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<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">abcimg</journal-id>
<journal-title-group>
<journal-title>ABC 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">abcimg.20230117i</article-id>
<article-id pub-id-type="doi">10.36660/abcimg.20230117i</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Case Report</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Ultrasound in the Diagnosis of Carotid Web: Report of Two Cases and Review</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0001-6186-1531</contrib-id>
<name><surname>Petisco</surname><given-names>Ana Claudia Gomes Pereira</given-names></name>
<xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref>
<xref ref-type="corresp" rid="c1"/>
<role>Conception and design of the research</role>
<role>acquisition of data and analysis and interpretation of the data</role>
<role>writing of the manuscript</role>
<role>critical revision of the manuscript for intellectual content</role>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0002-6723-5758</contrib-id>
<name><surname>Dourado</surname><given-names>Paulo Magno Martins</given-names></name>
<xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="aff" rid="aff3"><sup>3</sup></xref>
<role>acquisition of data and analysis and interpretation of the data</role>
<role>critical revision of the manuscript for intellectual content</role></contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0009-0001-8500-9244</contrib-id>
<name><surname>Dourado</surname><given-names>Larissa Almeida</given-names></name>
<xref ref-type="aff" rid="aff2"><sup>2</sup></xref>
<role>Conception and design of the research</role>
<role>critical revision of the manuscript for intellectual content</role>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0009-0001-5780-4726</contrib-id>
<name><surname>Dourado</surname><given-names>João Paulo Almeida</given-names></name>
<xref ref-type="aff" rid="aff2"><sup>2</sup></xref>
<role>Conception and design of the research</role>
<role>critical revision of the manuscript for intellectual content</role>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0009-0000-3342-9469</contrib-id>
<name><surname>Tebaldi</surname><given-names>Ricardo Thomaz</given-names></name>
<xref ref-type="aff" rid="aff2"><sup>2</sup></xref>
<role>acquisition of data and analysis and interpretation of the data</role>
<role>critical revision of the manuscript for intellectual content</role>
</contrib>
<aff id="aff1">
<label>1</label>
<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>
<aff id="aff2">
<label>2</label>
<institution content-type="orgname">Clínica Procoração Cardiologia Preventiva</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">Clínica Procoração Cardiologia Preventiva, São Paulo, SP – Brazil</institution>
</aff>
<aff id="aff3">
<label>3</label>
<institution content-type="orgname">Universidade de São Paulo Faculdade de Medicina</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">Universidade de São Paulo Faculdade de Medicina, São Paulo, SP – Brazil</institution>
</aff>
</contrib-group>
<author-notes>
<corresp id="c1"><bold>Mailing Address: Ana Claudia Gomes Pereira Petisco •</bold> Instituto Dante Pazzanese de Cardiologia. Rua Dr. Dante Pazzanese, 500. Postal code: <postal-code>04012-909</postal-code>. São Paulo, SP – Brazil E-mail: <email>anapetisco@outlook.com</email></corresp>
<fn fn-type="conflict"><p><bold>Potential Conflict of Interest</bold></p>
<p>No potential conflict of interest relevant to this article was reported.</p></fn>
<fn fn-type="edited-by"><p>Editor responsible for the review: Simone Nascimento dos Santos</p></fn>
</author-notes>
<pub-date publication-format="electronic" date-type="pub">
<day>28</day>
<month>03</month>
<year>2024</year></pub-date>
<pub-date publication-format="electronic" date-type="collection">
<year>2024</year></pub-date>
<volume>37</volume>
<issue>1</issue>
<elocation-id>e20230117</elocation-id>
<history>
<date date-type="received">
<day>19</day>
<month>12</month>
<year>2023</year>
</date>
<date date-type="rev-recd">
<day>26</day>
<month>01</month>
<year>2024</year>
</date>
<date date-type="accepted">
<day>14</day>
<month>02</month>
