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<article xlink="http://www.w3.org/1999/xlink" dtd-version="1.0" article-type="vascular-surgery" lang="en">
  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher">JOHS</journal-id>
      <journal-id journal-id-type="nlm-ta">Journ of Health Scien</journal-id>
      <journal-title-group>
        <journal-title>Journal of HealthCare Sciences</journal-title>
        <abbrev-journal-title abbrev-type="pubmed">Journ of Health Scien</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">2231-2196</issn>
      <issn pub-type="opub">0975-5241</issn>
      <publisher>
        <publisher-name>Radiance Research Academy</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id">445</article-id>
      <article-id pub-id-type="doi">http://dx.doi.org/10.52533/JOHS.2025.51105</article-id>
      <article-id pub-id-type="doi-url"/>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Vascular Surgery</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Impact of Chronic Inflammatory States on Aneurysm Wall Stability and Rupture Risk&#13;
</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Alanezi</surname>
            <given-names>Sami Abdullah</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alghamdi</surname>
            <given-names>Faisal Abdullah</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Almalki</surname>
            <given-names>Fahad Hussein</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Takrouni</surname>
            <given-names>Tharaa Younis</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alanazi</surname>
            <given-names>Ahmed Abdulhamid</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Fallaj</surname>
            <given-names>Ahlam Hamed Al</given-names>
          </name>
        </contrib>
      </contrib-group>
      <pub-date pub-type="ppub">
        <day>11</day>
        <month>11</month>
        <year>2025</year>
      </pub-date>
      <volume>5</volume>
      <issue>11</issue>
      <fpage>569</fpage>
      <lpage>577</lpage>
      <permissions>
        <copyright-statement>This article is copyright of Popeye Publishing, 2009</copyright-statement>
        <copyright-year>2009</copyright-year>
        <license license-type="open-access" href="http://creativecommons.org/licenses/by/4.0/">
          <license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 4.0) Licence. You may share and adapt the material, but must give appropriate credit to the source, provide a link to the licence, and indicate if changes were made.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>The frequency of cardiovascular diseases, such as aneurysms, continues to play a significant role in the current high death rates that are observed, even though life expectancy has increased in recent decades. In the event of an aneurysm rupture in the cerebral circulation or the abdominal aorta, the patient may experience sudden death or severe impairment. Morphological criteria like aneurysm size and growth rate have guided rupture risk assessment. Structure-only measures are limited since clinical findings show that small aneurysms can rupture while larger aneurysms stay stable. According to recent research, chronic inflammation is considered one of the most important factors that determine the stability of an aneurysm. The progressive breakdown of the wall is caused by the entry of inflammatory cells, the release of cytokines, and the activation of proteolytic enzymes. Apoptosis of vascular smooth muscle cells is induced by these mechanisms, which additionally promote neovascularization within the aneurysm wall. These mechanisms collectively enhance wall rupture risk and degradation. Consequently, hemodynamic or structural forces cannot explain aneurysm formation. However, it must be acknowledged that biological and mechanical variables interact complexly to trigger it. The intriguing techniques, such as positron emission tomography (PET) and vascular wall magnetic resonance imaging, can supplement current surveillance strategies, but study heterogeneity suggests standardization and validation. This narrative review explains chronic inflammation__ampersandsign#39;s effects on aneurysm wall biology using clinical, imaging, and experimental evidence. It contrasts abdominal aortic and cerebral aneurysms and explores therapeutic implications. These include risk classification models using inflammatory signs and anti-inflammatory drugs to reduce rupture risk.&#13;
</p>
      </abstract>
      <kwd-group>
        <kwd>chronic</kwd>
        <kwd> inflammation</kwd>
        <kwd> aneurysm</kwd>
        <kwd> aneurysm wall stability</kwd>
        <kwd> rupture risk</kwd>
      </kwd-group>
    </article-meta>
  </front>
</article>