&#231;a arterial coronariana (DAC) foram prospectivamente coletados de mar&#231;o/1993 a agosto/2001 em 593 mulheres com diagn&#243;stico de AI/IAMSS submetidas &#224; cinecoronariografia. Les&#245;es coronarianas definidas como graves estenoses &gt; 70%. RESULTADOS: Idade m&#233;dia de 59,2&#177;11,2 anos, significantemente mais alta nas pacientes com DAC: 61,9 &#177; 10,8 anos vs 56.4 &#177; 10,8 anos; tabagismo, diabetes e climat&#233;rio foram mais freq&#252;entes nas pacientes com DAC. As m&#233;dias das press&#245;es sist&#243;lica e arterial m&#233;dia foram iguais nos dois grupos, entretanto as m&#233;dias das press&#245;es diast&#243;licas do ventr&#237;culo esquerdo (17.6 &#177; 8.7 x 15.1 &#177; 8.1, p=0.001) e da press&#227;o de pulso a&#243;rtica foram significantemente maiores nas pacientes com DAC (75.5 &#177; 22 x 70 &#177; 19, p=0.002), enquanto a m&#233;dia da press&#227;o diast&#243;lica a&#243;rtica foi significantemente mais alta nas pacientes sem DAC (75.3 &#177; 17.5 x 79.8 &#177; 16, p=0.003). Na an&#225;lise multivariada a press&#227;o de pulso &gt; 80 mmHg e press&#227;o sist&#243;lica &gt; 165 foram independentemente associadas a DAC com raz&#227;o de chance de 2.12 e 2.09, p&lt;0.05, respectivamente. CONCLUS&#195;O: A doen&#231;a arterial coronariana est&#225; associada &#224; press&#227;o de pulso mais elevada e press&#227;o diast&#243;lica mais baixa em mulheres com AI/IAMSS. Embora a m&#233;dia da press&#227;o sist&#243;lica n&#227;o tenha se associado com DAC, valores dicotomisados de press&#227;o de pulso &gt; 80 mmHg e press&#227;o sist&#243;lica &gt; 165 mmHg determinaram risco duas vezes maior de les&#227;o coronariana grave.</p>
      </abstract>
      <kwd-group xml:lang="pt" kwd-group-type="author-generated">
        <kwd>doen&#231;a ateroscler&#243;tica coronariana grave</kwd>
        <kwd>angina inst&#225;vel</kwd>
        <kwd>infarto agudo do mioc&#225;rdio</kwd>
        <kwd>hipertens&#227;o</kwd>
      </kwd-group>
      <pub-date publication-format="electronic" date-type="pub">
        <day>08</day>
        <month>06</month>
        <year>2004</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>ARTIGO ORIGINAL</bold>
    </p>
    <p>Avalia&#231;&#227;o das press&#245;es sist&#243;lica, diast&#243;lica e press&#227;o de pulso como fator de risco para doen&#231;a ateroscler&#243;tica coronariana grave em mulheres com angina inst&#225;vel ou infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST</p>
    <p>
      <bold>Jos&#233; Marconi Almeida de Sousa; Jo&#227;o L. V. Hermann; Jo&#227;o B. Guimar&#227;es; Pedro Paulo O. Menezes; Antonio Carlos Camargo Carvalho</bold>
    </p>
    <p> Universidade Federal de S&#227;o Paulo e Hospital Santa Marcelina - S&#227;o Paulo, SP</p>
    <p>
      <xref ref-type="corresp" rid="back10">Endere&#231;o para correspond&#234;ncia</xref>
    </p>
    <p>
      <bold>RESUMO</bold>
    </p>
    <p><bold>OBJETIVO: </bold>Avaliar se as press&#245;es, medidas na raiz da aorta, s&#227;o fatores de risco para doen&#231;a ateroscler&#243;tica coronariana grave em mulheres com angina inst&#225;vel ou infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST (AI/IAMSS). </p>
    <p><bold>M&#201;TODO: </bold>As press&#245;es, assim como os fatores de risco para doen&#231;a arterial coronariana (DAC) foram prospectivamente coletados de mar&#231;o/1993 a agosto/2001 em 593 mulheres com diagn&#243;stico de AI/IAMSS submetidas &#224; cinecoronariografia. Les&#245;es coronarianas definidas como graves estenoses &gt; 70%. </p>
    <p>RESULTADOS: Idade m&#233;dia de 59,2&#177;11,2 anos, significantemente mais alta nas pacientes com DAC: 61,9 &#177; 10,8 anos vs 56.4 &#177; 10,8 anos; tabagismo, diabetes e climat&#233;rio foram mais freq&#252;entes nas pacientes com DAC. As m&#233;dias das press&#245;es sist&#243;lica e arterial m&#233;dia foram iguais nos dois grupos, entretanto as m&#233;dias das press&#245;es diast&#243;licas do ventr&#237;culo esquerdo (17.6 &#177; 8.7 x 15.1 &#177; 8.1, p=0.001) e da press&#227;o de pulso a&#243;rtica foram significantemente maiores nas pacientes com DAC (75.5 &#177; 22 x 70 &#177; 19, p=0.002), enquanto a m&#233;dia da press&#227;o diast&#243;lica a&#243;rtica foi significantemente mais alta nas pacientes sem DAC (75.3 &#177; 17.5 x 79.8 &#177; 16, p=0.003). Na an&#225;lise multivariada a press&#227;o de pulso <underline>&gt;</underline> 80 mmHg e press&#227;o sist&#243;lica <underline>&gt;</underline> 165 foram independentemente associadas a DAC com raz&#227;o de chance de 2.12 e 2.09, p&lt;0.05, respectivamente. </p>
    <p>CONCLUS&#195;O: A doen&#231;a arterial coronariana est&#225; associada &#224; press&#227;o de pulso mais elevada e press&#227;o diast&#243;lica mais baixa em mulheres com AI/IAMSS. Embora a m&#233;dia da press&#227;o sist&#243;lica n&#227;o tenha se associado com DAC, valores dicotomisados de press&#227;o de pulso <underline>&gt;</underline> 80 mmHg e press&#227;o sist&#243;lica <underline>&gt;</underline> 165 mmHg determinaram risco duas vezes maior de les&#227;o coronariana grave.</p>
    <p>Palavras-chave: doen&#231;a ateroscler&#243;tica coronariana grave, angina inst&#225;vel, infarto agudo do mioc&#225;rdio, hipertens&#227;o</p>
    <p>As press&#245;es sist&#243;lica, diast&#243;lica e a de pulso est&#227;o bem estabelecidas como fator de risco cardiovascular<sup>1</sup>. A press&#227;o de pulso &#233; o resultado da contra&#231;&#227;o card&#237;aca e das propriedades da circula&#231;&#227;o arterial, representando o componente puls&#225;til da press&#227;o arterial<sup>2</sup>, &#233; influenciada pela fra&#231;&#227;o de eje&#231;&#227;o, rigidez das grandes art&#233;rias, redu&#231;&#227;o precoce da onda de pulso e tamb&#233;m pela freq&#252;&#234;ncia card&#237;aca<sup>2</sup>. A press&#227;o arterial m&#233;dia representa o componente fixo da press&#227;o arterial e &#233; uma fun&#231;&#227;o da contratilidade ventricular esquerda, freq&#252;&#234;ncia card&#237;aca e da resist&#234;ncia vascular sist&#234;mica<sup>3</sup>.</p>
    <p>Dados do estudo de Framingham<sup>4</sup> demonstram que a press&#227;o sist&#243;lica aumenta continuamente com a idade em todos os grupos, ao passo que a press&#227;o diast&#243;lica aumenta at&#233; os 60 anos, diminuindo a seguir. Estudos epidemiol&#243;gicos t&#234;m demonstrado que os aumentos da press&#227;o sist&#243;lica e da press&#227;o de pulso est&#227;o mais relacionados a eventos coronarianos, enquanto a hipertens&#227;o diast&#243;lica aos acidentes vasculares cerebrais<sup>5,6</sup>. Essas press&#245;es podem ser verificadas n&#227;o invasivamente atrav&#233;s do manguito de press&#227;o e, de forma invasiva, em uma art&#233;ria perif&#233;rica ou na raiz da aorta. N&#227;o est&#225; claro ainda que tipo de press&#227;o, isolada ou combinada, apresenta melhor correla&#231;&#227;o com eventos cardiovasculares. Em homens jovens (&lt;60 anos) foi demonstrado recentemente<sup>7</sup> que a m&#233;dia das press&#245;es sist&#243;lica, diast&#243;lica e m&#233;dia foi um potente preditor de doen&#231;a cardiovascular, ao passo que a m&#233;dia de press&#227;o sist&#243;lica ou press&#227;o de pulso foi o preditor mais importante em homens mais velhos (&gt;60 anos).</p>
    <p>O objetivo deste estudo foi avaliar as press&#245;es medidas na raiz da aorta, como fator de risco para doen&#231;a ateroscler&#243;tica coronariana grave, em mulheres com angina inst&#225;vel ou infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST.</p>
    <p>
      <bold>M&#233;todo</bold>
    </p>
    <p>De mar&#231;o de 1993 a agosto de 2000 foram realizados 6.135 cateterismos card&#237;acos, em hospital terci&#225;rio do estado de S&#227;o Paulo, dos quais 645 realizados em mulheres com diagn&#243;stico de AI/IAMSS.</p>
    <p>Antes do procedimento, as pacientes foram submetidos &#224; hist&#243;ria cl&#237;nica padronizada, contendo dados referentes aos antecedentes e fatores de risco cardiovascular de acordo com o relato da paciente. Nesses fatores foram inclu&#237;dos: hipertens&#227;o arterial sist&#234;mica, diabetes mellitus tipo 1 ou 2, tabagismo, uso de anticoncepcional oral, sedentarismo, hist&#243;ria familiar para doen&#231;a cardiovascular, climat&#233;rio e dislipidemia.</p>
    <p>Foram consideradas diab&#233;ticas as pacientes com hist&#243;ria de diabetes, tratadas com dieta ou hipoglicemiantes orais, insulina ou ambos.</p>
    <p>Foi considerada hist&#243;ria familiar de doen&#231;a cardiovascular: hipertens&#227;o arterial sist&#234;mica e acidente vascular cerebral.</p>
