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  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia - SBC</publisher-name>
        <publisher-loc>S&#227;o Paulo, SP, Brazil</publisher-loc>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v3">rvgZSdggHFXWW5cWvShXTwq</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2012001200016</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v1">S0066-782X(12)09900300016</article-id>
      <article-id pub-id-type="doi">10.1590/S0066-782X2012001200016</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Relatos de Caso</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Supradesnivelamento do segmento ST no tromboembolismo pulmonar</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Montenegro</surname>
            <given-names>Fernando Santiago</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Barzan</surname>
            <given-names>Valmir</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>De Lorenzo</surname>
            <given-names>Andrea Rocha</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Pittella</surname>
            <given-names>Felipe Jos&#233; Monassa</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Rocha</surname>
            <given-names>Ant&#244;nio S&#233;rgio Cordeiro da</given-names>
          </name>
          <xref ref-type="aff" rid="aff01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <addr-line>
          <named-content content-type="city">Rio de Janeiro</named-content>
          <named-content content-type="state"/>
        </addr-line>
        <institution content-type="orgname">Instituto Nacional de Cardiologia</institution>
        <country country="BR">Brazil</country>
      </aff>
      <pub-date date-type="collection" publication-format="electronic">
        <month>09</month>
        <year>2012</year>
      </pub-date>
      <volume>99</volume>
      <issue>3</issue>
      <fpage>e131</fpage>
      <lpage>e133</lpage>
      <permissions>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/" xml:lang="en">
          <license-p>This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.</license-p>
        </license>
      </permissions>
      <pub-date publication-format="electronic" date-type="pub">
        <day>20</day>
        <month>09</month>
        <year>2012</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <p>
      <bold>RELATO DE CASO</bold>
    </p>
    <p>
      <bold>Supradesnivelamento do segmento ST no tromboembolismo pulmonar </bold>
    </p>
    <p>
      <bold>Fernando Santiago Montenegro; Valmir Barzan; Andrea Rocha De Lorenzo; Felipe Jos&#233; Monassa Pittella; Ant&#244;nio S&#233;rgio Cordeiro da Rocha</bold>
    </p>
    <p>Instituto Nacional de Cardiologia de Laranjeiras, Rio de Janeiro, RJ - Brasil</p>
    <p>
      <xref ref-type="corresp" rid="end">Correspond&#234;ncia</xref>
    </p>
    <p><bold>Palavras-chave: </bold>Embolia pulmonar; eletrocardiografia/m&#233;todos.</p>
    <p>
      <bold>Introdu&#231;&#227;o</bold>
    </p>
    <p>Al&#233;m do infarto agudo do mioc&#225;rdio (IAM), h&#225; v&#225;rias causas de supradesnivelamento do segmento ST<sup>1</sup>. Repolariza&#231;&#227;o precoce, varia&#231;&#227;o do padr&#227;o normal (padr&#227;o masculino), hipertrofia ventricular esquerda, bloqueio completo do ramo esquerdo, pericardite aguda, miocardite, s&#237;ndrome de Brugada, p&#243;s-cardiovers&#227;o, hipercalemia e tromboembolismo pulmonar (TEP) representam a maioria delas. No entanto, a distin&#231;&#227;o entre essas condi&#231;&#245;es e o IAM ganha relev&#226;ncia cl&#237;nica por conta do benef&#237;cio proporcionado pela reperfus&#227;o precoce na vig&#234;ncia do IAM com supradesnivelamento do ST. O presente relato apresenta o caso de um paciente com o diagn&#243;stico de TEP cujo ECG mimetizava IAM.</p>