<year>2024</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</license-p>
</license>
</permissions>
<kwd-group xml:lang="en">
<title>Keywords</title>
<kwd>Carotid Artery Diseases</kwd>
<kwd>Carotid Arteries Ultrasonography</kwd>
<kwd>Fibromuscular Dysplasia</kwd>
</kwd-group>
<counts>
<fig-count count="8"/>
<table-count count="0"/>
<equation-count count="0"/>
<ref-count count="10"/>
</counts>
</article-meta>
</front>
<body>
<sec sec-type="intro">
<title>Introduction</title>
<p>Carotid web (CW) is a nonatherosclerotic disease of the extracranial carotid artery, described as an atypical, still little known, and poorly diagnosed focal fibromuscular dysplasia (FMD). CW has been associated with the occurrence of cerebral vascular accidents (CVAs) and transient ischemic attacks (TIAs), affecting young patients, with no other known causes.</p>
</sec>
<sec sec-type="cases">
<title>Case report</title>
<p><bold>Case 1:</bold> A 51-year-old female teacher, married, asymptomatic until September 2022, when she developed sudden motor deficit of left hemibody, and was admitted with the diagnosis of CVA. The patient reported complete regression of motor deficit one month after hospital discharge, and use of atorvastatin 40mg and aspirin 100mg. The patient has smoked for 30 years and denied diabetes and hypertension. Her mother has a history of cerebral aneurysm. Physical examination was normal (blood pressure: 120×80mmHg; heart rate = 76bpm).</p>
<p>The patient underwent laboratory tests, electrocardiogram (ECG), transthoracic and transesophageal echocardiograms, 24h Holter monitoring, and treadmill test, with normal results. Vascular ultrasound (VUS) of carotid and vertebral arteries revealed an echogenic image in left carotid bifurcation, projecting into the carotid artery lumen, apparently fixed, without significant stenosis, raising the possibility of CW. On the surface, there was a small pedunculated echogenic mobile mass, towards the flow, measuring 0.66 mm (possible thrombus) – <xref ref-type="fig" rid="f1">Figures 1A</xref>-<xref ref-type="fig" rid="f1">F</xref>. Computed tomography angiography (CTA) of cervical vessels corroborated the ultrasound findings, showing a luminal thin band or folding, at the bulb of the left internal carotid artery (<xref ref-type="fig" rid="f2">Figures 2A</xref> and <xref ref-type="fig" rid="f2">2B</xref>). Contrast angiography was performed, which revealed a filling defect, compatible with CW, projecting into the left bulb in a turbulent flow, and no intracranial changes (<xref ref-type="fig" rid="f2">Figures 2C</xref> and <xref ref-type="fig" rid="f2">D</xref>). A surgical intervention was indicated.</p>
<fig id="f1">
<label>Figure 1</label>
<caption><title>Case 1 – Visualization of the carotid web (yellow arrows) by Vascular Ultrasonography; A – B mode cross section view; B- Power Doppler cross section view; C- B mode longitudinal section view; D – Color Doppler longitudinal section view; E- B mode longitudinal section view; F – Pedunculated and mobile image in the direction of flow (magnifying glass – suggests a small thrombus).</title></caption>
<graphic xlink:href="2675-312X-abcimg-37-01-e20230117-gf01.tif"/>
</fig>
<fig id="f2">
<label>Figure 2</label>
<caption><title>A and B) Case 1: Carotid web visualization in the bulb-emergence of the left internal carotid artery by tomography angiography (white arrows); C and D) Case 1: filling failure on contrast angiography, compatible with carotid web with flow turbulence.</title></caption>
<graphic xlink:href="2675-312X-abcimg-37-01-e20230117-gf02.tif"/>
</fig>
<p><bold>Case 2:</bold> A 42-year-old woman, service assistant, single. The patient was asymptomatic, with a history of hypertension, using losartan 75 mg/d, and preparing for elective hysterectomy. The patient underwent a cardiovascular <italic>check-up</italic> and reported that her mother had dyslipidemia and hypertension. The VUS of carotid and vertebral arteries showed an echogenic image in the posterolateral wall, near the right carotid bifurcation, projecting into the arterial lumen, apparently fixed, suggestive of CW, with flow disturbance, peak systolic velocity (PSV) = 134 cm/s and narrowing of the lumen by nearly 50%. A cross-sectional view reviewed that the membrane acted as a &quot;web&quot; (<xref ref-type="fig" rid="f3">Figures 3A</xref>-<xref ref-type="fig" rid="f3">F</xref>).</p>
