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  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">dic</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia Imagem cardiovascular</journal-title>
        
        <abbrev-journal-title abbrev-type="publisher">Arq Bras Cardiol: Imagem cardiovasc</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="epub">2675-312X</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia</publisher-name>
        
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id">2318-8219.20180029</article-id>
      <article-id pub-id-type="doi">10.5935/2318-8219.20180029</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Review Article</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>What’s New in Cardiac Amyloidosis?</article-title>
        <trans-title-group xml:lang="pt">
          <trans-title>O Que Há de Novo na Amiloidose Cardíaca?</trans-title>
        </trans-title-group>
      </title-group>
      <contrib-group><contrib contrib-type="author"><name><surname>Quagliato</surname><given-names>Priscila Cestari</given-names></name><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Vieira</surname><given-names>Elry M .</given-names><suffix>Segundo Neto</suffix></name><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Assef</surname><given-names>Jorge Eduardo</given-names></name><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Barretto</surname><given-names>Rodrigo B. de Mattos</given-names></name><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Correia</surname><given-names>Edilaide de Barros</given-names></name><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Savioli</surname><given-names>Felicio</given-names><suffix>Neto</suffix></name><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Lin-Wang</surname><given-names>Hui Tzu</given-names></name><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Hirata</surname><given-names>Mario Hiroyuki</given-names></name><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Smanio</surname><given-names>Paola Emanuela Poggio</given-names></name><xref ref-type="aff" rid="aff1"/></contrib></contrib-group>
      <aff id="aff1"><institution content-type="normalized"/><institution content-type="orgname">Instituto Dante Pazzanese de Cardiologia</institution><addr-line><named-content content-type="city">São Paulo</named-content><named-content content-type="state">SP</named-content></addr-line><country country="BR">Brazil</country><institution content-type="original">Instituto Dante Pazzanese de Cardiologia, São Paulo, SP - Brazil</institution></aff>
      <author-notes>
        <corresp id="c01"> Mailing Address: Priscila Cestari Quagliato • Av. Dr. Dante Pazzanese, 500. Postal Code 05410-000, Vila Mariana, São Paulo, SP − Brazil E-mail: <email>cestari.fpriscila@gmail.com</email> </corresp>
        <fn fn-type="con">
	<p>Authors’ contributions</p>
	<p>Manuscript writing: Quagliato PC; Critical revision of the manuscript as for important intellectual content: Quagliato PC.</p></fn><fn fn-type="conflict">

	<p>Potential Conflicts of Interest</p>
	<p>There are no relevant conflicts of interest.</p></fn>
      </author-notes>
      <pub-date date-type="pub" publication-format="electronic">
				<day>20</day>
				<month>01</month>
				<year>2022</year>
			</pub-date>
			<pub-date date-type="collection" publication-format="electronic">
        <season>Jul-Sep</season>
        <year>2018</year>
      </pub-date>
      <volume>31</volume>
      <issue>3</issue>
      <fpage>198</fpage>
      <lpage>203</lpage>
      <permissions>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/">
<license-p>
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
</license-p>
</license>
</permissions>
      <abstract><title>Abstract</title><sec><title>These are</title><p>Amyloidosis is characterized by the localized or systemic deposition of proteins with unstable tertiary structure, which aggregate and form amyloid fibrils. Cardiac amyloidosis is a frequently underdiagnosed condition and it is an important cause of heart failure. There are more than 30 known types of amyloid proteins, but only five often infiltrate the heart, causing cardiac amyloidosis. light chain immunoglobulin, heavy chain immunoglobulin, transthyretin, serum amyloid A and apolipoprotein AI, mostly in light chain immunoglobulin or transthyretin forms. According to the type of fibrillar protein deposited, cardiac amyloidosis has different clinical courses, prognosis and different forms of treatment. In this review, we address new techniques that allow the diagnosis of this entity, especially in situations of heart failure with preserved ejection fraction and restrictive heart diseases. Early diagnosis is fundamental in defining the best therapeutic approach and in the prognosis of these patients.</p></sec></abstract>
      <trans-abstract xml:lang="pt"><title>Resumo</title><sec><title>São elas</title><p>A amiloidose caracteriza-se pela deposição localizada ou sistêmica de proteínas com estrutura terciária instável, que se agregam e formam as fibrilas amiloidóticas. A amiloidose cardíaca é uma condição frequentemente subdiagnosticada e causa importante de insuficiência cardíaca. Existem mais de 30 tipos de proteínas amiloides conhecidas, mas somente cinco frequentemente infiltram o coração, causando a amiloidose cardíaca. imunoglobulina de cadeia leve, imunoglobulina de cadeia pesada, transtirretina, amiloide sérica A e apolipoproteína AI, sendo em sua maioria nas formas de imunoglobulina de cadeia leve ou transtirretina. De acordo com o tipo de proteína fibrilar depositado, a amiloidose cardíaca possui diferentes cursos clínicos, prognóstico e formas distintas de tratamento. Nesta revisão abordamos novas técnicas, que possibilitam o diagnóstico desta entidade, principalmente em situações de insuficiência cardíaca com fração de ejeção preservada e cardiopatias restritivas. O diagnóstico precoce é fundamental na definição da melhor abordagem terapêutica e no prognóstico desses pacientes.</p></sec></trans-abstract>
      <kwd-group xml:lang="en"><kwd>Amyloidosis/physiopathology</kwd><kwd>Heart Failure</kwd><kwd>Amyloid</kwd><kwd>Echocardiography, Doppler</kwd><kwd>Immunoglobulin Light-Chain Amyloidosis</kwd><kwd>Drug Therapy</kwd></kwd-group>
      <kwd-group xml:lang="pt"><kwd>Amiloidose/fisiopatologia</kwd><kwd>Insuficiência Cardíaca</kwd><kwd>Amilóide</kwd><kwd>Ecocardiografia Dopple</kwd><kwd>Amiloidose de Cadeia Leve de Imunoglobulina</kwd><kwd>Tratamento Farmacológico</kwd></kwd-group>
      <counts><fig-count count="0"/><table-count count="0"/><equation-count count="0"/><ref-count count="0"/><page-count count="6"/></counts>
    </article-meta>
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