    <p>
      <bold>Relato do caso</bold>
    </p>
    <p>Trata-se de paciente feminina com 55 anos, negra, obesa (IMC = 31 kg/m<sup>2</sup>), que deu entrada na unidade de pronto-atendimento de outra institui&#231;&#227;o ap&#243;s quatro epis&#243;dios seguidos de s&#237;ncope acompanhados por dor retroesternal e dispneia. A primeira s&#237;ncope ocorreu durante caminhada e as outras em repouso. As s&#237;ncopes foram sucedidas por dor retroesternal em aperto, sem irradia&#231;&#227;o, e dispneia. N&#227;o havia hist&#243;ria de diabetes ou hipertens&#227;o arterial, mas ex-tabagismo, com carga tab&#225;gica de 60 ma&#231;os-ano e tratamento radioter&#225;pico para c&#226;ncer de &#250;tero h&#225; 12 anos. </p>
    <p>No relato de admiss&#227;o, havia refer&#234;ncia &#224; taquicardia (150 bpm), press&#227;o arterial de 132/74 mmHg e satura&#231;&#227;o de O<sub>2</sub> de 91% em ar ambiente. O ritmo card&#237;aco era irregular, sem bulhas acess&#243;rias e sem sopros. Havia descri&#231;&#227;o de leve redu&#231;&#227;o do murm&#250;rio vesicular em ter&#231;o inferior de ambos os hemit&#243;races. O ECG de admiss&#227;o mostrava ritmo de fibrila&#231;&#227;o atrial com resposta ventricular de 150 bpm, padr&#227;o S1Q3, bloqueio de ramo direito (BRD) de 2&#186; grau, supradesnivelamento do segmento ST em AVR e V1 e infradesnivelamento do segmento ST em deriva&#231;&#245;es D1, D2, aVF e de V2-V6 (<xref ref-type="fig" rid="a16fig01">Figura 1A</xref>). Os marcadores de necrose mioc&#225;rdica estavam positivos e o pico de troponina I foi de 4,42. Dois dias ap&#243;s iniciado o tratamento para s&#237;ndrome coronariana aguda (SCA), a paciente foi submetida &#224; cineangiocoronariografia em nossa institui&#231;&#227;o, que demonstrou art&#233;rias coron&#225;rias sem obstru&#231;&#245;es. Onze dias ap&#243;s o epis&#243;dio inicial, transferida para nossa institui&#231;&#227;o, ainda em tratamento para SCA (dupla antiagrega&#231;&#227;o plaquet&#225;ria com anticoagula&#231;&#227;o profil&#225;tica) foi verificado edema doloroso e assim&#233;trico de perna esquerda, sem empastamento de panturrilha ou sinais flog&#237;sticos. O ecocardiograma transtor&#225;cico revelou fun&#231;&#227;o ventricular esquerda e direita normais e o ecodoppler venoso de membro inferior, trombose recente de veia popl&#237;tea e safena parva. </p>
    <p><fig id="a16fig01"/>&#13;
&#160;&#13;
</p>
    <p>
      <fig id="a16fig01a">
        <graphic xlink:href="1678-4170-abc-99-03-e131-00016-gf01.jpg"/></fig>
    </p>
    <p>&#13;
  <fig id="a16fig01xfig1b"/><fig id="a16fig01b"><graphic xlink:href="1678-4170-abc-99-03-e131-00016-gf02.jpg"/></fig></p>
    <p>A angiotomografia contrastada de art&#233;rias pulmonares demonstrou trombos em ambas as art&#233;rias pulmonares principais (<xref ref-type="fig" rid="a16fig02">Figura 2</xref>). Um ECG realizado 10 dias ap&#243;s o epis&#243;dio inicial mostrou desaparecimento do padr&#227;o S1Q3 e do bloqueio de ramo direito, al&#233;m de invers&#227;o de onda T nas deriva&#231;&#245;es V1-V3 (<xref ref-type="fig" rid="a16fig01">Figura 1B</xref>). Em fun&#231;&#227;o da estabilidade cl&#237;nica, a paciente foi tratada inicialmente com anticoagulante venoso e, posteriormente, mantida com anticoagula&#231;&#227;o oral, sendo encaminhada para um servi&#231;o de oncologia para investigar poss&#237;vel recidiva de neoplasia.</p>
    <p content-type="asset">
      <fig id="a16fig02">
        <graphic xlink:href="1678-4170-abc-99-03-e131-00016-gf03.jpg"/></fig>
    </p>
    <p>
      <bold>Discuss&#227;o</bold>
    </p>
