Acute ST-elevation myocardial infarction in a young patient with antiphospholipid syndrome
Identifieur interne : 000323 ( Pmc/Corpus ); précédent : 000322; suivant : 000324Acute ST-elevation myocardial infarction in a young patient with antiphospholipid syndrome
Auteurs : Ariel González-Cordero ; Melissa Ruiz-Rodríguez ; Bayoan Ramos-Parra ; Juan Carrillo-Vanas ; Marcel Mesa-Pab N ; Hilton Franqui-RiveraSource :
- SAGE Open Medical Case Reports [ 2050-313X ] ; 2019.
Abstract
Acute coronary syndrome rarely occurs in young individuals and is seldomly associated with antiphospholipid syndrome. We report the case of a 26-year-old Hispanic man who presented with acute ST-elevation myocardial infarction and was treated with urgent percutaneous transluminal coronary angioplasty. He experienced stent thrombosis within 48 h of intervention and subsequently developed a left apical thrombus. Hypercoagulable state studies were obtained at admission and 12 weeks after the event establishing the diagnosis of antiphospholipid syndrome.
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DOI: 10.1177/2050313X19848597
PubMed: 31205708
PubMed Central: 6537053
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Acute ST-elevation myocardial infarction in a young patient with
antiphospholipid syndrome</title><author><name sortKey="Gonzalez Cordero, Ariel" sort="Gonzalez Cordero, Ariel" uniqKey="Gonzalez Cordero A" first="Ariel" last="González-Cordero">Ariel González-Cordero</name><affiliation><nlm:aff id="aff1-2050313X19848597">Internal Medicine Residency Program, Department of Medicine, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Ruiz Rodriguez, Melissa" sort="Ruiz Rodriguez, Melissa" uniqKey="Ruiz Rodriguez M" first="Melissa" last="Ruiz-Rodríguez">Melissa Ruiz-Rodríguez</name><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Ramos Parra, Bayoan" sort="Ramos Parra, Bayoan" uniqKey="Ramos Parra B" first="Bayoan" last="Ramos-Parra">Bayoan Ramos-Parra</name><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Carrillo Vanas, Juan" sort="Carrillo Vanas, Juan" uniqKey="Carrillo Vanas J" first="Juan" last="Carrillo-Vanas">Juan Carrillo-Vanas</name><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Mesa Pab N, Marcel" sort="Mesa Pab N, Marcel" uniqKey="Mesa Pab N M" first="Marcel" last="Mesa-Pab N">Marcel Mesa-Pab N</name><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Franqui Rivera, Hilton" sort="Franqui Rivera, Hilton" uniqKey="Franqui Rivera H" first="Hilton" last="Franqui-Rivera">Hilton Franqui-Rivera</name><affiliation><nlm:aff id="aff3-2050313X19848597">Cardiovascular Disease Training Program, Department of Medicine, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation><affiliation><nlm:aff id="aff4-2050313X19848597">Pavia Santurce Hospital, San Juan, Puerto Rico</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31205708</idno><idno type="pmc">6537053</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6537053</idno><idno type="RBID">PMC:6537053</idno><idno type="doi">10.1177/2050313X19848597</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000323</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000323</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Acute ST-elevation myocardial infarction in a young patient with
antiphospholipid syndrome</title><author><name sortKey="Gonzalez Cordero, Ariel" sort="Gonzalez Cordero, Ariel" uniqKey="Gonzalez Cordero A" first="Ariel" last="González-Cordero">Ariel González-Cordero</name><affiliation><nlm:aff id="aff1-2050313X19848597">Internal Medicine Residency Program, Department of Medicine, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Ruiz Rodriguez, Melissa" sort="Ruiz Rodriguez, Melissa" uniqKey="Ruiz Rodriguez M" first="Melissa" last="Ruiz-Rodríguez">Melissa Ruiz-Rodríguez</name><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Ramos