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	<front>
		<journal-meta>
			<journal-id journal-id-type="publisher-id">ABC HF</journal-id>
			<journal-title-group>
				<journal-title>Phenomenology, Humanities and Sciences - Fenomenologia, Humanidades e Ciências</journal-title>
				<abbrev-journal-title abbrev-type="publisher">ABC Heart Fail Cardiomyop</abbrev-journal-title>
			</journal-title-group>
			<issn pub-type="epub">0000-0000</issn>
			<publisher>
				<publisher-name>Instituto de Treinamento e Pesquisa em Gestalt-terapia de Goiânia (ITGT); Associação Brasileira de Psicologia Fenomenológica (Abrapfe)</publisher-name>
			</publisher>
		</journal-meta>
		<article-meta>
			<article-id pub-id-type="publisher-id">abchf.20210032</article-id>
			<article-id pub-id-type="doi">10.36660/abchf.20210032</article-id>
			<article-categories>
				<subj-group subj-group-type="heading">
					<subject>Viewpoint</subject>
				</subj-group>
			</article-categories>
			<title-group>
				<article-title>Indications for Anticoagulation in Cardiac Amyloidosis</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0001-8922-4075</contrib-id>
					<name>
						<surname>Montera</surname>
						<given-names>Marcelo Westerlund</given-names>
					</name>
					<xref ref-type="aff" rid="aff1"/>
				</contrib>
			</contrib-group>
			<aff id="aff1">
				<institution content-type="orgname">Hospital Pró Cardíaco</institution>
				<institution content-type="orgdiv1">Centro de Insuficiência Cardíaca</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">Hospital Pró Cardíaco, Centro de Insuficiência Cardíaca, Rio de Janeiro, RJ - Brazil</institution>
			</aff>
			<author-notes>
				<corresp id="c01"> Mailing Address: Marcelo Montera <bold>•</bold> Rua Redentor, 111/301. Postal Code: 22421030, Ipanema , Rio de Janeiro, RJ - Brazil. E-mail: <email>mmontera@uol.com.br</email>
				</corresp>
				<fn fn-type="con">
					<p>Author Contributions</p>
					<p>Writing of the manuscript and Critical revision of the manuscript for intellectual content: Montera MW.</p>
				</fn>
				<fn fn-type="conflict">
					<p>Potential Conflict of Interest</p>
					<p>No potential conflict of interest relevant to this article was reported.</p>
				</fn>
			</author-notes>
			<pub-date date-type="pub" publication-format="electronic">
				<day>10</day>
				<month>12</month>
				<year>2021</year>
			</pub-date>
			<pub-date date-type="collection" publication-format="electronic">
				<season>Oct-Dec</season>
				<year>2021</year>
			</pub-date>
			<volume>1</volume>
			<issue>2</issue>
			<fpage>147</fpage>
			<lpage>148</lpage>
			<history>
				<date date-type="received">
					<day>04</day>
					<month>10</month>
					<year>2021</year>
				</date>
				<date date-type="rev-recd">
					<day>15</day>
					<month>10</month>
					<year>2021</year>
				</date>
				<date date-type="accepted">
					<day>15</day>
					<month>10</month>
					<year>2021</year>
				</date>
			</history>
			<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>Cardiac Amyloidosis</kwd>
				<kwd>Intracardiac Thrombosis: Anticoagulation</kwd>
				<kwd>Stroke Prevention</kwd>
			</kwd-group>
			<counts>
				<fig-count count="0"/>
				<table-count count="0"/>
				<equation-count count="0"/>
				<ref-count count="13"/>
				<page-count count="2"/>
			</counts>
		</article-meta>
	</front>
	<body>
		<p>In cardiac amyloidosis, amyloid infiltrate at the atrial level promotes atrial dilation and contractile dysfunction as well as a higher prevalence of atrial fibrillation which, when associated with ventricular diastolic and systolic dysfunction, favors blood stasis and the consequent development of intracardiac thrombosis (ICT) and cardioembolic events.</p>