    <p>As altera&#231;&#245;es eletrocardiogr&#225;ficas cl&#225;ssicas do tromboembolismo pulmonar (TEP) incluem invers&#227;o da onda T em precordiais direitas, altera&#231;&#245;es simult&#226;neas de invers&#227;o da onda T, eleva&#231;&#227;o do segmento ST em deriva&#231;&#245;es anterosseptais e inferiores, padr&#227;o S1Q3T3, BRD completo ou incompleto, e taquicardia sinusal. A presen&#231;a de arritmias atriais, BRD e supra ou infradesnivelamento do segmento ST est&#227;o associadas &#224; fal&#234;ncia do ventr&#237;culo direito (VD) e mau progn&#243;stico<sup>2</sup>. </p>
    <p>Livaditis e cols.<sup>3</sup> descrevem um paciente com TEP maci&#231;o e supradesnivelamento do ST em aVR e de V1-V3, que com tratamento trombol&#237;tico evoluiu para revers&#227;o completa das altera&#231;&#245;es<sup>3</sup>. O caso aqui descrito, apesar de n&#227;o ter sofrido tratamento trombol&#237;tico, apresentou melhora cl&#237;nica e eletrocardiogr&#225;fica com o tratamento anticoagulante. </p>
    <p>Em outro relato, h&#225; descri&#231;&#227;o de tr&#234;s casos de supradesnivelamento do segmento ST em aVR e troponina elevadas, dos quais apenas um apresentava oclus&#227;o aguda do tronco da coron&#225;ria esquerda. Dos outros com art&#233;rias coron&#225;rias normais, sendo que em um o supradesnivelamento do ST em aVR foi atribu&#237;do &#224; taquicardia juncional parox&#237;stica e o outro &#224; TEP, confirmada na angiotomografia<sup>4</sup>. </p>
    <p>Lin e cols.<sup>5</sup> descrevem um caso de TEP, no qual o paciente apresentava s&#237;ncope acompanhada de dor tor&#225;cica e dispneia, como no presente relato, e o ECG inicial, al&#233;m do supradesnivelamento do segmento ST de V1 a V4, mostrava BRD incompleto, ondas S em D1, V5 e V6 e onda Q em D3. Como no caso aqui relatado, houve normaliza&#231;&#227;o das altera&#231;&#245;es eletrocardiogr&#225;ficas com o tratamento e o diagn&#243;stico inicial foi de IAM<sup>5</sup>. </p>
    <p>As altera&#231;&#245;es eletrocardiogr&#225;ficas do TEP s&#227;o atribu&#237;das &#224;s mudan&#231;as na hemodin&#226;mica card&#237;aca. A sobrecarga volum&#233;trica aumentaria a tens&#227;o parietal e o trabalho muscular do VD. O abaulamento do septo interventricular em dire&#231;&#227;o ao VE reduziria o d&#233;bito card&#237;aco, diminuindo o fluxo coronariano que, associado &#224; hipoxemia e ao aumento do trabalho card&#237;aco, contribuiria para isquemia mioc&#225;rdica<sup>6</sup>, justificando a eleva&#231;&#227;o dos marcadores de necrose mioc&#225;rdica.</p>
    <p>Embora a eleva&#231;&#227;o do segmento ST esteja associada a TEP maci&#231;o e seja, portanto, um importante marcador progn&#243;stico, &#233; uma altera&#231;&#227;o incomum e com poucos relatos na literatura. Em um estudo envolvendo 246 pacientes, no qual se avaliou o valor do ECG no diagn&#243;stico do TEP, verificou-se que apenas 9,3% dos pacientes com o diagn&#243;stico confirmado apresentavam alguma altera&#231;&#227;o do segmento ST<sup>7</sup>.</p>
    <p>De acordo com o escore de Wells, a paciente do presente relato possu&#237;a probabilidade intermedi&#225;ria de TEP, ou seja, 4,5 pontos: 3 pontos pelos sintomas cl&#237;nicos de trombose venosa profunda (edema assim&#233;trico com dor &#224; palpa&#231;&#227;o) e 1,5 pontos pela frequ&#234;ncia card&#237;aca superior a 100 bpm<sup>6</sup>. Somando-se a isto as altera&#231;&#245;es eletrocardiogr&#225;ficas encontradas, a probabilidade de TEP se tornaria maior. Todavia, o supradesnivelamento do segmento ST em aVR e V1 poderia tamb&#233;m indicar les&#227;o grave de tronco de coron&#225;ria esquerda e/ou les&#227;o proximal da art&#233;ria descendente anterior<sup>8</sup>. Deste modo, a presen&#231;a de eleva&#231;&#227;o do segmento ST em aVR e V1 poderia significar tanto TEP maci&#231;o quanto les&#227;o coronariana grave. </p>