<fig id="f3">
<label>Figure 3</label>
<caption><title>Case 2: Visualization of the carotid web (yellow arrows) by Vascular Ultrasonography; A) Longitudinal section with color Doppler; B and C) B mode longitudinal section view; D) B mode cross section view; E) Color Doppler cross section view; F) Pulsed Doppler demonstrating flow turbulence (peak systolic velocity = 134cm/s).</title></caption>
<graphic xlink:href="2675-312X-abcimg-37-01-e20230117-gf03.tif"/>
</fig>
<p>CTA of carotid arteries corroborated the ultrasonographic diagnosis, showing a filling defect in the right carotid bulb / origin of the right internal carotid artery, suggestive of CW (variant of FMD), and causing discrete stenosis (<xref ref-type="fig" rid="f4">Figures 4A</xref> and <xref ref-type="fig" rid="f4">B</xref>). The patient is still asymptomatic and clinically followed-up.</p>
<fig id="f4">
<label>Figure 4</label>
<caption><title>A and B) Case 2: Visualization of the carotid web (white arrows) by CT angiography</title></caption>
<graphic xlink:href="2675-312X-abcimg-37-01-e20230117-gf04.tif"/>
</fig>
</sec>
<sec sec-type="discussion">
<title>Discussion</title>
<p>CW was first described in 1968.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> It consists of a little known and poorly diagnosed nonatherosclerotic disease of the extracranial carotid artery.<sup><xref ref-type="bibr" rid="B2">2</xref></sup> CW is described as a discrete membrane (web or net) defined as an intraluminal filling defect that usually affects the posterolateral wall of the carotid artery, more commonly in the proximal internal carotid artery. Of unknown cause, CW is considered an atypical focal carotid FMD, with intimal fibrous proliferation.<sup><xref ref-type="bibr" rid="B2">2</xref>,<xref ref-type="bibr" rid="B3">3</xref></sup> CWs are more prevalent in proximal internal carotid artery and carotid bifurcation and may be unilateral or bilateral.<sup><xref ref-type="bibr" rid="B3">3</xref></sup></p>
<p>CW may be the cause of CVA and TIAs, accounting for 9.4-37% of cryptogenic stroke, mainly in young patients.<sup><xref ref-type="bibr" rid="B3">3</xref>-<xref ref-type="bibr" rid="B5">5</xref></sup> CW patients may be asymptomatic or develop recurrent neurological events.<sup><xref ref-type="bibr" rid="B3">3</xref>,<xref ref-type="bibr" rid="B5">5</xref></sup> Sajedi et al.<sup><xref ref-type="bibr" rid="B5">5</xref></sup> assessed cryptogenic stroke patients and demonstrated a CW prevalence of 21.2% (95% CI, 8.9–38.9%). Mean age was 38.9 years, and CW was more common among African American (86%) and women (86%). The mechanism by which CW leads to neurological events is not well established. Although CW does not commonly result in significant stenosis, flow disturbance may occur, with blood recirculation and stasis, which would increase the risk of platelet aggregation. CW is a shelf-like membrane that allows the blood to be retained and in longer contact with the endothelium, favoring thrombus formation and thromboembolic events.<sup><xref ref-type="bibr" rid="B3">3</xref>,<xref ref-type="bibr" rid="B5">5</xref></sup> It is believed that the pattern of flow abnormalities caused by CWs differs from those caused by atherosclerotic plaques, since while CWs are focal lesions, atherosclerotic plaques may affect longer segments of the artery and have more irregular surface.<sup><xref ref-type="bibr" rid="B6">6</xref></sup> The detection of a thrombus adherent to CW, similar to that found in our first case, was reported in 16.2% of the cases.<sup><xref ref-type="bibr" rid="B7">7</xref></sup></p>
<p>CW may be diagnosed by CTA, contrast angiography, magnetic resonance angiography, or VUS.<sup><xref ref-type="bibr" rid="B8">8</xref></sup> It is radiologically described as a focal protrusion, a tissue fold from the posterior wall of the carotid bulb, on sagittal or on oblique sagittal image, also visible on the axial image as a septum.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