Parra, Bayoan" sort="Ramos Parra, Bayoan" uniqKey="Ramos Parra B" first="Bayoan" last="Ramos-Parra">Bayoan Ramos-Parra</name><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Carrillo Vanas, Juan" sort="Carrillo Vanas, Juan" uniqKey="Carrillo Vanas J" first="Juan" last="Carrillo-Vanas">Juan Carrillo-Vanas</name><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Mesa Pab N, Marcel" sort="Mesa Pab N, Marcel" uniqKey="Mesa Pab N M" first="Marcel" last="Mesa-Pab N">Marcel Mesa-Pab N</name><affiliation><nlm:aff id="aff2-2050313X19848597">Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation></author><author><name sortKey="Franqui Rivera, Hilton" sort="Franqui Rivera, Hilton" uniqKey="Franqui Rivera H" first="Hilton" last="Franqui-Rivera">Hilton Franqui-Rivera</name><affiliation><nlm:aff id="aff3-2050313X19848597">Cardiovascular Disease Training Program, Department of Medicine, University of Puerto Rico, San Juan, Puerto Rico</nlm:aff></affiliation><affiliation><nlm:aff id="aff4-2050313X19848597">Pavia Santurce Hospital, San Juan, Puerto Rico</nlm:aff></affiliation></author></analytic><series><title level="j">SAGE Open Medical Case Reports</title><idno type="eISSN">2050-313X</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Acute coronary syndrome rarely occurs in young individuals and is seldomly
associated with antiphospholipid syndrome. We report the case of a 26-year-old
Hispanic man who presented with acute ST-elevation myocardial infarction and was
treated with urgent percutaneous transluminal coronary angioplasty. He
experienced stent thrombosis within 48 h of intervention and subsequently
developed a left apical thrombus. Hypercoagulable state studies were obtained at
admission and 12 weeks after the event establishing the diagnosis of
antiphospholipid syndrome.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Ortel, Tl" uniqKey="Ortel T">TL. Ortel</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Pierangeli, Ss" uniqKey="Pierangeli S">SS Pierangeli</name></author><author><name sortKey="Espinola, Rg" uniqKey="Espinola R">RG Espinola</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Redecha, P" uniqKey="Redecha P">P Redecha</name></author><author><name sortKey="Tilley, R" uniqKey="Tilley R">R Tilley</name></author><author><name sortKey="Tencati, M" uniqKey="Tencati M">M Tencati</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cervera, R" uniqKey="Cervera R">R Cervera</name></author><author><name sortKey="Khamashta, Ma" uniqKey="Khamashta M">MA Khamashta</name></author><author><name sortKey="Font, J" uniqKey="Font J">J Font</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kattwinkel, N" uniqKey="Kattwinkel N">N. Kattwinkel</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ito, S" uniqKey="Ito S">S Ito</name></author><author><name sortKey="Hasuo, T" uniqKey="Hasuo T">T. Hasuo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Urbanus, Rt" uniqKey="Urbanus R">RT Urbanus</name></author><author><name sortKey="Siegerink, B" uniqKey="Siegerink B">B Siegerink</name></author><author><name sortKey="Roest, M" uniqKey="Roest M">M Roest</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pengo, V" uniqKey="Pengo V">V Pengo</name></author><author><name sortKey="Ruffatti, A" uniqKey="Ruffatti A">A Ruffatti</name></author><author><name sortKey="Legnani, C" uniqKey="Legnani C">C Legnani</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hernandez Molina, G" uniqKey="Hernandez Molina G">G Hernandez-Molina</name></author><author><name sortKey="Espericueta Arriola, G" uniqKey="Espericueta Arriola G">G Espericueta-Arriola</name></author><author><name sortKey="Cabral, Ar" uniqKey="Cabral A">AR. Cabral</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schomig, A" uniqKey="Schomig A">A Schomig</name></author><author><name sortKey="Kastrati, A" uniqKey="Kastrati A">A Kastrati</name></author><author><name