    <p>O presente caso ilustra a dificuldade do diagn&#243;stico diferencial entre as duas s&#237;ndromes, especialmente na sala de emerg&#234;ncia, onde a tomada de decis&#227;o &#233; realizada em um curto intervalo de tempo visando salvar a vida dos pacientes. No presente caso, a equipe da sala de emerg&#234;ncia optou pelo tratamento da causa mais prevalente, a SCA. Nessa circunst&#226;ncia, a disponibilidade de um exame ecocardiogr&#225;fico seria uma ferramenta proped&#234;utica importante para auxiliar no diagn&#243;stico diferencial e orientar o tratamento, posto que poderia demonstrar altera&#231;&#245;es nas press&#245;es da art&#233;ria pulmonar, na fun&#231;&#227;o do VD ou a presen&#231;a de trombo no tronco ou nos ramos principais da art&#233;ria pulmonar vigentes no TEP maci&#231;o.</p>
    <p>
      <bold>Potencial Conflito de Interesses</bold>
    </p>
    <p>Declaro n&#227;o haver conflito de interesses pertinentes.</p>
    <p>
      <bold>Fontes de Financiamento</bold>
    </p>
    <p>O presente estudo n&#227;o teve fontes de financiamento externas.</p>
    <p>
      <bold>Vincula&#231;&#227;o Acad&#234;mica</bold>
    </p>
    <p>N&#227;o h&#225; vincula&#231;&#227;o deste estudo a programas de p&#243;s-gradua&#231;&#227;o.</p>
    <p>
      <fn id="end" fn-type="corresp">
        <label>
          <bold>Correspond&#234;ncia:</bold>
        </label>
        <p> Fernando Santiago Montenegro </p>
        <p> Avenida Epit&#225;cio Pessoa, 2330/906, Lagoa </p>
        <p> CEP 22411-071, Rio de Janeiro, RJ - Brasil </p>
        <p> E-mail: </p>
        <p>
          <email xlink:href="fernandomonte03@gmail.com">fernandomonte03@gmail.com</email>
        </p>
      </fn>
    </p>
    <p>Artigo recebido em 22/08/11; revisado em 22/08/11; aceito em 19/12/11.</p>
  </body>
  <back>
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  </back>
  <sub-article article-type="translation" id="TRen" xml:lang="en">
    <front-stub>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Case Reports</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">ST-segment elevation in pulmonary thromboembolism</article-title>
      </title-group>
    </front-stub>
    <body>
      <p>
        <bold>CASE REPORT</bold>
      </p>
      <p>
        <fn id="enda-body2">
          <label>
            <bold>ST-segment elevation in pulmonary thromboembolism</bold>
          </label>
          <p>
            <bold>Fernando Santiago Montenegro; Valmir Barzan; Andrea Rocha De Lorenzo; Felipe Jos&#233; Monassa Pittella; Ant&#244;nio S&#233;rgio Cordeiro da Rocha</bold>
          </p>
        </fn>
      </p>
      <p>Instituto Nacional de Cardiologia de Laranjeiras, Rio de Janeiro, RJ - Brasil</p>
      <p>Mailing Address</p>
      <p><bold>Keywords: </bold>Pulmonary embolism; electrocardiography/methods</p>
      <p>
        <bold>Introduction</bold>
      </p>
      <p>In addition to acute myocardial infarction (AMI), there are several causes of ST-segment elevation,<sup>1</sup> such as early repolarization, variation of the normal pattern (male pattern), left ventricular hypertrophy, complete left bundle branch block, acute pericarditis, myocarditis, Brugada syndrome, post-cardioversion, hyperkalemia, and pulmonary thromboembolism (PTE). However, the distinction between those conditions and AMI is clinically relevant, because of the benefit provided by early reperfusion in the presence of AMI with ST-segment elevation. This case report is about a patient diagnosed with PTE, whose electrocardiogram (ECG) mimicked AMI.</p>
      <p>
        <bold>Case report</bold>
      </p>