<p>As described in the two cases presented here, VUS can detect CW. In the two-dimensional image, CW is seen as a thin membrane formed by an abnormal endothelial fold, with variable-diameter orifices, similar to a web, causing a partial flow in the carotid artery.<sup><xref ref-type="bibr" rid="B4">4</xref>,<xref ref-type="bibr" rid="B6">6</xref>,<xref ref-type="bibr" rid="B9">9</xref></sup> The use of the VUS resources like color Doppler, power Doppler, and contrast VUS whenever possible, helps in MW visualization.<sup><xref ref-type="bibr" rid="B9">9</xref></sup> Madaelil et al.<sup><xref ref-type="bibr" rid="B6">6</xref></sup> reported a moderate agreement between VUS and contrast angiography (k=0.62; p=0.01). However, a more recent study reported an 85.7% agreement between CTA and contrast-enhanced VUS.<sup><xref ref-type="bibr" rid="B8">8</xref></sup></p>
<p>Due to is high resolution and images in multiple planes, CTA allows the identification of filling defect projecting from the carotid wall into the lumen, in addition to thrombi and calcium. It is useful for the exclusion of atherosclerosis and other vascular lesions and, so far, it is considered the method of choice for the diagnosis of CW.<sup><xref ref-type="bibr" rid="B4">4</xref>,<xref ref-type="bibr" rid="B6">6</xref>-<xref ref-type="bibr" rid="B8">8</xref></sup></p>
<p>Digital subtraction angiography can be used in the CW diagnosis, however, since CW usually affects the posteromedial and posterolateral carotid artery wall, different angiographic projections may be necessary, with the disadvantage of being an invasive procedure.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> Magnetic resonance angiography can evaluate the morphology and composition of CW, but there are few data in this regard.<sup><xref ref-type="bibr" rid="B4">4</xref>,<xref ref-type="bibr" rid="B8">8</xref></sup></p>
<p>Differential diagnoses of CW are atherosclerotic plaque, carotid dissection, and intraluminal thrombus.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> Fontaine et al.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> compared ultrasound images (B-mode and microflow imaging) of 24 patients with CW and 24 patients with atherosclerotic plaques and reported that none of patients with atherosclerotic plaques presented ultrasonographic features suggestive of CW. The treatment of CW patients is still debatable. Therapeutic options include medical treatment with antiplatelet or anticoagulant agents, and/or interventions via stents or endarterectomy. Patel et al.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> conducted a systematic review of 289 symptomatic CW patients across 15 series. Interventional management was performed in 151 (52.2%) (stent implantation in 87 and carotid endarterectomy in 64) and medical management was performed in 138 (47.8%), including antiplatelet therapy and anticoagulants. Baseline characteristics and time from index CVA were similar between medical and interventional patients. In the interventional group, no recurrent ischemic events were observed over a follow-up of up to 60 months. In the medical group, over a follow-up of up to 55 months, recurrence rate was 26.8%, with no statistical difference between patients receiving any antithrombotic vs. no antithrombotic.</p>
<p>Therefore, the diagnosis of CW depends on a greater knowledge about the disease, to identify those patients with neurological events, frequently young patients, to provide proper treatment and prevent recurrence. In this context, VUS stands out as a low-cost, reliable, and accessible diagnostic method.</p>
</sec>
</body>
<back>
<fn-group>
<fn fn-type="financial-disclosure" id="fn1"><p><bold>Sources of Funding</bold></p>
<p>There were no external funding sources for this study.</p></fn>
<fn fn-type="other" id="fn2"><p><bold>Study Association</bold></p>
<p>This study is not associated with any thesis or dissertation work.</p></fn>
<fn fn-type="other" id="fn3"><p><bold>Ethics Approval and Consent to Participate</bold></p>
<p>This article does not contain any studies with human participants or animals performed by any of the authors.</p></fn>
</fn-group>
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</back>
<sub-article article-type="translation" id="S1" xml:lang="pt">
<front-stub>
<article-id pub-id-type="doi">10.36660/abcimg.20230117</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Relato de Caso</subject></subj-group></article-categories>