    <p>Foi considerado infarto agudo do mioc&#225;rdio sem supradesnivelamento ST: hist&#243;ria cl&#237;nica compat&#237;vel associada a aumento nas enzimas card&#237;acas (CPK total e CK-MB) acima de duas vezes o valor padr&#227;o utilizado no hospital, sem a presen&#231;a de novas ondas Q no eletrocardiograma.</p>
    <p>No final do cateterismo card&#237;aco eram registradas em papel milimetrado as press&#245;es do ventr&#237;culo esquerdo e da aorta.</p>
    <p>Neste estudo foram analisadas as press&#245;es sist&#243;lica e diast&#243;lica final do ventr&#237;culo esquerdo e as press&#245;es sist&#243;lica e diast&#243;lica da aorta. Foi calculada ainda a press&#227;o de pulso a&#243;rtica, definida como a diferen&#231;a entre a press&#227;o sist&#243;lica e a press&#227;o diast&#243;lica a&#243;rtica, assim como a press&#227;o arterial m&#233;dia calculada pela f&#243;rmula: 2xPD/3+PS/3, sendo PD=Press&#227;o diast&#243;lica e PS=Press&#227;o sist&#243;lica.</p>
    <p>A coronariografia foi realizada pela t&#233;cnica de Sones ou Judkins e as coron&#225;rias filmadas em m&#250;ltiplas proje&#231;&#245;es ortogonais. Todos os vasos coronarianos principais e seus ramos, pontes de safena e enxerto de mam&#225;ria foram analisados visualmente por dois cardiologistas intervencionistas experientes, de forma cega para qualquer dado do paciente, inclusive o diagn&#243;stico de angina inst&#225;vel ou infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST, j&#225; que todos os exames realizados no servi&#231;o durante o per&#237;odo da coleta foram analisados conjuntamente. Estenose vascular <underline>&gt;</underline> 70%, visualmente, foi considerada grave<sup>8,9</sup>.</p>
    <p>A fra&#231;&#227;o de eje&#231;&#227;o foi calculada atrav&#233;s da ventriculografia esquerda em proje&#231;&#227;o obl&#237;qua anterior direita, no laborat&#243;rio de hemodin&#226;mica da Universidade Federal de S&#227;o Paulo, pelo m&#233;todo de Stanford, sempre pelo mesmo t&#233;cnico, com treinamento espec&#237;fico para esse procedimento. O m&#233;todo utiliza os contornos angiogr&#225;ficos em s&#237;stole e di&#225;stole, tendo como controle uma placa milimetrada ou uma esfera com di&#226;metro conhecido. Nos casos em que esses dois marcadores n&#227;o s&#227;o utilizados a refer&#234;ncia passa a ser o di&#226;metro do cateter utilizado na realiza&#231;&#227;o do procedimento. Um fator de calibra&#231;&#227;o que varia de acordo com a refer&#234;ncia usada tem que ficar em limites previamente definidos para evitar distor&#231;&#245;es. Nos casos em que a ventriculografia n&#227;o foi realizada a fra&#231;&#227;o de eje&#231;&#227;o foi determinada pelo ecocardiograma.</p>
    <p>As vari&#225;veis n&#227;o categ&#243;ricas foram comparadas por meio do teste do qui quadrado; vari&#225;veis cont&#237;nuas com distribui&#231;&#227;o normal foram comparadas atrav&#233;s da m&#233;dia, pelo teste t de Student, e vari&#225;veis cont&#237;nuas sem distribui&#231;&#227;o normal foram comparadas pela m&#233;dia e analisadas pelo teste de Mann-Whitney. Na an&#225;lise dos fatores de risco, foi constru&#237;do um modelo de regress&#227;o log&#237;stica envolvendo todos os fatores de risco e todas as press&#245;es que foram comparados pelo qui quadrado. V&#225;rios modelos de regress&#227;o foram constru&#237;dos incluindo apenas uma press&#227;o e associa&#231;&#245;es de press&#245;es. O modelo que mais contribuiu foi quando se analisou a press&#227;o sist&#243;lica dicotomizada <underline>&gt;</underline> 165 mmHg e a press&#227;o de pulso <underline>&gt;</underline> 80 mmHg. Em toda a an&#225;lise diferen&#231;a estatisticamente significante foi considerada quando o valor de p foi menor do que 0,05.</p>
    <p>
      <bold>Resultados</bold>
    </p>
    <p>Neste estudo foram analisadas 593 mulheres e exclu&#237;das 52 por falta de dados na ficha antes do exame ou por registro da manometria incompleto. Das 593 pacientes quase metade, 48%, era proveniente da enfermaria, um ter&#231;o de sua resid&#234;ncia e apenas 16,5% provinham da UTI. Angina inst&#225;vel foi o diagn&#243;stico em 512 (86,3%) pacientes e infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST em 81 (13,7%). N&#227;o houve diferen&#231;a entre os dois grupos (com e sem doen&#231;a arterial coronariana grave) em rela&#231;&#227;o ao diagn&#243;stico. Infarto agudo do mioc&#225;rdio sem supra e angina inst&#225;vel foi o diagn&#243;stico de 47 (16,1%) e 245 (83,9%) pacientes com doen&#231;a arterial coronariana versus 34 (11,3%) e 267 (88,7%) pacientes sem a doen&#231;a, respectivamente.</p>
    <p>A m&#233;dia de idade foi de 59,2&#177;11,2 anos, com varia&#231;&#227;o de 29 a 90 anos. As pacientes com doen&#231;a arterial coronariana foram significantemente mais idosas: 61,9 &#177; 10,8 anos versus 56,4 &#177; 10,8 anos. Dos fatores de risco, o tabagismo, diabetes e climat&#233;rio foram significantemente mais freq&#252;entes nas pacientes com doen&#231;a arterial coronariana. N&#227;o houve diferen&#231;a significante em rela&#231;&#227;o aos outros fatores de risco. Hist&#243;ria pr&#233;via de infarto agudo do mioc&#225;rdio e cirurgia de revasculariza&#231;&#227;o mioc&#225;rdica foram mais comuns nas pacientes com doen&#231;a arterial coronariana, entretanto n&#227;o houve diferen&#231;a significante entre os grupos em rela&#231;&#227;o &#224; presen&#231;a de angioplastia pr&#233;via (<xref ref-type="table" rid="tab1">tab. I</xref>).</p>
    <table-wrap id="tab1">
      <graphic xlink:href="1678-4170-abc-82-05-0426-00005-gt01.jpg"/></table-wrap>
    <p>Nos pacientes internados, o estudo hemodin&#226;mico foi realizado em m&#233;dia seis dias ap&#243;s a interna&#231;&#227;o. As m&#233;dias das press&#245;es sist&#243;lica e arterial m&#233;dia foram iguais nos dois grupos, entretanto as m&#233;dias das press&#245;es diast&#243;licas do ventr&#237;culo esquerdo e da press&#227;o de pulso a&#243;rtica foram significantemente mais elevadas nas pacientes com doen&#231;a arterial coronariana, enquanto a m&#233;dia da press&#227;o diast&#243;lica a&#243;rtica foi significantemente mais alta nas pacientes sem a doen&#231;a. (<xref ref-type="table" rid="tab2">tab. II</xref>)</p>
    <table-wrap id="tab2">
      <graphic xlink:href="1678-4170-abc-82-05-0426-00005-gt02.jpg"/></table-wrap>
    <p>Na an&#225;lise univariada de press&#227;o dicotomizada em valores crescentes de 5 mmHg, observou-se que n&#227;o houve diferen&#231;a entre os dois grupos na faixa de press&#227;o diast&#243;lica a&#243;rtica <underline>&gt;</underline> 95 mmHg at&#233; 120 mmHg. A faixa de press&#227;o diast&#243;lica a&#243;rtica <underline>&lt;</underline> 90 mmHg at&#233; 65 mmHg, foi significantemente mais freq&#252;ente nas pacientes sem doen&#231;a arterial coronariana (<xref ref-type="table" rid="tab3">tab. III</xref>).</p>
    <table-wrap id="tab3">
      <graphic xlink:href="1678-4170-abc-82-05-0426-00005-gt03.jpg"/></table-wrap>
    <p>Em rela&#231;&#227;o &#224; press&#227;o sist&#243;lica n&#227;o houve nenhum valor na an&#225;lise univariada que se correlacionasse com doen&#231;a ateroscler&#243;tica, entretanto a press&#227;o de pulso para qualquer valor &gt; 75 mmHg predominou nas pacientes com doen&#231;a arterial coronariana (55,8% x 44,0%), p=0.004. A press&#227;o arterial m&#233;dia apresentou comportamento irregular.</p>
    <p>Na an&#225;lise multivariada, levando-se em considera&#231;&#227;o a intera&#231;&#227;o entre a press&#227;o sist&#243;lica e a idade, com todos os fatores de risco e as press&#245;es sist&#243;lica, diast&#243;lica, m&#233;dia e de pulso n&#227;o houve qualquer correla&#231;&#227;o com doen&#231;a arterial coronariana em nenhuma dessas press&#245;es. Quando apenas uma press&#227;o entrou no modelo de regress&#227;o, a press&#227;o de pulso <underline>&gt;</underline> 80 mmHg e a press&#227;o sist&#243;lica <underline>&gt;</underline> 165 mmHg foram associadas significantemente com a doen&#231;a. Independente da associa&#231;&#227;o de press&#245;es analisadas, a press&#227;o de pulso e a press&#227;o sist&#243;lica acima desses valores se mantiveram significantemente associadas com doen&#231;a arterial coronariana. Al&#233;m disso, no modelo de regress&#227;o em que se utilizou as press&#245;es de pulso e sist&#243;lica associadas, elas se mantiveram preditores independentes de doen&#231;a arterial coronariana, com <italic>odds ratio</italic> de 1,9 e 2,1, respectivamente. (<xref ref-type="table" rid="tab4">tab. IV</xref>).</p>
    <table-wrap id="tab4">
