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  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">ijcs</journal-id>
      <journal-title-group>
        <journal-title>International Journal of Cardiovascular Sciences</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Int J Cardiovasc Sci</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">2359-4802</issn>
      <issn pub-type="epub">2359-5647</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id specific-use="scielo-v3" pub-id-type="publisher-id">vPBdbfwgw3fKTZT6h4znySq</article-id>
      <article-id specific-use="scielo-v2" pub-id-type="publisher-id">S2359-56472025000100108</article-id>
      <article-id pub-id-type="doi">10.36660/ijcs.20250032</article-id>
      <article-id pub-id-type="other">00108</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Short Editorial</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Obstructive Sleep Apnea in Acute Myocardial Infarction: A Prognostic Risk Factor beyond Traditional Players?</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Wollmann</surname>
            <given-names>Carlos</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
        </contrib>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-2081-6846</contrib-id>
          <name>
            <surname>Drager</surname>
            <given-names>Luciano F.</given-names>
          </name>
          <xref ref-type="aff" rid="aff2">
            <sup>2</sup>
          </xref>
          <xref ref-type="corresp" rid="c1"/>
        </contrib>
        <aff id="aff1">
          <label>1</label>
          <institution content-type="orgname">Universidade de S&#227;o Paulo</institution>
          <institution content-type="orgdiv1">Faculdade de Medicina</institution>
          <addr-line>
            <named-content content-type="city">Bauru</named-content>
            <named-content content-type="state">SP</named-content>
          </addr-line>
          <country country="BR">Brazil</country>
          <institution content-type="original">Faculdade de Medicina, Universidade de S&#227;o Paulo, Bauru, SP - Brazil</institution>
        </aff>
        <aff id="aff2">
          <label>2</label>
          <institution content-type="orgname">Universidade de S&#227;o Paulo</institution>
          <institution content-type="orgdiv1">Instituto do Cora&#231;&#227;o (InCor) e Disciplina de Nefrologia</institution>
          <institution content-type="orgdiv2">Unidades de Hipertens&#227;o</institution>
          <addr-line>
            <named-content content-type="city">S&#227;o Paulo</named-content>
            <named-content content-type="state">SP</named-content>
          </addr-line>
          <country country="BR">Brazil</country>
          <institution content-type="original">Unidades de Hipertens&#227;o, Instituto do Cora&#231;&#227;o (InCor) e Disciplina de Nefrologia, Universidade de S&#227;o Paulo, S&#227;o Paulo, SP - Brazil</institution>
        </aff>
      </contrib-group>
      <author-notes>
        <corresp id="c1"><label>Mailing Address:</label><bold>Luciano F. Drager &#8226;</bold> Universidade de S&#227;o Paulo. Av., En&#233;as de Carvalho Aguiar, 44, 2&#186; andar, bloco 2, sala 8. Postal code: <postal-code>05403-900</postal-code>. S&#227;o Paulo, SP &#8211; Brazil E-mail: <email>luciano.drager@incor.usp.br</email></corresp>
      </author-notes>
      <pub-date publication-format="electronic" date-type="pub">
        <day>08</day>
        <month>05</month>
        <year>2025</year>
      </pub-date>
      <pub-date publication-format="electronic" date-type="collection">
        <year>2025</year>
      </pub-date>
      <volume>38</volume>
      <elocation-id>e20250032</elocation-id>
      <permissions>
        <license license-type="open-access" xml:lang="en" xlink:href="https://creativecommons.org/licenses/by/4.0/">
          <license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
        </license>
      </permissions>
      <kwd-group xml:lang="en">
        <title>Keywords</title>
        <kwd>Sleep</kwd>
        <kwd>Myocardial Infarction</kwd>
        <kwd>Prognosis</kwd>
        <kwd>Risk Factors</kwd>
        <kwd>Obstructive Sleep Apnea</kwd>
      </kwd-group>
      <counts>
        <fig-count count="0"/>
        <table-count count="0"/>
        <equation-count count="0"/>
        <ref-count count="13"/>
      </counts>
    </article-meta>
  </front>
  <body>
    <p>The high prevalence of obstructive sleep apnea (OSA) and its worrisome association with various cardiovascular diseases, particularly ischemic heart disease, demand our attention.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> This common sleep disordered breathing, characterized by partial or complete upper airway obstructions during sleep, profoundly impacts overall health.<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup> In the cardiovascular context, intermittent hypoxia, sleep fragmentation, and intrathoracic pressure swings promoted by repeated respiratory events during sleep promote several potentially deleterious phenomena, including increased sympathetic activity, blood pressure fluctuations, chronic systemic inflammation, reactive oxygen species production, and endothelial dysfunction.