sortKey="Mudra, H" uniqKey="Mudra H">H Mudra</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Weissman, A" uniqKey="Weissman A">A Weissman</name></author><author><name sortKey="Coplan, Nl" uniqKey="Coplan N">NL. Coplan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Prashanth, P" uniqKey="Prashanth P">P Prashanth</name></author><author><name sortKey="Mukhaini, M" uniqKey="Mukhaini M">M Mukhaini</name></author><author><name sortKey="Riyami, A" uniqKey="Riyami A">A. Riyami</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Ruiz Irastorza, G" uniqKey="Ruiz Irastorza G">G Ruiz-Irastorza</name></author><author><name sortKey="Khamashta, Ma" uniqKey="Khamashta M">MA Khamashta</name></author><author><name sortKey="Hunt, Bj" uniqKey="Hunt B">BJ Hunt</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lim, W" uniqKey="Lim W">W Lim</name></author><author><name sortKey="Crowther, Ma" uniqKey="Crowther M">MA Crowther</name></author><author><name sortKey="Eikelboom, Jw" uniqKey="Eikelboom J">JW. Eikelboom</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Merashli, M" uniqKey="Merashli M">M Merashli</name></author><author><name sortKey="Noureldine, Mh" uniqKey="Noureldine M">MH Noureldine</name></author><author><name sortKey="Uthman, I" uniqKey="Uthman I">I Uthman</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="case-report"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">SAGE Open Med Case Rep</journal-id><journal-id journal-id-type="iso-abbrev">SAGE Open Med Case Rep</journal-id><journal-id journal-id-type="publisher-id">SCO</journal-id><journal-id journal-id-type="hwp">spsco</journal-id><journal-title-group><journal-title>SAGE Open Medical Case Reports</journal-title></journal-title-group><issn pub-type="epub">2050-313X</issn><publisher><publisher-name>SAGE Publications</publisher-name><publisher-loc>Sage UK: London, England</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31205708</article-id><article-id pub-id-type="pmc">6537053</article-id><article-id pub-id-type="doi">10.1177/2050313X19848597</article-id><article-id pub-id-type="publisher-id">10.1177_2050313X19848597</article-id><article-categories><subj-group subj-group-type="heading"><subject>Case Report</subject></subj-group></article-categories><title-group><article-title>Acute ST-elevation myocardial infarction in a young patient with
antiphospholipid syndrome</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-9185-9635</contrib-id><name><surname>González-Cordero</surname><given-names>Ariel</given-names></name><xref ref-type="aff" rid="aff1-2050313X19848597">1</xref><xref ref-type="aff" rid="aff2-2050313X19848597">2</xref><xref ref-type="corresp" rid="corresp1-2050313X19848597"></xref></contrib><contrib contrib-type="author"><name><surname>Ruiz-Rodríguez</surname><given-names>Melissa</given-names></name><xref ref-type="aff" rid="aff2-2050313X19848597">2</xref></contrib><contrib contrib-type="author"><name><surname>Ramos-Parra</surname><given-names>Bayoan</given-names></name><xref ref-type="aff" rid="aff2-2050313X19848597">2</xref></contrib><contrib contrib-type="author"><name><surname>Carrillo-Vanas</surname><given-names>Juan</given-names></name><xref ref-type="aff" rid="aff2-2050313X19848597">2</xref></contrib><contrib contrib-type="author"><name><surname>Mesa-Pabón</surname><given-names>Marcel</given-names></name><xref ref-type="aff" rid="aff2-2050313X19848597">2</xref></contrib><contrib contrib-type="author"><name><surname>Franqui-Rivera</surname><given-names>Hilton</given-names></name><xref ref-type="aff" rid="aff3-2050313X19848597">3</xref><xref ref-type="aff" rid="aff4-2050313X19848597">4</xref></contrib></contrib-group><aff id="aff1-2050313X19848597"><label>1</label>Internal Medicine Residency Program, Department of Medicine, University of Puerto Rico, San Juan, Puerto Rico</aff><aff id="aff2-2050313X19848597"><label>2</label>Section of Cardiology, University of Puerto Rico, San Juan, Puerto Rico</aff><aff id="aff3-2050313X19848597"><label>3</label>Cardiovascular Disease Training Program, Department of Medicine, University of Puerto Rico, San Juan, Puerto Rico</aff><aff id="aff4-2050313X19848597"><label>4</label>Pavia Santurce Hospital, San Juan, Puerto Rico</aff><author-notes><corresp id="corresp1-2050313X19848597">Ariel González-Cordero, Internal Medicine