      <graphic xlink:href="1678-4170-abc-82-05-0426-00005-gt04.jpg"/></table-wrap>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>O principal achado deste estudo &#233; a associa&#231;&#227;o da press&#227;o de pulso, em an&#225;lise univariada, a partir de 75 mmHg e na an&#225;lise multivariada a partir de 80 mmHg, com doen&#231;a arterial coronariana grave em mulheres com angina inst&#225;vel ou infarto agudo do mioc&#225;rdio sem supradesnivelamento. Al&#233;m disso, a press&#227;o sist&#243;lica acima de 165 mmHg tamb&#233;m se associou &#224; doen&#231;a grave sendo essas duas press&#245;es, a partir desses valores, preditores independentes de doen&#231;a arterial coronariana.</p>
    <p>O valor progn&#243;stico da press&#227;o de pulso j&#225; foi avaliado na popula&#231;&#227;o geral<sup>4,10,11</sup>, em pacientes hipertensos<sup>12,13</sup>, e em pacientes com d&#233;ficit da fun&#231;&#227;o ventricular com ou sem infarto agudo do mioc&#225;rdio pr&#233;vio<sup>14,15</sup> . A press&#227;o de pulso medida ao n&#237;vel da art&#233;ria braquial mostrou-se preditor independente da massa ventricular esquerda, hipertrofia vascular, eventos coronarianos e insufici&#234;ncia card&#237;aca<sup>10,16-19</sup>.</p>
    <p>Nosso estudo demonstra que press&#227;o de pulso <underline>&gt;</underline> 80 mmHg &#233; preditor independente de doen&#231;a arterial coronariana grave em mulheres com angina inst&#225;vel/infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST. Lee e cols<sup>5</sup>. analisaram a press&#227;o de pulso de forma invasiva e n&#227;o invasiva, em 159 pacientes com estenose mitral e demonstraram que press&#227;o de pulso <underline>&gt;</underline> 60 mmHg foi preditor independente da doen&#231;a arterial coronariana grave. Al&#233;m disso, press&#227;o de pulso <underline>&gt;</underline> 60 mmHg apresentou sensibilidade e especificidade de 88% e 77% para o diagn&#243;stico da doen&#231;a grave, respectivamente. O valor preditivo negativo foi de 93%.</p>
    <p>A maioria dos estudos da literatura que avaliou as v&#225;rias press&#245;es como fatores de risco para doen&#231;a cardiovascular foram estudos de coortes. Sesso e cols.<sup>7</sup> analisaram as press&#245;es sist&#243;lica, diast&#243;lica, m&#233;dia e press&#227;o de pulso como preditores de risco para eventos cardiovasculares, inclu&#237;dos infarto do mioc&#225;rdio, angina, cirurgia de revasculariza&#231;&#227;o mioc&#225;rdica, angioplastia coronariana percut&#226;nea, acidente vascular cerebral e morte card&#237;aca. Nesse estudo 11.150 homens foram acompanhados por 10,8 anos em m&#233;dia. Nos pacientes &lt; 60 anos a press&#227;o sist&#243;lica, diast&#243;lica e m&#233;dia foram preditores importantes de risco cardiovascular ao passo que nos homens acima de 60 anos, apenas as press&#245;es sist&#243;lica e de pulso foram associados com esse risco. A diferen&#231;a entre nosso estudo e este &#250;ltimo &#233; que mesmo corrigindo para a idade, a press&#227;o sist&#243;lica e de pulso foram fatores de risco independente para doen&#231;a arterial coronariana grave. Outro fator &#233; que nossa popula&#231;&#227;o &#233; exclusivamente feminina, o que pode explicar esse resultado, j&#225; que nas mulheres a press&#227;o sist&#243;lica continua aumentando at&#233; cerca de 80 anos de forma que hipertens&#227;o sist&#243;lica isolada &#233; mais freq&#252;ente nas mulheres do que nos homens<sup>18</sup>.</p>
    <p>Em outro estudo Pope e cols.<sup>19</sup> avaliaram 10.689 pacientes com quadro de dor precordial, tendo verificado uma associa&#231;&#227;o entre a press&#227;o de pulso mais alta e os pacientes que tiveram um diagn&#243;stico final de isquemia (P&lt;0,001); j&#225; no estudo de Framingham <sup>4</sup>, a press&#227;o de pulso foi um preditor mais potente de eventos cardiovasculares do que a press&#227;o diast&#243;lica ou a sist&#243;lica isoladamente. Mais recentemente, Millar e Lever <sup>20</sup> estudando homens hipertensos, desenvolveram um modelo de regress&#227;o log&#237;stica emp&#237;rico e complexo que levou em considera&#231;&#227;o a intera&#231;&#227;o das press&#227;o sist&#243;lica e diast&#243;lica bem como da press&#227;o de pulso na determina&#231;&#227;o do risco de eventos coronarianos. Esses autores demonstraram que a press&#227;o de pulso foi o fator preditivo mais potente para determina&#231;&#227;o do risco card&#237;aco, todavia foi dif&#237;cil de discerni-la da press&#227;o sist&#243;lica. Em todos esses estudos a press&#227;o de pulso foi medida de maneira n&#227;o invasiva, o que difere do nosso estudo em que essa avalia&#231;&#227;o foi central, medida na raiz da aorta, podendo neste caso ser menor do que a medida perif&#233;rica, j&#225; que a press&#227;o sist&#243;lica perif&#233;rica &#233; um pouco mais alta do que a central <sup>21</sup>.</p>
    <p>Com rela&#231;&#227;o &#224; press&#227;o diast&#243;lica como fator de risco nos dois grupos, a nossa casu&#237;stica corrobora alguns estudos epidemiol&#243;gicos, que demonstraram uma associa&#231;&#227;o inversa entre a press&#227;o diast&#243;lica e doen&#231;a arterial coronariana. De acordo com o estudo de Framingham, a press&#227;o sist&#243;lica aumenta com a idade em todos os grupos populacionais, ao passo que a press&#227;o diast&#243;lica eleva-se at&#233; os 60 anos e diminui a seguir.</p>
    <p>A press&#227;o de pulso &#233; um &#237;ndice da rigidez da parede arterial, que se altera com a idade; assim, al&#233;m da press&#227;o sist&#243;lica, a press&#227;o de pulso pode representar um fator mais importante associado &#224; doen&#231;a arterial coronariana tamb&#233;m em mulheres com angina inst&#225;vel/infarto agudo do mioc&#225;rdio sem supradesnivelamento do segmento ST. Al&#233;m disso, a hipertens&#227;o sist&#243;lica &#233; mais importante nas mulheres, o que pode tamb&#233;m ter influenciado este resultado. &#201; importante ressaltar que todos os estudos citados previamente avaliaram as v&#225;rias press&#245;es como fatores de risco para eventos coronarianos de qualquer natureza, diferente deste estudo em que essas press&#245;es foram avaliadas como risco para doen&#231;a arterial coronariana grave.</p>
    <p>O nosso estudo apresenta algumas limita&#231;&#245;es: foi um estudo retrospectivo, n&#227;o discriminando quem tomava ou n&#227;o medica&#231;&#245;es antihipertensivas; o diagn&#243;stico de hipertens&#227;o n&#227;o foi de acordo com os crit&#233;rios estabelecidos pela AHA/ACC e a popula&#231;&#227;o foi heterog&#234;nea em rela&#231;&#227;o a este diagn&#243;stico. Entretanto este &#233; o primeiro estudo numa popula&#231;&#227;o espec&#237;fica de pacientes a demonstrar a import&#226;ncia da press&#227;o de pulso n&#227;o para o diagn&#243;stico de eventos cardiovasculares, mas para a presen&#231;a de doen&#231;a ateroscler&#243;tica coronariana grave.</p>
    <p>
      <fn id="back10" fn-type="corresp">
        <p>Endere&#231;o para correspond&#234;ncia</p>
        <p> Dr. Jos&#233; Marconi Almeida de Sousa </p>
        <p> R: Vicente Felix, 60/121 &#150; Cerqueira C&#233;sar </p>
        <p> S&#227;o Paulo, SP Cep 01410-020 </p>
        <p> E-mail: </p>
        <p>
          <email xlink:href="jmarconi@cardiol.br">jmarconi@cardiol.br</email>
        </p>
      </fn>
    </p>
    <p>Recebido para Publica&#231;&#227;o em 7/1/03 </p>
    <p> Aceito em 3/4/03</p>
  </body>
  <back>
    <ref-list>
      <ref id="B1">
        <mixed-citation>1. Joint    National Committee by the Detection, Evaluation, and Treatment of High Blood    Pressure. The sixth report of the Joint National Committee on prevention, detection,    evaluation, and treatment of high blood pressure. Arch Intern Med 1997; 157:    2413-46.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure</article-title>
          <source>Arch Intern Med</source>
          <date>
            <year>1997</year>
          </date>
          <fpage>2413</fpage>
          <lpage>46</lpage>
          <volume>157</volume>
        </element-citation>
      </ref>
      <ref id="B2">
        <mixed-citation>2. Franklin    SS, Gustin W IV, Wong ND et al. Hemodynamic patterns of age-related changes    in blood pressure: the Framingham Heart Study. Circulation 1997; 96: 308-15.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Hemodynamic patterns of age-related changes in blood pressure: the Framingham Heart Study</article-title>
          <source>Circulation</source>
          <date>
            <year>1997</year>
          </date>
          <fpage>308</fpage>
          <lpage>15</lpage>
          <volume>96</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Franklin</surname>
              <given-names>SS</given-names>
            </name>
            <name>
              <surname>Gustin</surname>