<title-group>
<article-title>A Ultrassonografia no Diagnóstico da Membrana Carotídea: Relato de Dois Casos e Revisão da Literatura</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0001-6186-1531</contrib-id>
<name><surname>Petisco</surname><given-names>Ana Claudia Gomes Pereira</given-names></name>
<xref ref-type="aff" rid="aff4"><sup>1</sup></xref><xref ref-type="aff" rid="aff5"><sup>2</sup></xref>
<xref ref-type="corresp" rid="c2"/>
<role>Concepção e desenho da pesquisa</role>
<role>obtenção de dados, análise e interpretação dos dados</role>
<role>redação do manuscrito</role>
<role>revisão crítica do manuscrito quanto ao conteúdo intelectual importante</role>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0000-0002-6723-5758</contrib-id>
<name><surname>Dourado</surname><given-names>Paulo Magno Martins</given-names></name>
<xref ref-type="aff" rid="aff5"><sup>2</sup></xref><xref ref-type="aff" rid="aff6"><sup>3</sup></xref>
<role>obtenção de dados, análise e interpretação dos dados</role>
<role>revisão crítica do manuscrito quanto ao conteúdo intelectual importante</role>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0009-0001-8500-9244</contrib-id>
<name><surname>Dourado</surname><given-names>Larissa Almeida</given-names></name>
<xref ref-type="aff" rid="aff5"><sup>2</sup></xref>
<role>Concepção e desenho da pesquisa</role>
<role>revisão crítica do manuscrito quanto ao conteúdo intelectual importante</role>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0009-0001-5780-4726</contrib-id>
<name><surname>Dourado</surname><given-names>João Paulo Almeida</given-names></name>
<xref ref-type="aff" rid="aff5"><sup>2</sup></xref>
<role>Concepção e desenho da pesquisa</role>
<role>revisão crítica do manuscrito quanto ao conteúdo intelectual importante</role>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">0009-0000-3342-9469</contrib-id>
<name><surname>Tebaldi</surname><given-names>Ricardo Thomaz</given-names></name>
<xref ref-type="aff" rid="aff5"><sup>2</sup></xref>
<role>obtenção de dados, análise e interpretação dos dados</role>
<role>revisão crítica do manuscrito quanto ao conteúdo intelectual importante</role>
</contrib>
<aff id="aff4">
<label>1</label>
<addr-line>
<named-content content-type="city">São Paulo</named-content>
<named-content content-type="state">SP</named-content>
</addr-line>
<country country="BR">Brasil</country>
<institution content-type="original">Instituto Dante Pazzanese de Cardiologia, São Paulo, SP – Brasil</institution>
</aff>
<aff id="aff5">
<label>2</label>
<addr-line>
<named-content content-type="city">São Paulo</named-content>
<named-content content-type="state">SP</named-content>
</addr-line>
<country country="BR">Brasil</country>
<institution content-type="original">Clínica Procoração Cardiologia Preventiva, São Paulo, SP – Brasil</institution>
</aff>
<aff id="aff6">
<label>3</label>
<addr-line>
<named-content content-type="city">São Paulo</named-content>
<named-content content-type="state">SP</named-content>
</addr-line>
<country country="BR">Brasil</country>
<institution content-type="original">Universidade de São Paulo Faculdade de Medicina, São Paulo, SP – Brasil</institution>
</aff>
</contrib-group>
<author-notes>
<corresp id="c2"><bold>Correspondência: Ana Claudia Gomes Pereira Petisco</bold> Instituto Dante Pazzanese de Cardiologia. Rua Dr. Dante Pazzanese, 500. CEP: <postal-code>04012-909</postal-code>. São Paulo, SP – Brasil E-mail: <email>anapetisco@outlook.com</email></corresp>
<fn fn-type="conflict"><p><bold>Potencial Conflito de Interesse</bold></p>
<p>Declaro não haver conflito de interesses pertinentes.</p></fn>
<fn fn-type="edited-by"><p>Editor responsável pela revisão: Simone Nascimento dos Santos</p></fn>
</author-notes>
<kwd-group xml:lang="pt">
<title>Palavras-chave</title>
<kwd>Doenças das Artérias Carótidas</kwd>
<kwd>Ultrassonografia das Artérias Carótidas</kwd>
<kwd>Displasia Fibromuscular</kwd>
</kwd-group>
</front-stub>
<body>
<sec sec-type="intro">
<title>Introdução</title>