      <p>The patient is a 55-year-old, black, obese (BMI = 31 kg/m<sup>2</sup>) female, who was admitted to the emergency unit of another institution after four episodes of syncope accompanied by retrosternal pain and dyspnea. The first syncope occurred when she was walking, and the others when resting. The syncope episodes were followed by a retrosternal pressure sensation, with no radiation, and dyspnea. There was no history of diabetes or arterial hypertension, but she reported being an ex-smoker (tobacco load of 60 packs per year) and undergoing radiotherapy for uterus cancer 12 years before. </p>
      <p>The report of her admission was as follows: tachycardia (150 bpm); blood pressure of 132/74 mmHg; and O<sub>2</sub> saturation of 91% at room air. Her heart rhythm was irregular, with neither accessory heart sounds nor murmurs. The respiratory sounds were reduced in the lower third of both hemithoraces. The ECG on admission showed atrial fibrillation with ventricular response of 150 bpm, S1Q3 pattern, incomplete right bundle-branch block (RBBB), ST-segment elevation in the leads aVR and V1, and ST-segment depression in the leads D1, D2, aVF, and V2-V6 (<xref ref-type="fig" rid="en_a16fig01-body2">Figure 1A</xref>). The markers of myocardial necrosis were positive and the troponin I peak was 4.42. Two days after starting the treatment for acute coronary syndrome (ACS), the patient underwent coronary angiography at our institution, which showed no coronary artery obstruction. Eleven days after the initial episode, after being transferred to our institution, still undergoing treatment for ACS (double platelet antiaggregation with prophylactic anticoagulation), painful and asymmetric swelling of the left leg was evidenced, with neither calf changes nor inflammatory signs. A transthoracic echocardiogram revealed normal left and right ventricular (RV) function, while venous Doppler echography of the lower limb evidenced recent thrombosis of the popliteal and small saphenous veins. </p>
      <p content-type="html"><fig id="en_a16fig01-body2"><graphic xlink:href="https://minio.scielo.br/documentstore/1678-4170/rvgZSdggHFXWW5cWvShXTwq/a6d062e389268cbee13fceb914ac6253239cda98.jpg"/><graphic xlink:href="1678-4170-abc-99-03-e131-00016-gf01-en.jpg"/></fig>&#13;
&#160;&#13;
</p>
      <p>Computed tomographic angiography of the pulmonary arteries showed thrombi in both main pulmonary arteries (<xref ref-type="fig" rid="en_a16fig02-body2">Figure 2</xref>). An ECG performed ten days after the initial episode showed disappearance of the S1Q3 pattern and of the RBBB, in addition to T wave inversion in the leads V1-V3 (<xref ref-type="fig" rid="en_a16fig01-body2">Figure 1B</xref>). Because of clinical stability, the patient was initially treated with venous anticoagulation, later maintained on oral anticoagulation, and referred to an oncology service to investigate possible recurrence of the neoplasia.</p>
      <p content-type="asset">
        <fig id="en_a16fig02-body2">
          <graphic xlink:href="1678-4170-abc-99-03-e131-00016-gf02-en.jpg"/></fig>
      </p>
      <p>
        <bold>Discussion</bold>
      </p>
      <p>The classical ECG changes of PTE are as follows: T wave inversion on the right precordial leads; simultaneous T wave inversion and ST-segment elevation on the anteroseptal and inferior leads; S1Q3T3 pattern; complete or incomplete RBBB; and sinus tachycardia. The presence of atrial arrhythmias, RBBB, and ST-segment elevation or depression is associated with RV failure and poor prognosis<sup>2</sup>. </p>