              <given-names>W IV</given-names>
            </name>
            <name>
              <surname>Wong</surname>
              <given-names>ND</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B3">
        <mixed-citation>3. Benetos    A, Laurent S, Asmar RG, Lacolley P. Large artery stiffness in hypertension.    J Hypertens 1997; 15 Suppl: S89-97.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Large artery stiffness in hypertension</article-title>
          <source>J Hypertens</source>
          <date>
            <year>1997</year>
          </date>
          <fpage>S89</fpage>
          <lpage>97</lpage>
          <volume>15 Suppl</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Benetos</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Laurent</surname>
              <given-names>S</given-names>
            </name>
            <name>
              <surname>Asmar</surname>
              <given-names>RG</given-names>
            </name>
            <name>
              <surname>Lacolley</surname>
              <given-names>P</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B4">
        <mixed-citation>4. Franklin    SS, Khan SA, Wong ND, Larson MG, Levy D. Is pulse pressure useful in predicting    risk for coronary heart disease? The Framingham Heart Study. Circulation 1999;    100: 354-60.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Is pulse pressure useful in predicting risk for coronary heart disease?: The Framingham Heart Study</article-title>
          <source>Circulation</source>
          <date>
            <year>1999</year>
          </date>
          <fpage>354</fpage>
          <lpage>60</lpage>
          <volume>100</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Franklin</surname>
              <given-names>SS</given-names>
            </name>
            <name>
              <surname>Khan</surname>
              <given-names>SA</given-names>
            </name>
            <name>
              <surname>Wong</surname>
              <given-names>ND</given-names>
            </name>
            <name>
              <surname>Larson</surname>
              <given-names>MG</given-names>
            </name>
            <name>
              <surname>Levy</surname>
              <given-names>D</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B5">
        <mixed-citation>5. Lee ML,    Rosner BA, Vokonas PS, Weiss ST. Longitudinal analysis of adult male blood pressure:    the Normative Aging Study, 1963-1992. J Epidemiol Biostat 1996; 1: 79-87.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Longitudinal analysis of adult male blood pressure: the Normative Aging Study, 1963-1992</article-title>
          <source>J Epidemiol Biostat</source>
          <date>
            <year>1996</year>
          </date>
          <fpage>79</fpage>
          <lpage>87</lpage>
          <volume>1</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Lee</surname>
              <given-names>ML</given-names>
            </name>
            <name>
              <surname>Rosner</surname>
              <given-names>BA</given-names>
            </name>
            <name>
              <surname>Vokonas</surname>
              <given-names>PS</given-names>
            </name>
            <name>
              <surname>Weiss</surname>
              <given-names>ST</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B6">
        <mixed-citation>6. Tate    RB, Manfreda J, Krahn AD, Cuddy TE. Tracking of blood pressure over a 40-year    period in the University of Manitoba Follow-up Study, 1948-1988. Am J Epidemiol    1995; 142: 946-54.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Tracking of blood pressure over a 40-year period in the University of Manitoba Follow-up Study, 1948-1988</article-title>
          <source>Am J Epidemiol</source>
          <date>
            <year>1995</year>
          </date>
          <fpage>946</fpage>
          <lpage>54</lpage>
          <volume>142</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Tate</surname>
              <given-names>RB</given-names>
            </name>
            <name>
              <surname>Manfreda</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Krahn</surname>
              <given-names>AD</given-names>
            </name>
            <name>
              <surname>Cuddy</surname>
              <given-names>TE</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B7">
        <mixed-citation>7. Sesso    HD, Stampfer MJ, Rosner B et al. Systolic and diastolic blood pressure, pulse    pressure, and mean arterial pressure as predictors of cardiovascular disease    risk in men. Hypertension 2000; 36: 801-7.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Systolic and diastolic blood pressure, pulse pressure, and mean arterial pressure as predictors of cardiovascular disease risk in men</article-title>
          <source>Hypertension</source>
          <date>
            <year>2000</year>
          </date>
          <fpage>801</fpage>
          <lpage>7</lpage>
          <volume>36</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Sesso</surname>
              <given-names>HD</given-names>
            </name>
            <name>
              <surname>Stampfer</surname>
              <given-names>MJ</given-names>
            </name>
            <name>
              <surname>Rosner</surname>
              <given-names>B</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B8">
        <mixed-citation>8. Ellis    SG, Vandormael MG, Cowley MJ et al. Coronary morphology and clinical determinants    of procedural outcome with angioplasty for multivessel coronary disease. Implications    for patient selection. Multivessel angioplasty prognosis study group. Circulation    1990; 82: 1193-202.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Coronary morphology and clinical determinants of procedural outcome with angioplasty for multivessel coronary disease</article-title>
          <source>Implications for patient selection. Multivessel angioplasty prognosis study group. Circulation</source>
          <date>
            <year>1990</year>
          </date>
          <fpage>1193</fpage>
          <lpage>202</lpage>
          <volume>82</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Ellis</surname>
              <given-names>SG</given-names>
            </name>
            <name>
              <surname>Vandormael</surname>
              <given-names>MG</given-names>
            </name>
            <name>
              <surname>Cowley</surname>
              <given-names>MJ</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B9">
        <mixed-citation>9. Ryan    TJ, Bauman WB, Kennedy JW et al - Guidelines for percutaneous transluminal coronary    angioplasty: A report of the American Heart Association/American College of    Cardiology Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular    Procedures (Subcommittee on Percutaneous Transluminal Coronary Angioplasty).    Circulation 1993; 88: 2987-3007.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Guidelines for percutaneous transluminal coronary angioplasty: A report of the American Heart Association/American College of Cardiology Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee on Percutaneous Transluminal Coronary Angioplasty)</article-title>
          <source>Circulation</source>
          <date>
            <year>1993</year>
          </date>
          <fpage>2987</fpage>
          <lpage>3007</lpage>
          <volume>88</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Ryan</surname>
              <given-names>TJ</given-names>
            </name>
            <name>
              <surname>Bauman</surname>
              <given-names>WB</given-names>
            </name>
            <name>
              <surname>Kennedy</surname>
              <given-names>JW</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B10">
        <mixed-citation>10. Mandhavan    S, Ooi WL, Cohen H, Alderman MH. Relation of pulse pressure and blood pressure    reduction to the incidence of myocardial infarction. Hypertension 1994; 23:    395-401.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Relation of pulse pressure and blood pressure reduction to the incidence of myocardial infarction</article-title>
          <source>Hypertension</source>
          <date>
            <year>1994</year>
          </date>
          <fpage>395</fpage>
          <lpage>401</lpage>
          <volume>23</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Mandhavan</surname>
              <given-names>S</given-names>
            </name>
            <name>
