<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.1 20151215//EN" "http://jats.nlm.nih.gov/publishing/1.1/JATS-journalpublishing1.dtd">
<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" article-type="editorial" dtd-version="1.1" specific-use="sps-1.9" xml:lang="en">
  <front>
    <journal-meta>
      <journal-id journal-id-type="nlm-ta">Int J Cardiovasc Sci</journal-id>
      <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">k453DZ458m9QZKp5TFbXVRn</article-id>
      <article-id specific-use="scielo-v2" pub-id-type="publisher-id">S2359-56472020000200143</article-id>
      <article-id pub-id-type="publisher-id">ijcs.20200023</article-id>
      <article-id pub-id-type="doi">10.36660/ijcs.20200023</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>EDITORIAL</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Arterial Stiffness: The New Frontier in Hypertension and Cardiovascular Disease</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <contrib-id contrib-id-type="orcid">0000-0002-6352-3330</contrib-id>
          <name>
            <surname>Campana</surname>
            <given-names>Erika Maria Gon&#231;alves</given-names>
          </name>
          <xref ref-type="aff" rid="aff1">
            <sup>1</sup>
          </xref>
          <xref ref-type="aff" rid="aff2">
            <sup>2</sup>
          </xref>
        </contrib>
      </contrib-group>
      <aff id="aff1">
        <label>1</label>
        <institution content-type="orgname">Universidade de Nova Igua&#231;u</institution>
        <addr-line>
          <named-content content-type="city">Nova Igua&#231;u</named-content>
          <named-content content-type="state">RJ</named-content>
        </addr-line>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade de Nova Igua&#231;u, Nova Igua&#231;u, RJ - Brazil</institution>
      </aff>
      <aff id="aff2">
        <label>2</label>
        <institution content-type="orgname">Universidade do Estado do Rio de Janeiro</institution>
        <addr-line>
          <named-content content-type="city">Rio de Janeiro</named-content>
          <named-content content-type="state">RJ</named-content>
        </addr-line>
        <country country="BR">Brazil</country>
        <institution content-type="original">Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ &#8211; Brazil</institution>
      </aff>
      <author-notes>
        <corresp id="c01"> Mailing Address: Erika Maria Gon&#231;alves Campana. Av. Ab&#237;lio Augusto T&#225;vora, 2134. Postal Code: 26275-580, Dom Rodrigo, Nova Igua&#231;u &#8211; Brazil. E-mail: <email>campanaemg@predialnet.com.br</email>, <email>campanaemg@gmail.com</email> </corresp>
      </author-notes>
      <pub-date date-type="pub" publication-format="electronic">
        <day>03</day>
        <month>04</month>
        <year>2020</year>
      </pub-date>
      <pub-date date-type="collection" publication-format="electronic">
        <season>Mar-Apr</season>
        <year>2020</year>
      </pub-date>
      <volume>33</volume>
      <issue>02</issue>
      <fpage>143</fpage>
      <lpage>144</lpage>
      <permissions>
        <license license-type="open-access" xlink:href="https://creativecommons.org/licenses/by/4.0/" xml:lang="en">
          <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">
        <kwd>Vascular Stiffness</kwd>
        <kwd>Hypertension</kwd>
        <kwd>Blood Pressure</kwd>
        <kwd>Indicators of Morbidity and Mortality</kwd>
        <kwd>Target Organs, Risk Factors</kwd>
      </kwd-group>
      <counts>
        <fig-count count="1"/>
        <table-count count="0"/>
        <equation-count count="0"/>
        <ref-count count="11"/>
        <page-count count="2"/>
      </counts>
    </article-meta>
  </front>
  <body>
    <p>Vascular age is a reflection of cardiovascular and non-cardiovascular factors that contribute to accelerated vascular aging (AVA) and stiffness of large elastic arteries, leading to increased cardiovascular morbidity and mortality.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> Arterial stiffness has been regarded as an important biomarker in the assessment of subclinical atherosclerosis and cardiovascular risk.<sup><xref ref-type="bibr" rid="B1">1</xref>-<xref ref-type="bibr" rid="B4">4</xref></sup> The addition of pulse wave velocity (PWV) measurements to traditional risk factors has improved the prediction of the ten-year risk of cardiovascular diseases in 13% of individuals at intermediate risk.<sup><xref ref-type="bibr" rid="B5">5</xref></sup></p>