      <p>Livaditis et als.<sup>3</sup> have reported the case of a patient with massive PTE and ST-segment elevation in the leads aVR and V1-V3, which, with thrombolytic treatment, reverted completely<sup>3</sup>. Although our patient did not undergo thrombolytic treatment, she improved clinically and electrocardiographically with the anticoagulant treatment. </p>
      <p>Another study has reported three patients with ST-segment elevation in aVR and elevated troponin, of whom only one showed acute occlusion of the left main coronary artery. Considering the two other patients with normal coronary arteries, in one the ST-segment elevation in aVR was attributed to paroxysmal junctional tachycardia, while, in the other, to PTE, confirmed on computed tomographic angiography <sup>4</sup>. </p>
      <p>Lin et als.<sup>5</sup> have reported a case of PTE, in which the patient had syncope, chest pain and dyspnea, similarly to the findings of the present report, and the initial ECG, in addition to ST-segment elevation from leads V1 to V4, showed incomplete RBBB, S waves in D1, V5, and V6, and Q wave in D3. Similarly to the case presently reported, the ECG changes normalized with treatment, and the initial diagnosis was AMI<sup>5</sup>. </p>
      <p>The ECG changes of PTE are attributed to changes in the cardiac hemodynamics. Volume overload increases the parietal tension and the RV muscle work. The ventricular septum bulging into the left ventricle reduces cardiac output, decreasing coronary flow, which, associated with hypoxemia and the increased heart work, contributes to myocardial ischemia<sup>6</sup>, justifying the elevation of myocardial necrosis markers.</p>
      <p>Although the ST-segment elevation is associated with massive PTE, being, thus, an important prognostic marker, it is a rare alteration with few reports in the literature. A study with 246 patients, assessing the value of the ECG for the diagnosis of PTE, has reported that only 9.3% of the patients with the confirmed diagnosis had a change in the ST segment<sup>7</sup>.</p>
      <p>According to her Wells score (4.5 points), the patient here reported had an intermediate probability of PTE: 3 points for the clinical symptoms of deep venous thrombosis (asymmetric swelling with tenderness on palpation) and 1.5 points for heart rate greater than 100 bpm<sup>6</sup>. Adding the ECG changes found increased the probability of PTE. However, the ST-segment elevation in the leads aVR and V1 could also indicate severe damage to the left main coronary artery and/or proximal lesion of the anterior descending artery<sup>8</sup>. Thus, the presence of the ST-segment elevation in the leads aVR and V1 could mean both massive PTE and severe coronary artery lesion. </p>
      <p>This case report illustrates the difficulty of differentiating between both syndromes, especially at the emergency room, where decisions should be made rapidly aiming at saving patients' lives. In the present case, the emergency room team chose to treat the most prevalent cause, ACS. In that circumstance, echocardiography availability would be an important tool to help in the differential diagnosis and in guiding the treatment, because it could demonstrate changes in pulmonary artery pressures or RV function, or the presence of a thrombus in the pulmonary trunk or pulmonary artery main branches occurring in massive PTE.</p>
      <p>
        <bold>Potential Conflict of Interest</bold>
      </p>
      <p>No potential conflict of interest relevant to this article was reported.</p>
      <p>
        <bold>Sources of Funding</bold>
      </p>
      <p>There were no external funding sources for this study.</p>
      <p>
        <bold>Study Association</bold>
      </p>
      <p>This study is not associated with any post-graduation program.</p>
      <p>
        <bold>References</bold>
      </p>
    </body>
  </sub-article>
</article>