Residency Program, Department of Medicine, School of Medicine, University of
Puerto Rico, Medical Sciences Campus, 365067, San Juan, Puerto Rico. Email:
<email>Ariel.gonzalez1@upr.edu</email></corresp><corresp id="corresp2-2050313X19848597">Hilton Franqui-Rivera, Cardiovascular
Disease Training Program, Department of Medicine, School of Medicine, University
of Puerto Rico, Medical Sciences Campus, 365067, San Juan, Puerto Rico. Email:
<email>Hilton.franqui@upr.edu</email></corresp></author-notes><pub-date pub-type="epub"><day>14</day><month>5</month><year>2019</year></pub-date><pub-date pub-type="collection"><year>2019</year></pub-date><volume>7</volume><elocation-id>2050313X19848597</elocation-id><history><date date-type="received"><day>16</day><month>8</month><year>2018</year></date><date date-type="accepted"><day>11</day><month>4</month><year>2019</year></date></history><permissions><copyright-statement>© The Author(s) 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder content-type="sage">SAGE Publications</copyright-holder><license license-type="creative-commons" xlink:href="http://www.creativecommons.org/licenses/by-nc/4.0/"><license-p>This article is distributed under the terms of the Creative Commons
Attribution-NonCommercial 4.0 License (<ext-link ext-link-type="uri" xlink:href="http://www.creativecommons.org/licenses/by-nc/4.0/">http://www.creativecommons.org/licenses/by-nc/4.0/</ext-link>) which
permits non-commercial use, reproduction and distribution of the work
without further permission provided the original work is attributed as
specified on the SAGE and Open Access pages (<ext-link ext-link-type="uri" xlink:href="https://us.sagepub.com/en-us/nam/open-access-at-sage">https://us.sagepub.com/en-us/nam/open-access-at-sage</ext-link>).</license-p></license></permissions><abstract><p>Acute coronary syndrome rarely occurs in young individuals and is seldomly
associated with antiphospholipid syndrome. We report the case of a 26-year-old
Hispanic man who presented with acute ST-elevation myocardial infarction and was
treated with urgent percutaneous transluminal coronary angioplasty. He
experienced stent thrombosis within 48 h of intervention and subsequently
developed a left apical thrombus. Hypercoagulable state studies were obtained at
admission and 12 weeks after the event establishing the diagnosis of
antiphospholipid syndrome.</p></abstract><kwd-group><kwd>Antiphospholipid syndrome</kwd><kwd>anti-cardiolipin</kwd><kwd>antiphospholipid anticoagulant</kwd><kwd>lupus antibody</kwd><kwd>stent thrombosis</kwd><kwd>ST elevation</kwd><kwd>ST-elevation myocardial infarction</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>cover-date</meta-name><meta-value>January-December 2019</meta-value></custom-meta></custom-meta-group></article-meta></front><body><sec sec-type="intro" id="section1-2050313X19848597"><title>Introduction</title><p>Antiphospholipid syndrome (APS) is an immune-mediated, acquired hypercoagulable state
that can cause arterial and venous thrombosis. Its incidence is estimated around 5
per 100,000 per year, with a median age of diagnosis of 34 years.<sup><xref rid="bibr1-2050313X19848597" ref-type="bibr">1</xref></sup> In rare occasions, acute coronary syndrome (ACS) can occur in patients with
APS.</p></sec><sec sec-type="cases" id="section2-2050313X19848597"><title>Case report</title><p>A 26-year-old man presented with severe mid-sternal chest pain of 3-h evolution.