    <p>In addition, the altered behavior of central hemodynamic parameters, such as central systolic blood pressure (cSBP) and the (heart rate-corrected) augmentation index (AI), is influenced by arterial stiffness and plays a crucial role in the interface between the traditional cardiovascular continuum vascular aging continuum, which represents the current view of the pathophysiology of cardiovascular diseases.<sup><xref ref-type="bibr" rid="B6">6</xref>-<xref ref-type="bibr" rid="B8">8</xref></sup> (<xref ref-type="fig" rid="f01">Figure 1</xref>)</p>
    <p>
      <fig id="f01">
        <label>Figure 1</label>
        <caption>
          <title>&#8211; Interaction between the traditional cardiovascular continuum and the vascular aging continuum (Adapted from Mikael et al.;6 and Dzau et al.8)</title>
          <p>
            <italic>LVH: left ventricular hypertrophy; CHD: coronary heart disease; AMI: acute myocardial infarction; AVA: accelerated vascular aging; isolated systolic hypertension</italic>
          </p>
        </caption>
        <graphic xlink:href="2359-5647-ijcs-33-02-0143-00023-gf01.tif"/></fig>
    </p>
    <p>Part of the residual cardiovascular risk in hypertensive patients, a concept that has gained much attention in recent years, has been related to the AVA process. An early detection of this condition allows a more effective cardiovascular protection. In the pathophysiology of the residual risk and development of cardiovascular disease, there is a bidirectional interaction of AVA and hypertension. The accumulation of risk factors contributes to changes in the vessel wall that lead to vascular aging and stiffening of elastic arteries, and consequent elevation of blood pressure levels. In the opposite direction, increased blood pressure promotes arterial stiffening, providing a feedback to the AVA process.<sup><xref ref-type="bibr" rid="B2">2</xref>-<xref ref-type="bibr" rid="B4">4</xref></sup></p>
    <p>The CAFE study<sup><xref ref-type="bibr" rid="B9">9</xref></sup> has presented the first evidence of the clinical impact of central hemodynamic parameters and arterial stiffness on the reduction of cardiovascular events. The therapeutic strategy of amlodipine plus perindopril promoted greater reductions in cSBP and cardiovascular events compared with atenolol plus thiazide (control intervention).</p>
    <p>Vlachopoulos et al.,<sup><xref ref-type="bibr" rid="B10">10</xref></sup>produced one of the most striking evidences of the clinical application of arterial stiffness in predicting the risk for cardiovascular events. In a meta-analysis, the authors showed that an increase in aortic PWV by 1 m/s was associated with an increase of 15% in cardiovascular mortality and 15% in all-cause mortality.</p>
    <p>Thus, the main guidelines on cardiovascular disease prevention have incorporated the assessment of arterial stiffness and central hemodynamics for risk stratification, aiming at early recognition of subclinical target organ lesions in patients&#8217; follow-up.<sup><xref ref-type="bibr" rid="B2">2</xref>-<xref ref-type="bibr" rid="B4">4</xref></sup></p>
    <p>In the article published in this issue, Barroso et al.,<sup><xref ref-type="bibr" rid="B11">11</xref></sup> present the results of the comparison of two methods of central pressure and arterial stiffness evaluation &#8211; applanation tonometry, considered the gold standard, and the oscillometric method that has been recently validated for clinical use. Twenty-seven patients were assessed using both methods. There was no difference in mean cSBP between the methods, but PWV and pulse pressure were underestimated by the oscillometric method. These results validate the oscillometric method for clinical application in the Brazilian population and suggest that patients with elevated PWV detected by the oscillometric method are at elevated cardiovascular risk, expressed by a more aggressive AVA process.</p>
    <p>The incorporation of arterial stiffness measures to traditional risk scores and its recognition as a biomarker of subclinical target organ lesion, significantly improves the capacity to predict cardiovascular events. This concept adds to the knowledge about the AVA in guiding the diagnosis, risk stratification and treatment of hypertensive patients, allowing a personalization of therapeutic strategies and reduction of hypertension-related risk.</p>
  </body>
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