              <surname>Ooi</surname>
              <given-names>WL</given-names>
            </name>
            <name>
              <surname>Cohen</surname>
              <given-names>H</given-names>
            </name>
            <name>
              <surname>Alderman</surname>
              <given-names>MH</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B11">
        <mixed-citation>11. Khattar    RS, Acharya DU, Kinsey C, Senior R, Lahiri A. Longitudinal association of ambulatory    blood pressure with left ventricular mass and vascular hypertrophy in essential    hypertension. J Hypertens 1997; 15: 737-43.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Longitudinal association of ambulatory blood pressure with left ventricular mass and vascular hypertrophy in essential hypertension</article-title>
          <source>J Hypertens</source>
          <date>
            <year>1997</year>
          </date>
          <fpage>737</fpage>
          <lpage>43</lpage>
          <volume>15</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Khattar</surname>
              <given-names>RS</given-names>
            </name>
            <name>
              <surname>Acharya</surname>
              <given-names>DU</given-names>
            </name>
            <name>
              <surname>Kinsey</surname>
              <given-names>C</given-names>
            </name>
            <name>
              <surname>Senior</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Lahiri</surname>
              <given-names>A</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B12">
        <mixed-citation>12. Benetos    A, Rudnichi A, Safar M, Guize L. Pulse pressure and cardiovascular mortality    in normotensive and hypertensive subjects. Hypertension 1998; 32: 560-4.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects</article-title>
          <source>Hypertension</source>
          <date>
            <year>1998</year>
          </date>
          <fpage>560</fpage>
          <lpage>4</lpage>
          <volume>32</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Benetos</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Rudnichi</surname>
              <given-names>A</given-names>
            </name>
            <name>
              <surname>Safar</surname>
              <given-names>M</given-names>
            </name>
            <name>
              <surname>Guize</surname>
              <given-names>L</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B13">
        <mixed-citation>13. Antikainen    RL, Jousilathi P, Vanhanen H, Tuomilehto J. Excess mortality associated with    pulse pressure among middle-aged men and women is explained by high systolic    pressure. J Hypertens 2000; 18: 417-23.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Excess mortality associated with pulse pressure among middle-aged men and women is explained by high systolic pressure</article-title>
          <source>J Hypertens</source>
          <date>
            <year>2000</year>
          </date>
          <fpage>417</fpage>
          <lpage>23</lpage>
          <volume>18</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Antikainen</surname>
              <given-names>RL</given-names>
            </name>
            <name>
              <surname>Jousilathi</surname>
              <given-names>P</given-names>
            </name>
            <name>
              <surname>Vanhanen</surname>
              <given-names>H</given-names>
            </name>
            <name>
              <surname>Tuomilehto</surname>
              <given-names>J</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B14">
        <mixed-citation>14. Domanski    MJ, Mitchell GF, Norman JE, Exner DV, Pitt B, Pfeffer MA. Independent prognostic    information provided by sphygmomanometrically determined pulse pressure and    mean arterial pressure in patients with left ventricular dysfunction. J Am Coll    Cardiol 1999; 33: 951-8.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Independent prognostic information provided by sphygmomanometrically determined pulse pressure and mean arterial pressure in patients with left ventricular dysfunction</article-title>
          <source>J Am Coll Cardiol</source>
          <date>
            <year>1999</year>
          </date>
          <fpage>951</fpage>
          <lpage>8</lpage>
          <volume>33</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Domanski</surname>
              <given-names>MJ</given-names>
            </name>
            <name>
              <surname>Mitchell</surname>
              <given-names>GF</given-names>
            </name>
            <name>
              <surname>Norman</surname>
              <given-names>JE</given-names>
            </name>
            <name>
              <surname>Exner</surname>
              <given-names>DV</given-names>
            </name>
            <name>
              <surname>Pitt</surname>
              <given-names>B</given-names>
            </name>
            <name>
              <surname>Pfeffer</surname>
              <given-names>MA</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B15">
        <mixed-citation>15. Wenger    NK. The natural history of coronary artery disease in women. In Pamela Charney    (ed). Coronary Artery Disease in Women. Philadelphia: American College of Physicians     American Society of Internal Medicine;1999: 3-35.</mixed-citation>
        <element-citation publication-type="book">
          <source>Coronary Artery Disease in Women</source>
          <date>
            <year>1999</year>
          </date>
          <fpage>3</fpage>
          <lpage>35</lpage>
          <person-group person-group-type="author">
            <name>
              <surname>Wenger</surname>
              <given-names>NK</given-names>
            </name>
            <name>
              <surname>Charney</surname>
              <given-names>Pamela</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B16">
        <mixed-citation>16. Blacher    J, Staessen JA, Girerd X et al. Pulse pressure  not mean pressure  determines    cardiovascular risk in older hypertensive patients. Arch Intern Med 2000; 160:    1085-9.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Pulse pressure - not mean pressure - determines cardiovascular risk in older hypertensive patients</article-title>
          <source>Arch Intern Med</source>
          <date>
            <year>2000</year>
          </date>
          <fpage>1085</fpage>
          <lpage>9</lpage>
          <volume>160</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Blacher</surname>
              <given-names>J</given-names>
            </name>
            <name>
              <surname>Staessen</surname>
              <given-names>JA</given-names>
            </name>
            <name>
              <surname>Girerd</surname>
              <given-names>X</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B17">
        <mixed-citation>17. Millar    JA, Lever AF, Burke V. Pulse pressure as a risk factor for cardiovascular events    in the MRC Mild Hypertension trial. J Hypertens 1999: 17: 1065-72.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Pulse pressure as a risk factor for cardiovascular events in the MRC Mild Hypertension trial</article-title>
          <source>J Hypertens</source>
          <date>
            <year>1999</year>
          </date>
          <fpage>1065</fpage>
          <lpage>72</lpage>
          <volume>17</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Millar</surname>
              <given-names>JA</given-names>
            </name>
            <name>
              <surname>Lever</surname>
              <given-names>AF</given-names>
            </name>
            <name>
              <surname>Burke</surname>
              <given-names>V</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B18">
        <mixed-citation>18. Mitchell    GF, Moyle LA, Braunwald E et al. Sphygmomanometrically determined pulse pressure    is a powerful independent predictor of recurrent events after myocardial infarction    in patients with impaired left ventricular function. Circulation 1997; 96: 4254-60.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Sphygmomanometrically determined pulse pressure is a powerful independent predictor of recurrent events after myocardial infarction in patients with impaired left ventricular function</article-title>
          <source>Circulation</source>
          <date>
            <year>1997</year>
          </date>
          <fpage>4254</fpage>
          <lpage>60</lpage>
          <volume>96</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Mitchell</surname>