<sup><xref ref-type="bibr" rid="B1">1</xref>-<xref ref-type="bibr" rid="B3">3</xref></sup> These factors create a fertile ground for the development and progression of atherosclerosis,<sup><xref ref-type="bibr" rid="B4">4</xref>,<xref ref-type="bibr" rid="B5">5</xref></sup> significantly increasing the likelihood of ischemic events if the condition remains undetected and untreated.<sup><xref ref-type="bibr" rid="B6">6</xref>,<xref ref-type="bibr" rid="B7">7</xref></sup> However, the relationship between OSA and acute myocardial infarction (AMI) is complex.<sup><xref ref-type="bibr" rid="B8">8</xref></sup> Patients with OSA often share risk factors that also increase AMI risk, notably age, male sex, and obesity. While some evidence suggests an independent role for OSA in the cardiovascular risk,<sup><xref ref-type="bibr" rid="B6">6</xref></sup> its contribution remains controversial in high-risk patients with multiple comorbidities.<sup><xref ref-type="bibr" rid="B8">8</xref></sup> Further research in this area is therefore warranted in order to provide additional insights.</p>
    <p>In this issue of the <italic>International Journal of Cardiovascular Sciences</italic>, Carrijo et al. explore the complex relationship between OSA and traditional risk factors in 145 patients with ST-segment elevation myocardial infarction (STEMI).<sup><xref ref-type="bibr" rid="B9">9</xref></sup> The authors used employed the widely used STOP-BANG questionnaire to assess OSA risk. The initial results were consistent with previous literature: a high frequency (58.6%) of patients exhibited a high risk for OSA. This highlights the urgent need for increased attention to this comorbidity, particularly in this specific patient population.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> In the multivariate analysis, the authors found an independent association of OSA with both male sex and hypertension in these patients. The presence of hypertension in OSA patients is not coincidental. Some of the aforementioned mechanisms associated with OSA directly contribute to elevated blood pressure, thereby increasing cardiovascular risk.<sup><xref ref-type="bibr" rid="B2">2</xref>,<xref ref-type="bibr" rid="B3">3</xref></sup></p>
    <p>While studies addressing OSA in the cardiovascular context are welcome, some aspects of the study warrant careful interpretation: 1) the study highlights the utility of screening tools such as the STOP-BANG questionnaire for identifying patients with a higher probability of OSA.<sup><xref ref-type="bibr" rid="B11">11</xref></sup> Despite being simple and easily applicable, several questionnaires (including the STOP-BANG) lack appropriate sensitivity and specificity in detecting OSA. In addition, questionnaires are not able to characterize OSA severity. Instead, full polysomnography (the gold standard for OSA diagnosis)<sup><xref ref-type="bibr" rid="B1">1</xref>,<xref ref-type="bibr" rid="B2">2</xref></sup> or even portable monitoring devices would provide more comprehensive information on OSA severity, including the analysis of metrics of nocturnal hypoxia, a key factor in cardiovascular risk;<sup><xref ref-type="bibr" rid="B10">10</xref></sup> 2) Although the authors found independent associations of OSA with male sex and hypertension, the limited sample size precluded exploration of whether OSA independently worsens the prognosis in these AMI patients or whether the cardiovascular risk attributable to OSA is partially mediated by sex and comorbidities such as hypertension. Two recent studies from the same group addressed this issue.<sup><xref ref-type="bibr" rid="B12">12</xref>,<xref ref-type="bibr" rid="B13">13</xref></sup> In the first, Wang and colleagues analyzed the relationship between OSA severity (assessed by the apnea-hypopnea index, AHI) and adverse cardiovascular events (AMI, stroke, and cardiovascular death) in a prospective cohort of patients with acute coronary syndrome (ACS).<sup><xref ref-type="bibr" rid="B12">12</xref></sup> The main results demonstrated an association between higher AHI and adverse cardiovascular events in both men and women with ACS. In the second study,<sup><xref ref-type="bibr" rid="B13">13</xref></sup> the same authors investigated the association between OSA (also measured by AHI) and major long-term cardiovascular events (stroke, non-fatal AMI, and cardiovascular death) in ACS patients with and without hypertension. The main results indicated an independent association between higher AHI and increased risk of major cardiovascular events, irrespective of hypertension status.<sup><xref ref-type="bibr" rid="B13">13</xref></sup> These studies shed light on the potential role of OSA in the context of ACS.</p>
    <p>In conclusion, the high frequency of increased OSA risk in AMI patients reinforces the existing literature and highlights the growing need to raise suspicion for this important sleep disorder in high-risk cardiovascular patients. The significant impact of this comorbidity on clinical outcomes underscores the urgent need for research focused on optimizing practical early diagnosis and developing effective therapeutic strategies for this patient population.</p>
  </body>
  <back>
    <fn-group>
      <fn fn-type="other" id="fn1">
        <label>Editorial referring to the article:</label>
        <p>Associated Factors to the Risk of Obstructive Sleep Apnea in the Acute Phase of Myocardial Infarction</p>
      </fn>
    </fn-group>
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