		<p>In a study of 116 autopsies of patients with cardiac amyloidosis, conducted at the Mayo Clinic, the presence of ICT was demonstrated in 33% of hearts, with a significantly higher prevalence in patients with the AL form of amyloidosis than in those with other forms (56% versus 16%, p &lt; 0.001).<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
		<p>When evaluating 324 patients with cardiac amyloidosis using cardiac magnetic resonance, we found an ICT prevalence of 6.2%, with 90% located in the atrial appendage. Among the patients, 70% had atrial fibrillation, and 30% had sinus rhythm, with a similar prevalence of ICT in the AL (5.2%) and ATTR forms (7.2%).<sup><xref ref-type="bibr" rid="B2">2</xref> , <xref ref-type="bibr" rid="B3">3</xref></sup></p>
		<p>Morphological and functional changes caused by atrial amyloid infiltrate favor the development of atrial fibrillation, with a prevalence ranging from 29% to 60%, depending on the population, and it is more prevalent in the ATTR form, given that it affects an older population. The presence of atrial fibrillation poses a high risk for the development of ICT and stroke, especially in patients with AL amyloidosis.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
		<p>Approximately 20% to 30% of patients who have ICT, as well as 27% of patients with cerebral ischemic events are in sinus rhythm.<sup><xref ref-type="bibr" rid="B3">3</xref> , <xref ref-type="bibr" rid="B5">5</xref></sup></p>
		<p>The probable mechanism responsible for the development of thrombotic events and thromboembolism in patients in sinus rhythm would be the presence of atrial myopathy due to amyloid infiltrate and high ventricular filling pressures, which induce atrial contractile dysfunction and favor blood stasis and ICT formation.<sup><xref ref-type="bibr" rid="B5">5</xref> - <xref ref-type="bibr" rid="B7">7</xref></sup></p>
		<p>By means of logistic regression analysis, several factors have been identified that are related to greater predisposition to ICT and thromboembolic events, such as biventricular systolic dysfunction, restrictive pattern of diastolic dysfunction, atrial dilatation, degree of atrial amyloid infiltration, and high NT-proBNP levels. In the presence of these factors, we must carry out a specific evaluation as to the possible benefit of anticoagulation for preventing cardioembolic events.<sup><xref ref-type="bibr" rid="B2">2</xref></sup></p>
		<p>In patients with cardiac amyloidosis who have ICT or atrial fibrillation, anticoagulation treatment is absolutely indicated, due to the benefits in reducing thromboembolic events and improving survival.<sup><xref ref-type="bibr" rid="B8">8</xref></sup></p>
		<p>New anticoagulants and coumarin are similar in terms of benefits in reducing stroke and increasing survival, as well as in terms of increasing the incidence of bleeding events. Approximately 55% to 68% of patients taking coumarin have difficulties reaching the stable therapeutic target of the international normalized ratio, especially in the elderly population, which we must take into account when making decisions regarding the choice of new anticoagulants as an alternative for anticoagulation.<sup><xref ref-type="bibr" rid="B9">9</xref> - <xref ref-type="bibr" rid="B11">11</xref></sup></p>
		<p>Even though anticoagulation in patients with amyloidosis has been associated with an increased risk of bleeding events due to amyloid angiopathy, especially in patients with the ATTR form, who are at risk of intracranial hemorrhage, this risk does not outweigh the benefits of preventing thromboembolic events; therefore, anticoagulation should be carried out when it is indicated.<sup><xref ref-type="bibr" rid="B12">12</xref> - <xref ref-type="bibr" rid="B13">13</xref></sup></p>