<p>A Membrana Carotídea (MC) (<italic>carotid web</italic>) é uma doença não aterosclerótica da artéria carótida extracraniana, descrita como uma Displasia Fibromuscular (DFM) focal atípica, ainda pouco conhecida e diagnosticada. A MC tem sido relacionada à ocorrência de Acidentes Vasculares Encefálicos (AVE) e Ataques Isquêmicos Transitórios (AIT), acometendo pacientes jovens, sem outra etiologia identificada.</p>
</sec>
<sec sec-type="cases">
<title>Relato de caso</title>
<p><bold>Caso 1</bold>: Paciente do sexo feminino, 51 anos, casada, professora. Assintomática até setembro de 2022, quando apresentou déficit motor súbito em dimídio direito, sendo hospitalizada com diagnóstico de AVE. Após a alta, refere regressão total do déficit motor em um mês, mantendo-se em uso de atorvastatina 40mg e AAS 100mg. Como antecedentes é tabagista há 30 anos, nega diabetes ou hipertensão. Mãe com história de aneurisma cerebral.</p>
<p>Exame físico normal. Pressão Arterial: 120×80mmHg; Frequência Cardíaca =76bpm.</p>
<p>Foram realizados exames laboratoriais, eletrocardiograma (ECG), ecocardiograma transtorácico e transesofágico, Holter de 24h e teste ergométrico (TE) em esteira, que estavam dentro da normalidade. A Ultrassonografia Vascular (USV) das artérias carótidas e vertebrais demonstrou imagem ecogênica na altura da bifurcação carotídea à esquerda, projetando-se para o lúmen carotídeo, aparentemente fixa, sem estenose significativa, levantando-se a possibilidade de MC. Em sua superfície observou-se pequena imagem ecogênica, pedunculada e móvel, na direção do fluxo, medindo 0,66mm (possível trombo) – <xref ref-type="fig" rid="f5">Figuras 1A</xref>-<xref ref-type="fig" rid="f5">F</xref>. A Angiotomografia Computadorizada (ATC) de vasos cervicais corroborou o diagnóstico ultrassonográfico, descrevendo delgada banda ou prega luminal no bulbo da carótida interna à esquerda (<xref ref-type="fig" rid="f6">Figuras 2A</xref> e <xref ref-type="fig" rid="f6">2B</xref>). Foi realizada angiografia contrastada que apresentou falha de enchimento compatível com MC, projetando-se para o interior do bulbo esquerdo com turbilhonamento, sem alterações intracranianas (<xref ref-type="fig" rid="f6">Figuras 2C</xref> e <xref ref-type="fig" rid="f6">D</xref>). Foi indicada intervenção cirúrgica.</p>
<fig id="f5">
<label>Figura 1</label>
<caption><title>Caso 1: Visualização da membrana carotídea (setas amarelas) pela Ultrassonografia Vascular; A) Corte transversal ao modo B; B) Corte transversal ao Power Doppler; C) Corte longitudinal ao modo B; D) Corte longitudinal com Doppler colorido; E) Corte longitudinal modo B; F) Imagem pedunculada e móvel na direção do fluxo (lupa – sugere pequeno trombo).</title></caption>
<graphic xlink:href="2675-312X-abcimg-37-01-e20230117-gf01-pt.tif"/>
</fig>
<fig id="f6">
<label>Figura 2</label>
<caption><title>A e B) Caso 1: Visualização da membrana carotídea no bulbo-emergência da carótida interna à esquerda pela angiotomografia (setas brancas); C e D) Caso 1: falha de enchimento à angiografia contrastada, compatível com membrana carotídea no bulbo esquerdo (setas azuis) com turbilhonamento</title></caption>
<graphic xlink:href="2675-312X-abcimg-37-01-e20230117-gf02-pt.tif"/>
</fig>
<p><bold>Caso 2</bold>: Paciente sexo feminino, 42 anos, solteira, auxiliar de serviços. Assintomática, com antecedente de hipertensão arterial, usando losartana 75mg/dia, em programação de histerectomia eletiva. Realizou exames de <italic>check-up</italic> cardiológico, onde referiu mãe portadora de dislipidemia e hipertensão. Exame físico sem alterações. Realizados, ECG, TE em esteira, exames laboratoriais, ecocardiograma transtorácico, que se apresentaram dentro da normalidade. A USV das artérias carótidas e vertebrais demonstrou imagem ecogênica na parede póstero-lateral próximo à bifurcação carotídea direita, projetando-se para o lúmen arterial, aparentemente fixa, sugerindo MC, com distúrbio de fluxo, velocidade de pico sistólico (VPS) =134cm/s e redução luminal anatômica em torno de 50%. Ao corte transversal, observou-se que a membrana se portava como uma &quot;rede&quot; (<xref ref-type="fig" rid="f7">Figuras 3A</xref>-<xref ref-type="fig" rid="f7">F</xref>).</p>
<fig id="f7">
<label>Figura 3</label>
<caption><title>Caso 2: Visualização da membrana carotídea (setas amarelas) pela Ultrassonografia Vascular; A) Corte longitudinal com Doppler colorido; B e C) Corte longitudinal ao modo B; D) Corte transversal ao modo B; E) Corte transversal ao Doppler colorido; F) Doppler pulsado demonstrando turbulência e velocidade de pico sistólico = 134cm/s</title></caption>