              <given-names>GF</given-names>
            </name>
            <name>
              <surname>Moyle</surname>
              <given-names>LA</given-names>
            </name>
            <name>
              <surname>Braunwald</surname>
              <given-names>E</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B19">
        <mixed-citation>19. Pope    JH, Ruthazer R, Beshansky JR, Griffith JL, Selker HP. Clinical features of emergency    departments patients presenting with symptoms suggestive of acute cardiac ischemia:    a multicenter study. J Thromb Thrombolysis 1998; 6: 63-74.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Clinical features of emergency departments patients presenting with symptoms suggestive of acute cardiac ischemia: a multicenter study</article-title>
          <source>J Thromb Thrombolysis</source>
          <date>
            <year>1998</year>
          </date>
          <fpage>63</fpage>
          <lpage>74</lpage>
          <volume>6</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Pope</surname>
              <given-names>JH</given-names>
            </name>
            <name>
              <surname>Ruthazer</surname>
              <given-names>R</given-names>
            </name>
            <name>
              <surname>Beshansky</surname>
              <given-names>JR</given-names>
            </name>
            <name>
              <surname>Griffith</surname>
              <given-names>JL</given-names>
            </name>
            <name>
              <surname>Selker</surname>
              <given-names>HP</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B20">
        <mixed-citation>20. Millar    JA, Lever AF. Implications of pulse pressure as a predictor of cardiac risk    in patients with hypertension. Hypertension 2000; 36: 907-11.</mixed-citation>
        <element-citation publication-type="journal">
          <article-title>Implications of pulse pressure as a predictor of cardiac risk in patients with hypertension</article-title>
          <source>Hypertension</source>
          <date>
            <year>2000</year>
          </date>
          <fpage>907</fpage>
          <lpage>11</lpage>
          <volume>36</volume>
          <person-group person-group-type="author">
            <name>
              <surname>Millar</surname>
              <given-names>JA</given-names>
            </name>
            <name>
              <surname>Lever</surname>
              <given-names>AF</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
      <ref id="B21">
        <mixed-citation>21. Lambert    CR, Pepine CJ. Nichols WW. Pressure measurement and determination of vascular    resistence. In: Pepine CJ, Hill JA, Lambert CR. Diagnostic and therapeutic cardiac    catheterization. Baltimore: Williams &amp; Wilkins; 1994: 355-71.</mixed-citation>
        <element-citation publication-type="book">
          <source>Diagnostic and therapeutic cardiac catheterization</source>
          <date>
            <year>1994</year>
          </date>
          <fpage>355</fpage>
          <lpage>71</lpage>
          <person-group person-group-type="author">
            <name>
              <surname>Lambert</surname>
              <given-names>CR</given-names>
            </name>
            <name>
              <surname>Pepine</surname>
              <given-names>CJ</given-names>
            </name>
            <name>
              <surname>Nichols</surname>
              <given-names>WW</given-names>
            </name>
            <name>
              <surname>Pepine</surname>
              <given-names>CJ</given-names>
            </name>
            <name>
              <surname>Hill</surname>
              <given-names>JA</given-names>
            </name>
            <name>
              <surname>Lambert</surname>
              <given-names>CR</given-names>
            </name>
          </person-group>
        </element-citation>
      </ref>
    </ref-list>
  </back>
  <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">Evaluation of systolic, diastolic, and pulse pressure as risk factors for severe coronary arteriosclerotic disease in women with unstable angina non-ST-elevation acute myocardial infarction</article-title>
      </title-group>
      <abstract xml:lang="en">
        <p>OBJECTIVE: To evaluate pressures assessed at the aortic root as risk factors for severe atherosclerotic coronary heart disease in women with unstable angina/compatible clinical history associated with increase in cardiac enzymes (total CPK and CK-MB) 2 times greater than the standard value used in the hospital, with the absence of new Q waves on the electrocardiogram (UA/NSTEMI). METHODS: Five hundred and ninety-three female patients with clinical diagnosis of UA/NSTEMI underwent cinecoronariography from March 1993 to August 2001, and the risk factors for CHD were studied. During examination the pressures, at the aortic root, and coronary obstructions were visually assessed by 2 interventional cardiologists, and those stenosis over 70% were considered severe. RESULTS: Eight-one per cent of the population was white and 18.3% was black. Mean age was 59.2&#177;11.2 years, and it was significantly higher in patients with severe coronary lesions: 61.9 &#177; 10.8 years versus 56.4 &#177; 10.8 years; smoking, diabetes mellitus and climacteric were more frequent in patients with CHD. The average mean arterial pressure and mean systolic blood pressure was the same in both groups, however, average left ventricle diastolic pressure (17.6 &#177; 8.7 x 15.1 &#177; 8.1, p=0.001), and aortic pulse pressure were significantly greater in patients with CHD (75.5 &#177; 22 x 70 &#177; 19, p=0.002), while average aortic diastolic pressure was significantly greater in patients without CHD (79.8 &#177; 16 x 75.3 &#177; 17.5, p=0.003). In the multivariated analysis, pulse pressure &gt; 80 mmHg and systolic blood pressure &gt; 165 were independently associated with severe CHD with odds ratio of 2.12 and 2.09, p&lt;0.05, respectively. CONCLUSION: CHD is associated with increased pulse pressure and lower diastolic blood pressure in women with UA/NSTEMI. Although average systolic blood pressure has not been associated with CHD in this population, dichotomized values of pulse pressure &gt; 80 mmHg and systolic blood pressure &gt; 165 mmHG determined risk two times greater of severe coronary disease.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <kwd>coronary arterioscherotic disease</kwd>
        <kwd>unstable angina</kwd>
        <kwd>acute myocardial infarction</kwd>
        <kwd>hypertension</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <p>
        <bold>ORIGINAL ARTICLE</bold>
      </p>
      <p>Evaluation of systolic, diastolic, and pulse pressure as risk factors for severe coronary arteriosclerotic disease in women with unstable angina non-ST-elevation acute myocardial infarction</p>
      <p>
        <bold>Jos&#233; Marconi Almeida de Sousa; Jo&#227;o L. V. Hermann; Jo&#227;o B. Guimar&#227;es; Pedro Paulo O. Menezes; Antonio Carlos Camargo Carvalho</bold>
      </p>
      <p> Universidade Federal de S&#227;o Paulo-UNIFESP and Hospital Santa Marcelina - S&#227;o Paulo, SP - Brazil</p>
      <p>
        <xref ref-type="corresp" rid="back10-body2">Correspondence</xref>
      </p>
      <p>
        <bold>ABSTRACT</bold>
      </p>
      <p><bold>OBJECTIVE:</bold> To evaluate pressures assessed at the aortic root as risk factors for severe atherosclerotic coronary heart disease in women with unstable angina/compatible clinical history associated with increase in cardiac enzymes (total CPK and CK-MB) 2 times greater than the standard value used in the hospital, with the absence of new Q waves on the electrocardiogram (UA/NSTEMI).</p>
      <p><bold>METHODS: </bold>Five hundred and ninety-three female patients with clinical diagnosis of UA/NSTEMI underwent cinecoronariography from March 1993 to August 2001, and the risk factors for CHD were studied. During examination the pressures, at the aortic root, and coronary obstructions were visually assessed by 2 interventional cardiologists, and those stenosis over 70% were considered severe.</p>