	</body>
	<back>
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		<fn-group>
			<fn fn-type="other">
				<p>Study Association</p>
				<p>This study is not associated with any thesis or dissertation work.</p>
			</fn>
			<fn fn-type="other">
				<p>Ethics approval and consent to participate</p>
				<p>This article does not contain any studies with human participants or animals performed by any of the authors.</p>
			</fn>
		</fn-group>
		<fn-group>
			<fn fn-type="supported-by">
				<p>Sources of Funding</p>
				<p>There were no external funding sources for this study.</p>
			</fn>
		</fn-group>
	</back>
	<sub-article article-type="translation" id="TRpt" xml:lang="pt">
		<front-stub>
			<article-categories>
				<subj-group subj-group-type="heading">
					<subject>Ponto de Vista</subject>
				</subj-group>
			</article-categories>
			<title-group>
				<article-title>Indicações de Anticoagulação na Amiloidose Cardíaca</article-title>
			</title-group>
			<contrib-group>
				<contrib contrib-type="author">
					<contrib-id contrib-id-type="orcid">0000-0001-8922-4075</contrib-id>
					<name>
						<surname>Montera</surname>
						<given-names>Marcelo Westerlund</given-names>
					</name>
					<xref ref-type="aff" rid="aff1"/>
				</contrib>
			</contrib-group>
			<aff id="aff1002">
				<country country="BR">Brasil</country>
				<institution content-type="original">Hospital Pró Cardíaco, Centro de Insuficiência Cardíaca, Rio de Janeiro, RJ - Brasil</institution>
			</aff>
			<author-notes>
				<corresp id="c01002">Correspondência: Marcelo Montera • Rua Redentor, 111/301. CEP: 22421030, Ipanema , Rio de Janeiro, RJ - Brasil. E-mail: mmontera@uol.com.br</corresp>
				<fn fn-type="con">
					<p>Contribuição dos autores</p>
					<p>Redação do manuscrito e Revisão crítica do manuscrito quanto ao conteúdo intelectual importante: Montera MW.</p>
				</fn>
				<fn fn-type="conflict">
					<p>Potencial conflito de interesse</p>
					<p>Não há conflito com o presente artigo.</p>
				</fn>
			</author-notes>
			<kwd-group xml:lang="pt">
				<kwd>Amiloidose Cardíaca</kwd>
				<kwd>Trombose Intracardíaca</kwd>
				<kwd>Anticoagulação</kwd>
				<kwd>Prevenção de Acidente Vascular Cerebral</kwd>
			</kwd-group>
		</front-stub>
		<body>
			<p>Na amiloidose cardíaca, o infiltrado amilóide a nível atrial promove dilatação e disfunção contrátil atrial e maior prevalência de fibrilação atrial que, associados à disfunção diastólica e sistólica ventricular, favorecem a estase sanguínea e ao consequente desenvolvimento de trombo intra-atrial (TIA) e de eventos cardioembólicos.</p>
			<p>Em estudo de 116 autopsias de pacientes com amiloidose cardíaca, realizado na Mayo Clinic, foi demonstrada a presença de TIA em 33% dos corações, sendo a prevalência significativamente maior nos portadores da forma AL de amiloidose quando comparada a outras formas de amiloidose (56% vs 16%, p &lt; 0,001).<sup><xref ref-type="bibr" rid="B1">1</xref></sup></p>
			<p>Na avaliação de 324 pacientes com amiloidose cardíaca por ressonância magnética cardíaca, encontramos uma prevalência de TIA de 6,2%, sendo 90% localizada no apêndice atrial. Entre os pacientes, 70% apresentavam fibrilação atrial e 30% em ritmo sinusal, com uma prevalência semelhante de TIA nas formas AL (5,2%) e ATTR (7,2%).<sup><xref ref-type="bibr" rid="B2">2</xref> , <xref ref-type="bibr" rid="B3">3</xref></sup></p>