<graphic xlink:href="2675-312X-abcimg-37-01-e20230117-gf03-pt.tif"/>
</fig>
<p>A ATC de artérias carótidas corroborou o diagnóstico ultrassonográfico, demonstrando falha de enchimento no bulbo carotídeo direito/origem da carótida interna direita sugestiva de MC (variante da displasia fibrosa), determinando estenose discreta (<xref ref-type="fig" rid="f8">Figuras 4A</xref> e <xref ref-type="fig" rid="f8">B</xref>). Mantém-se assintomática e em segmento clínico.</p>
<fig id="f8">
<label>Figura 4</label>
<caption><title>A e B) Caso 2: Visualização da membrana carotídea (setas brancas) pela angiotomografia</title></caption>
<graphic xlink:href="2675-312X-abcimg-37-01-e20230117-gf04-pt.tif"/>
</fig>
</sec>
<sec sec-type="discussion">
<title>Discussão</title>
<p>A MC, ou teia carotídea (<italic>carotid web</italic>), foi descrita em 1968.<sup><xref ref-type="bibr" rid="B1">1</xref></sup> Trata-se de doença não aterosclerótica da artéria carótida extracraniana pouco conhecida e diagnosticada.<sup><xref ref-type="bibr" rid="B2">2</xref></sup> É descrita como uma discreta membrana (teia ou rede), definida como defeito de enchimento intraluminal que, em geral, afeta a parede póstero lateral da artéria carótida, mais comumente, na porção mais proximal da artéria carótida interna. De causa desconhecida, é considerada uma DFM carotídea focal atípica, onde há proliferação fibrosa intimal.<sup><xref ref-type="bibr" rid="B2">2</xref>,<xref ref-type="bibr" rid="B3">3</xref></sup> Os sítios de maior prevalência das MCs são: a porção proximal da carótida interna e a bifurcação carotídea, podendo ser unilateral ou bilateral.<sup><xref ref-type="bibr" rid="B3">3</xref></sup></p>
<p>A MC pode ser causa de AVE e AIT, respondendo por 9,4% a 37% dos AVEs criptogênicos, mais comum em jovens.<sup><xref ref-type="bibr" rid="B3">3</xref>-<xref ref-type="bibr" rid="B5">5</xref></sup> Pacientes com MC podem ser assintomáticos ou apresentar eventos neurológicos recorrentes.<sup><xref ref-type="bibr" rid="B3">3</xref>,<xref ref-type="bibr" rid="B5">5</xref></sup> Sajedi et al.<sup><xref ref-type="bibr" rid="B5">5</xref></sup> avaliaram pacientes com AVE criptogênico e demostraram prevalência de MC de 21,2% (IC95%, 8,9–38,9%). A idade média foi de 38,9 anos, mais frequente em mulheres (86%), e em indivíduos afro-americanos (86%). O mecanismo pelo qual a MC leva aos eventos neurológicos não está bem estabelecido. Apesar de MC não determinar, comumente, estenose significativa, pode haver distúrbio de fluxo, com recirculação de sangue distal e estase, o que levaria a um aumento do risco de agregação plaquetária. A MC comporta-se como um anteparo, uma rede, uma teia, que permite que o sangue seja retido e fique em maior contato com o endotélio, podendo levar a formação de trombos, resultando em eventos tromboembólicos.<sup><xref ref-type="bibr" rid="B3">3</xref>,<xref ref-type="bibr" rid="B5">5</xref></sup> Acredita-se que haja padrão diferente de distúrbio de fluxo gerado pelas MCs em comparação com a placa aterosclerótica, pois, enquanto as MCs são protrusões focais, as placas ateroscleróticas podem acometer segmentos mais longos do vaso, com uma superfície mais irregular.<sup><xref ref-type="bibr" rid="B6">6</xref></sup> A visualização de imagem compatível com trombo aderido à MC, assim como observado em nosso primeiro caso, foi relatada em 16,2% dos casos.<sup><xref ref-type="bibr" rid="B7">7</xref></sup></p>
<p>O diagnóstico da MC pode ser feito por ATC, angiografia contrastada, angiorressonância ou USV.<sup><xref ref-type="bibr" rid="B8">8</xref></sup> Descreve-se, radiograficamente, como protuberância focal, uma teia ou prega de tecido, a partir da parede posterior do bulbo carotídeo, visualizada na imagem sagital ou sagital oblíqua, também sendo visível à imagem axial como um septo.<sup><xref ref-type="bibr" rid="B4">4</xref></sup></p>