      <p><bold>RESULTS: </bold>Eight-one per cent of the population was white and 18.3% was black. Mean age was 59.2&#177;11.2 years, and it was significantly higher in patients with severe coronary lesions: 61.9 &#177; 10.8 years versus 56.4 &#177; 10.8 years; smoking, diabetes mellitus and climacteric were more frequent in patients with CHD. The average mean arterial pressure and mean systolic blood pressure was the same in both groups, however, average left ventricle diastolic pressure (17.6 &#177; 8.7 x 15.1 &#177; 8.1, p=0.001), and aortic pulse pressure were significantly greater in patients with CHD (75.5 &#177; 22 x 70 &#177; 19, p=0.002), while average aortic diastolic pressure was significantly greater in patients without CHD (79.8 &#177; 16 x 75.3 &#177; 17.5, p=0.003). In the multivariated analysis, pulse pressure <underline>&gt;</underline> 80 mmHg and systolic blood pressure <underline>&gt;</underline> 165 were independently associated with severe CHD with odds ratio of 2.12 and 2.09, p&lt;0.05, respectively.</p>
      <p><bold>CONCLUSION: </bold>CHD is associated with increased pulse pressure and lower diastolic blood pressure in women with UA/NSTEMI. Although average systolic blood pressure has not been associated with CHD in this population, dichotomized values of pulse pressure <underline>&gt;</underline> 80 mmHg and systolic blood pressure <underline>&gt;</underline> 165 mmHG determined risk two times greater of severe coronary disease.</p>
      <p><bold>Key words: </bold>coronary arterioscherotic disease, unstable angina, acute myocardial infarction, hypertension</p>
      <p>Systolic blood pressure, diastolic blood pressure, and pulse pressure are well established as risk factors for cardiovascular disease <sup>1</sup>. Pulse pressure is the result of cardiac contraction and the properties of arterial circulation, representing the pulsatile component of blood pressure <sup>2</sup>. It is influenced by ejection fraction, large artery stiffness, early reduction of pulse wave, and also by heart rate <sup>2</sup>. Mean blood pressure represents the steady component of blood pressure and is a function of left ventricular contractility, heart rate, and systemic vascular resistance <sup>3</sup>.</p>
      <p>Data from the Framingham study <sup>4</sup> show that systolic blood pressure increases continuously with age in all groups, whereas diastolic blood pressure increases until the age of 60 and then decreases. Epidemiological studies have shown that the increase in systolic blood pressure and pulse pressure is more often related to coronary events, while diastolic hypertension is more often related to stroke <sup>5,6</sup>. These pressures may be assessed noninvasively with a sphygmomanometer and, invasively, in a peripheral artery or at the aortic root. It is still not clear what kind of pressure, isolated or combined, has a better correlation with cardiovascular events. A recent study <sup>7</sup> showed that the average of systolic, diastolic, and mean blood pressure was a strong predictor of cardiovascular disease in young men (&lt;60 years), whereas average systolic blood pressure or pulse pressure was a more important predictor in older men (&gt;60 years).</p>
      <p>The objective of this study was to evaluate pressures assessed at the aortic root as risk factors for severe atherosclerotic coronary heart disease in women with unstable angina/compatible clinical history associated with increase in cardiac enzymes (total CPK and CK-MB) 2 times greater than the standard value used in the hospital, with the absence of new Q waves on the electrocardiogram (UA/NSTEMI).</p>
      <p>
        <bold>Methods</bold>
      </p>
      <p>From March 1993 to August 2001, 6,135 cardiac catheterizations were performed in an acute care hospital in S&#227;o Paulo State, of which 645 were performed in women with a diagnosis of UA/NSTEMI.</p>
      <p>Before the procedure, patients underwent a standard clinical history that included data concerning previous cardiovascular risk factors. We included in these factors: systemic arterial hypertension, diabetes mellitus type 1 or 2, smoking status, use of oral contraceptive, lack of exercise, family history of cardiovascular disease, climacteric, and dyslipidemia (information provided by the patient).</p>
      <p>Diabetes mellitus &#150; We considered diabetic patients to be those with a history of diabetes mellitus, treated with diet or oral hypoglycemic drugs, insulin, or both.</p>
      <p>Family history of cardiovascular disease (CVD) &#150; We included in the family history of CVD, systemic blood hypertension and stroke. The age of occurrence was not investigated.</p>
      <p>NSTEMI &#150; Compatible clinical history associated with an increase in cardiac enzymes (total CPK and CK-MB) 2 times greater than the standard value used in the hospital, with the absence of new Q waves on the electrocardiogram.</p>
      <p>At the end of cardiac catheterization, left ventricle (LV) and aortic pressures were recorded on millimetric paper.</p>
      <p>Left ventricle systolic and diastolic blood pressures, as well as aortic systolic and diastolic blood pressures were studied. Aortic pulse pressure was also assessed, defined as the difference between aortic systolic pressure and aortic diastolic pressure, similar to mean blood pressure calculated by the formula: 2xDP/3+SP/3, in that, DP = diastolic pressure and SP = systolic pressure.</p>
      <p>Coronariography was performed using Sones or Judkins techniques, and the coronaries were recorded in several orthogonal projections. All main coronary vessels and their branches, bypass, and mammary grafts were visually analyzed by 2 experienced interventional cardiologists, without knowledge of the patient's data, including the diagnosis of unstable angina (UA) or NSTSEMI. Vascular stenosis visually <underline>&gt;</underline> 70% was considered severe <sup>8,9</sup>.</p>
      <p>Ejection fraction was assessed through left ventriculography in the right anterior oblique projection at the hemodynamic laboratory of the Universidade Federal de S&#227;o Paulo (University of S&#227;o Paulo), using the Stanford method. It was always performed by the same technician, with specific training for this procedure. This method used angiographic contours during systole and diastole with a millimetric plate or a sphere of known diameter. When these 2 markers are not used, the catheter's diameter used in the procedure becomes the reference. A caliper factor that varies according to the reference used has to have previously set limits to avoid distortions. In cases where ventriculography was not performed, ejection fraction was determined with echocardiography.</p>
      <p>Non categorical variables were compared using the chi-square test; continuous variables with normal distribution were compared through the average, using the Student <italic>t</italic> test; and continuous variables without normal distribution were compared by averages and analyzed using the Mann-Whitney test. In the analysis of risk factors, a model of logistic regression was made involving all risk factors and pressures that were compared using the chi-square test. Several regression models were made including only 1 pressure and associations of pressures. The statistical model that most contributed was that obtained when we analyzed dichotomized systolic blood pressure <underline>&gt;</underline> 165 mmHg and pulse pressure <underline>&gt;</underline> 80 mmHg.</p>
      <p>A significant statistical difference was considered when P was &lt; 0.05.</p>
      <p>
        <bold>Results</bold>
      </p>
      <p>We analyzed 593 women; 52 patients were excluded due to lack of data in the chart before the examination or due to incomplete manometry records. Of the 593 patients, almost half (48%) came from the hospital ward, a third came from their houses, and only 16.5% came from the ICU. Unstable angina was present in 512 (86.3%) patients, and NSTEMI was present in 81 (13.7%). No difference existed in the diagnosis in either group (with or without severe CHD). Non-ST segment elevation myocardial infarction and unstable angina was the diagnosis in 47 patients (16.1%) and 245 patients (83.9%) with severe CHD versus 34 patients (11.3%) and 267 patients (88.7%) without severe CHD, respectively.</p>
      <p>The mean age of this cohort was 59.2&#177;11.2 years, ranging from 29 to 90 years. Patients with CHD were significantly older: 61.9 &#177; 10.8 years versus 56.4 &#177; 10.8 years. Of the risk factors for CHD, smoking, diabetes mellitus, and climacteric were more frequent in patients with CHD. No significant difference existed in relation to other risk factors. A previous history of AMI and myocardial revascularization surgery were more frequent in patients with CHD; however, no significant difference occurred between the groups in relation to the presence of previous angioplasty (<xref ref-type="table" rid="tab1-body2">tab. I</xref>).</p>
      <table-wrap id="tab1-body2">
