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<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">CC</journal-id>
<journal-id journal-id-type="nlm-ta">Cardiol Croat</journal-id>
<journal-title-group>
<journal-title>Cardiologia Croatica</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Cardiol. Croat.</abbrev-journal-title>
</journal-title-group>
<issn pub-type="ppub">1848-543X</issn>
<issn pub-type="epub">1848-5448</issn>
<publisher><publisher-name>Croatian Cardiac Society</publisher-name></publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="publisher-id">CC_11(10-11)_530-531</article-id>
<article-id pub-id-type="doi">10.15836/ccar2016.530</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Extended Abstract</subject></subj-group>
</article-categories>
<title-group>
<article-title>Eosinophilic cardiomyopathy with thrombus in left ventricle: is there a place for new oral anticoagulants?</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0003-0490-3832</contrib-id><name><surname>Vujeva</surname><given-names>Bo&#x017E;o</given-names></name></contrib><contrib contrib-type="author"><name><surname>Cvitku&#x0161;i&#x0107;</surname><given-names>Katica </given-names></name></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0001-6188-0708</contrib-id><name><surname>Lukenda</surname></name></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">http://orcid.org/0000-0003-4600-0498</contrib-id><name><surname>Mi&#x0161;kovi&#x0107;</surname><given-names>Domagoj</given-names></name></contrib>
<aff id="aff1">General Hospital &#x201C;Dr. Josip Ben&#x010D;evi&#x0107;&#x201D;, Slavonski Brod, <country>Croatia</country></aff>
</contrib-group>
<author-notes>
<corresp id="cor1">Address for correspondence: Domagoj Mi&#x0161;kovi&#x0107;, Op&#x0107;a bolnica &#x201C;Dr. Josip Ben&#x010D;evi&#x0107;&#x201D;, Andrije &#x0160;tampara 42, HR-35000 Slavonski Brod, Croatia. / Phone: +385-98-760-767 / E-mail: <email xlink:href="domagoj1304@gmail.com">domagoj1304@gmail.com</email></corresp></author-notes>
<pub-date pub-type="epub-ppub"><month>11</month><year>2016</year></pub-date>
<volume>11</volume>
<issue>10-11</issue>
<fpage>530</fpage>
<lpage>531</lpage>
<history>
<date date-type="received"><day>24</day><month>09</month><year>2016</year></date><date date-type="accepted"><day>10</day><month>10</month><year>2016</year></date>
</history>
<permissions>
<copyright-year>2016</copyright-year>
<copyright-holder>Croatian Cardiac Society</copyright-holder>
</permissions>
<kwd-group kwd-group-type="author"><title>Keywords: </title><kwd>hypereosinophilic syndrome</kwd><kwd>thrombus in the left ventricle</kwd><kwd>imatinib</kwd><kwd>anticoagulation therapy</kwd></kwd-group>
</article-meta>
</front>
<body>
<p><bold>Background:</bold> Hypereosinophilic syndrome is a myeloproliferative disorder characterized by eosinophilia that is associated with damage to multiple organs. (<xref ref-type="bibr" rid="r1"><italic>1</italic></xref>-<xref ref-type="bibr" rid="r3"><italic>3</italic></xref>)</p>
<p><bold>Case report:</bold> 23-year-old patient, without comorbidity, was admitted to hospital because of weight loss, night&#x2019;s sweats and cough. Blood test result shows eosinophilia, anemia and thrombocytopenia. <xref ref-type="fig" rid="f1"><bold>Figure 1</bold></xref> shows 12-lead ECG. Transthoracic echocardiography (<xref ref-type="fig" rid="f2"><bold>Figure 2</bold></xref>) reveals endomyocardial fibrosis and restrictive diastolic dysfunction with moderate mitral regurgitation. Except the heart, there are no other organs involved. We started the treatment with beta-blockers, ACE inhibitors, aspirin and corticosteroids. Thirteen days after discharge, the patient was rehospitalized because of paroxysmal nocturnal dyspnea and angina. Acute coronary syndrome was ruled out. Right pleural effusion was seen on chest X-ray and further echocardiography showed worsening of mitral regurgitation. For the purpose of further diagnosis and treatment, patient was transferred to the University Hospital Center. Treatment by tyrosine kinase inhibitor imatinib was initiated. MRI exam verified thrombus in the left ventricle. The patient returned to our hospital with a recommendation by concomitant administration of imatinib 400 mg OD and subcutaneously enoxaparine 1 mg/kg BID.</p>
<fig id="f1" position="float" fig-type="figure"><label>Figure 1</label><caption><p>Electrocardiographic signs of left atrial dilatation and left ventricular hypertrophy.</p></caption><graphic xlink:href="CC_11(10-11)_530-531-f1"></graphic></fig>
<fig id="f2" position="float" fig-type="figure"><label>Figure 2</label><caption><p>Echocardiography &#x2013; thrombus in the left ventricle size 1.57x1.71 cm.</p></caption><graphic xlink:href="CC_11(10-11)_530-531-f2"></graphic></fig>
<p><bold>Conclusion:</bold> Concomitant usage of imatinib and warfarin is not recommended since both drugs excreted by the liver-they are substrates of the liver enzyme citokrom P450 3A4 and taking them together could increase the risk of bleeding. As an alternative to enoxaparine, new oral anticoagulants (NOAC) dabigatran could be used. As an advantage compared to enoxaparin, we emphasize oral administration and in comparison to warfarin, dabigatran avoids enzymatic system cytochrome P450 3A4. There are also disadvantages because dabigatran is a substrate of P-glycoprotein, a protein that acts as a pump to transfer the substance from the cells. Imatinib inhibits the activity of P-glycoprotein so that can boost the effect of dabigatran and potentially lead to hemorrhage. There are reported cases of successful treatment of mural thrombi with dabigatran and also the reports of concomitant usage of dabigatran and imatinib without bleeding disorders. However, studies of parallel usage of dabigatran or other NOACs with imatinib in the hypereosinophilic syndrome are needed.</p>
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