			<p>As alterações morfológicas e funcionais ocasionadas pelo infiltrado amiloide atrial favorecem o desenvolvimento de fibrilação atrial, com uma prevalência que varia de 29% a 60% de acordo com o população, sendo mais prevalente na forma ATTR, por ser uma população mais idosa. A presença de fibrilação atrial impõe um alto risco para desenvolvimento de TIA e acidente vascular cerebral, principalmente nos pacientes com a forma AL de amiloidose.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
			<p>Cerca de 20% a 30% dos pacientes que apresentam TIA estão em ritmo sinusal, como também 27% dos pacientes com evento isquêmico cerebral.<sup><xref ref-type="bibr" rid="B3">3</xref> , <xref ref-type="bibr" rid="B5">5</xref></sup></p>
			<p>O provável mecanismo responsável pelo desenvolvimento de evento trombótico e tromboembolismo em pacientes em ritmo sinusal, seriam a presença de miopatia atrial por infiltrado amiloide e pressões de enchimento ventricular elevadas, que induzem a disfunção da mecânica contrátil atrial, e favorecem a estase sanguínea e a formação de TIA.<sup><xref ref-type="bibr" rid="B5">5</xref> - <xref ref-type="bibr" rid="B7">7</xref></sup></p>
			<p>Através de análise de regressão logística, foram identificados vários fatores que estão relacionados com maior predisposição de TIA e de eventos de tromboembolismo como disfunção sistólica biventricular, padrão restritivo de disfunção diastólica, dilatação atrial, grau de infiltrado amilóide atrial e níveis elevados de NT-proBNP. Na presença destes fatores, devemos realizar uma avaliação particularizada quanto ao possível benefício de anticoagulação para a prevenção de eventos cardioembólicos.<sup><xref ref-type="bibr" rid="B2">2</xref></sup></p>
			<p>Os pacientes com amiloidose cardíaca que apresentam TIA ou fibrilação atrial, tem absoluta indicação de tratamento com anticoagulação, em decorrência dos benefícios na redução de eventos tromboembólicos e da melhora de sobrevida.<sup><xref ref-type="bibr" rid="B8">8</xref></sup></p>
			<p>Os novos anticoagulantes e cumarinico apresentam benefícios semelhantes na redução de acidente vascular cerebral e aumento da sobrevida e quanto à incidência de eventos hemorrágicos. Os pacientes em uso de cumarínico, cerca de 55% a 68%, apresentam dificuldades em alcançar o alvo terapêutico estável do razão normalizada internacional, principalmente na população idosa, o que devemos levar em consideração na tomada de decisão quanto à escolha dos novos anticoagulantes como alternativa para a anticoagulação.<sup><xref ref-type="bibr" rid="B9">9</xref> - <xref ref-type="bibr" rid="B11">11</xref></sup></p>
			<p>Embora a anticogulação nos pacientes com amiloidose esteja associada a um maior risco de eventos hemorrágicos em decorrência da angiopatia amiloide, especialmente em pacientes com a forma ATTR, que apresentam risco de hemorragia intracraniana, este risco não se sobrepõe aos benefícios da prevenção de eventos tromboembólicos, portanto, a anticoagulação deve ser feita quando indicada.<sup><xref ref-type="bibr" rid="B12">12</xref> - <xref ref-type="bibr" rid="B13">13</xref></sup></p>
		</body>
		<back>
			<fn-group>
				<fn fn-type="other">
					<p>Vinculação acadêmica</p>
					<p>Não há vinculação deste estudo a programas de pós-graduação.</p>
				</fn>
				<fn fn-type="other">
					<p>Aprovação Ética e consentimento informado</p>
					<p>Este artigo não contém estudos com humanos ou animais realizados por nenhum dos autores.</p>
				</fn>
			</fn-group>
			<fn-group>
				<fn fn-type="supported-by">
					<p>Fontes de financiamento</p>
					<p>O presente estudo não teve fontes de financiamento externas.</p>
				</fn>
			</fn-group>
		</back>
	</sub-article>
</article>