        <graphic xlink:href="1678-4170-abc-82-05-0426-00005-gt01-en.jpg"/></table-wrap>
      <p>In admitted patients, a hemodynamic study was performed, on average, 6 days after admittance. The average mean systolic blood pressure and mean arterial pressure were the same in both groups; however, the average left ventricle diastolic blood pressure and aortic pulse pressure were significantly greater in patients with CHD, while the average aortic diastolic pressure was significantly greater in patients without CHD (<xref ref-type="table" rid="tab2-body2">tab. II</xref>).</p>
      <table-wrap id="tab2-body2">
        <graphic xlink:href="1678-4170-abc-82-05-0426-00005-gt02-en.jpg"/></table-wrap>
      <p>In the univariate analysis of dichotomized pressure in crescent values of 5 mmHg, we observed that no difference existed between the 2 groups in the diastolic aortic pressure spectrum <underline>&gt;</underline> 95 mmHg up to 120 mmHg. Diastolic aortic pressure spectrum <underline>&lt;</underline> 90 mmHg down to 65 mmHg, was significantly more frequent in patients without CHD (<xref ref-type="table" rid="tab3-body2">tab. III</xref>).</p>
      <table-wrap id="tab3-body2">
        <graphic xlink:href="1678-4170-abc-82-05-0426-00005-gt03-en.jpg"/></table-wrap>
      <p>Regarding systolic blood pressure, no value in the univariate analysis correlated with atherosclerotic disease; however, pulse pressure for any value &gt;75 mmHg was predominant in patients with CHD (55.8% x 44.0%), P = 0.004. Mean arterial pressure had an irregular behavior.</p>
      <p>In multivariate analysis (taking into account interaction between systolic blood pressure and age), with all risk factors, and<strike>,</strike> systolic blood pressure, diastolic blood pressure, mean pressure, and pulse pressure, CHD was not correlated with any of these pressures. When we used only 1 pressure in the regression model, pulse pressure <underline>&gt;</underline> 80 mmHg and systolic blood pressure <underline>&gt;</underline> 165 mmHg, a significant association was noted with CHD. Regardless of the association of pressures assessed, pulse pressure and systolic blood pressure above these values were significantly associated with CHD. Additionally, in the regression model, where associated pulse and systolic pressure were used, these pressures acted as independent predictors of CHD, with odds ratios of 1.9 and 2.1, respectively. (<xref ref-type="table" rid="tab4-body2">tab. IV</xref>). </p>
      <table-wrap id="tab4-body2">
        <graphic xlink:href="1678-4170-abc-82-05-0426-00005-gt04-en.jpg"/></table-wrap>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>The main finding of this study is the association of pulse pressure, in univariate analysis, above 75 mmHg, and in the multivariate analysis above 80 mmHg, with severe CHD in women with UA/NSTEMI. Additionally, systolic blood pressure &gt;165 mmHg was also associated with severe CHD, and above these values, were independent predictors of severe CHD.</p>
      <p>The prognostic value of pulse pressure has already been assessed in the population <sup>4,10,11</sup> of hypertensive patients <sup>12,13</sup>, and in patients with ventricular function impairment with or without previous acute myocardial infarction <sup>14,15</sup>. Pulse pressure assessed at the level of the brachial artery proved to be an independent predictor of left ventricular mass, vascular hypertrophy, coronary events, and heart failure <sup>10,16-19</sup>.</p>
      <p>Our study shows that pulse pressure <underline>&gt;</underline> 80 mmHg is an independent predictor of severe CHD in women with UA/NSTEMI. Lee et al <sup>5</sup> analyzed pulse pressure invasively and noninvasively in 159 patients with mitral stenosis and showed that pulse pressure <underline>&gt;</underline> 60 mmHg was an independent predictor of severe CHD. In addition, pulse pressure <underline>&gt;</underline> 60 mmHg had a sensitivity and specificity of 88% and 77%, respectively, for the diagnosis of severe CHD. The negative predictive value was 93%.</p>
      <p>The majority of studies reported in the literature that assessed several pressures as risk factors for cardiovascular diseases were cohort studies. Sesso et al <sup>7</sup> analyzed systolic, diastolic, mean arterial pressures, and pulse pressure as predictors of risk for cardiovascular events, including myocardial infarction, angina, myocardial revascularization, percutaneous coronary angioplasty, stroke, and cardiac death. In this study, 11,150 men were followed-up for 10.8 years on average. In patients under age 60, systolic, diastolic, and mean arterial pressure were important predictors of cardiovascular risk, while in men over 60, only systolic blood pressure and pulse pressure were associated with this risk. The difference between our study and the latter is that regardless of age, systolic blood pressure, and pulse pressure were independent risk factors for severe CHD. Another factor is an exclusively female population, which may explain this result, because in women systolic blood pressure increases up to about age 80, thus systolic hypertension is more frequent in women than it is in men <sup>18</sup>.</p>
      <p>In another study, Pope et al <sup>19</sup> assessed 10,689 patients with a clinical picture of precordial pain, verifying an association between higher PP and those patients who had a final diagnosis of ischemia (P&lt;0.001). In the Framingham study <sup>4</sup>, pulse pressure was a stronger predictor of cardiovascular events than was diastolic or systolic blood pressure alone. Recently, Millar and Lever <sup>20</sup>, studying hypertensive men, developed an empirical and complex model of logistic regression that took into account the interaction between systolic and diastolic blood pressure as well as pulse pressure to determine risk of coronary events. These authors showed that pulse pressure was the strongest predictive factor to determine cardiac risk; however, it was difficult to distinguish it from systolic blood pressure. In all these studies, pulse pressure was assessed noninvasively, distinguishing our study in which this evaluation was central, assessed at the aortic root, and in this case it can be lower than the peripheral measure, since peripheral systolic pressure is slightly higher than central systolic pressure <sup>21</sup>.</p>
      <p>Regarding diastolic blood pressure as a risk factor in the 2 groups, our sample corroborates some epidemiological studies that showed an inverse association between diastolic blood pressure and CHD. According to the Framingham study, systolic blood pressure increases with age in all population groups, but diastolic blood pressure increases up to age 60 and then decreases.</p>
      <p>Pulse pressure is an index of arterial wall stiffness, which changes with age; thus, besides systolic blood pressure, pulse pressure can represent a more important risk factor associated with CHD in women with UA/NSTEMI. Additionally, systolic hypertension is more important in women, which may have also influenced this result. It is important to stress that all previously mentioned studies assessed each and all pressures as risk factors for coronary events of any nature, which is different from our study where pressures were assessed as risks for severe CHD.</p>
      <p>Our study has some limitations: it was a retrospective study, we did not eliminate those who were taking antihypertensive medications; diagnosis of hypertension was not done according to the criteria established by AHA/ACC, and the population was heterogeneous regarding this diagnosis. However, this is the first study in a specific population to demonstrate the importance of pulse pressure not for diagnosis of cardiovascular events, but for the presence of severe coronary disease.</p>
      <p>In conclusion, we demonstrated that pulse pressure seems to be the most important component of pressure associated with severe CHD in women with UA/NSTEMI. The implications for a therapeutic approach are clear.</p>
      <p>
        <bold>References</bold>
      </p>
      <p>
        <fn id="back10-body2" fn-type="corresp">
          <p>Correspondence to</p>
          <p> Jos&#233; Marconi Almeida de Sousa</p>
          <p> Rua Vicente Felix, 60/121</p>
          <p> S&#227;o Paulo, SP &#150; Brazil</p>
          <p> Cep 01410-020 </p>
          <p> E-mail: </p>
          <p>
            <email xlink:href="jmarconi@cardiol.br">jmarconi@cardiol.br</email>
          </p>
        </fn>
      </p>
      <p>Received: 1/7/03</p>
      <p> Accepted: 4/3/03</p>
    </body>
  </sub-article>
</article>