<p>Assim como nas pacientes relatadas neste artigo, a USV é capaz de identificar a MC. A imagem ao modo bidimensional, é de uma membrana fina, formada por uma prega endotelial anômala podendo apresentar orifícios de diâmetros variáveis, semelhante a uma teia, permitindo a passagem parcial de fluxo na carótida.<sup><xref ref-type="bibr" rid="B4">4</xref>,<xref ref-type="bibr" rid="B6">6</xref>,<xref ref-type="bibr" rid="B9">9</xref></sup> A utilização de recursos da USV como o Doppler colorido, o <italic>power</italic> Doppler e, quando possível, a USV com contraste, facilitam a visualização da MC.<sup><xref ref-type="bibr" rid="B9">9</xref></sup> Madaelil et al.<sup><xref ref-type="bibr" rid="B6">6</xref></sup> descreveram uma concordância moderada da USV com a angiografia contrastada (κ=0,62; p=0,01). Porém, a concordância entre a USV e a ATC foi recentemente descrita em 85,7% com uso de contraste ultrassonográfico.<sup><xref ref-type="bibr" rid="B8">8</xref></sup></p>
<p>A ATC, pela alta resolução espacial, com imagens em múltiplos planos, permite a identificação da falha de enchimento projetando-se da parede carotídea para o lúmen, além de trombos e cálcio. A técnica é útil para exclusão da aterosclerose ou outra lesão vascular, portanto, até o momento, tem sido considerada o método de escolha para o diagnóstico da MC.<sup><xref ref-type="bibr" rid="B4">4</xref>-<xref ref-type="bibr" rid="B6">6</xref>,<xref ref-type="bibr" rid="B8">8</xref></sup></p>
<p>A angiografia contrastada pode ser utilizada no diagnóstico da MC. Porém, pelo fato de a MC apresentar-se na região póstero-medial ou parede póstero-lateral do vaso, pode ser necessária a avaliação em diversas projeções, tendo a desvantagem de ser um procedimento invasivo <sup><xref ref-type="bibr" rid="B7">7</xref></sup>. A angiorressonância pode avaliar a morfologia e a composição da MC, porém não se tem muitas informações sobre sua utilização.<sup><xref ref-type="bibr" rid="B4">4</xref>,<xref ref-type="bibr" rid="B8">8</xref></sup></p>
<p>Os diagnósticos diferenciais da MC são as placas ateroscleróticas, dissecção carotídea e trombo intraluminal.<sup><xref ref-type="bibr" rid="B4">4</xref></sup> Fontaine et al.<sup><xref ref-type="bibr" rid="B10">10</xref></sup> compararam imagens ultrassonográficas (modo B e MFI – <italic>microflow imaging</italic>) de 24 pacientes com MC e 24 pacientes com placas ateroscleróticas e relataram que nenhum dos pacientes com placas ateroscleróticas mostrou características ultrassonográficas sugestivas de MC.</p>
<p>O tratamento dos pacientes com MC ainda é discutido. Entre as opções estão o tratamento clínico com antiagregantes plaquetários ou anticoagulantes, e/ou tratamento com intervenção, seja por via percutânea com <italic>stents,</italic> ou por endarterectomia. Patel et al.<sup><xref ref-type="bibr" rid="B7">7</xref></sup> realizaram revisão sistemática de 289 MC sintomáticas em 15 séries; o tratamento por intervenção foi realizado em 151 casos (52,2%) (implante de <italic>stent</italic> em 87 e endarterectomia em 64) e tratamento clínico em 138 (47,8%), incluindo terapia antiplaquetária e/ou anticoagulantes. As características clínicas basais e o tempo da ocorrência do AVE foram semelhantes nos pacientes com tratamento intervencionista e no grupo clínico. Nos pacientes submetidos à intervenção, nenhum evento isquêmico recorrente foi observado antes de 60 meses. No grupo clínico, durante acompanhamento (até 55 meses), a taxa de recorrência foi 26,8%, não havendo diferença estatística entre os pacientes que receberam e não receberam tratamento antitrombótico.</p>
<p>Assim, o diagnóstico da MC depende de um melhor conhecimento da doença para identificarmos pacientes com eventos neurológicos, muitas vezes jovens, para seu tratamento adequado e evitar recorrência. Nesse contexto, a USV desponta como um método diagnóstico de baixo custo, confiável e acessível.</p>
</sec>
</body>
<back>
<fn-group>
<fn fn-type="financial-disclosure" id="fn4"><p><bold>Fontes de Financiamento</bold></p>
<p>O presente estudo não teve fontes de financiamento externas.</p></fn>
<fn fn-type="other" id="fn5"><p><bold>Vinculação Acadêmica</bold></p>
<p>Não há vinculação deste estudo a programas de pós-graduação.</p></fn>
<fn fn-type="other" id="fn6"><p><bold>Aprovação Ética e Consentimento Informado</bold></p>
<p>Este artigo não contém estudos com humanos ou animais realizados por nenhum dos autores.</p></fn>
</fn-group>
</back>
</sub-article>
</article>