Associated symptoms included diaphoresis, shortness of breath, and dizziness. He
denied previous similar symptoms. He had no history of diabetes mellitus, cigarette
smoking, hypertension, hyperlipidemia, family history of early coronary artery
disease, or sudden cardiac death. He denied illicit drug or anabolic steroid use. He
did have a remote history of a pulmonary embolism (PE) at 7 years of age. At that
time, work-up for hypercoagulable state was negative, as per history.</p><p>Physical examination revealed tachycardia of 110 bpm and blood pressure of
130/70 mmHg. Cardiac auscultation revealed regular rhythm with normal S1 and S2;
there were no murmurs. Lungs were clear to auscultation. A 12-lead electrocardiogram
(ECG) showed 3–4 mm ST-segment elevations in leads I, aVL, and V2 through V6,
consistent with acute ST-elevation myocardial infarction (STEMI).</p><p>The patient was treated as per standard management of STEMI, including
low-molecular-weight heparin (LMWH), nitrates, enalapril, metoprolol succinate,
aspirin, and clopidogrel. He also underwent coronary angiography within 30 min of
arrival to the emergency room (ER), which demonstrated total occlusion of the
proximal left anterior descending (LAD) coronary artery (<xref ref-type="fig" rid="fig1-2050313X19848597">Figure 1</xref>). A bare metal stent, Vascular
Multi-Link Vision 3.5 mm × 18 mm (Abbott Santa Clara, CA), was selected based on the
probability of a hypercoagulable state and possible need for prolonged
anticoagulation.</p><fig id="fig1-2050313X19848597" orientation="portrait" position="float"><label>Figure 1.</label><caption><p>(a) Left coronary angiogram showing thrombus at the proximal left anterior
descending (LAD) coronary artery (arrow). (b) Successful deployment of a
bare metal stent at the proximal LAD (arrow). Vascular Multi-Link Vision
3.5 mm × 18 mm (Abbott Santa Clara, CA).</p></caption><graphic xlink:href="10.1177_2050313X19848597-fig1"></graphic></fig><p>Following thromboaspiration of the LAD, pre-stent ballooning was performed with
application of 6 ATM, for 30 s. After baseline angioplasty, the balloon was removed.
After that, the stent was inspected for normal catheter centering. Distal LAD and D1
arteries were ballooned with 2.0 cm catheter at 6 ATM for 30 s and then repeating
the process four times each, achieving a post-stent measurement of minimal luminal
diameter (MLD) of 3.5 mm.</p><p>After the procedure, he was started on intravenous eptifibatide for 24 h, as well as
LMWH and dual antiplatelet therapy. Two days later, the patient developed severe
chest pain, similar to initial presentation. ECG showed new ST-segment elevations in
leads I, aVL, and V2 through V6. A repeat coronary angiography demonstrated stent
thrombosis; thrombus aspiration and ballooning of the LAD and first diagonal
coronaries were successful (<xref ref-type="fig" rid="fig2-2050313X19848597">Figure
2</xref>).</p><fig id="fig2-2050313X19848597" orientation="portrait" position="float"><label>Figure 2.</label><caption><p>(a) Left coronary angiogram showing thrombosed stent at the proximal left
anterior descending coronary artery (arrow). (b) Angiography after
successful thrombus aspiration and ballooning of the distal left anterior
descending (LAD) and first diagonal coronary arteries (arrow).</p></caption><graphic xlink:href="10.1177_2050313X19848597-fig2"></graphic></fig><p>A follow-up echocardiogram showed severe global hypokinesia and an ejection fraction
of <30%. Contrast echocardiogram confirmed the presence of a left ventricular
apical thrombus. Partial thromboplastin time mixing studies for lupus anticoagulant
(PTT-LA) was prolonged at 53 s, dilute Russell viper venom test (dRVVT-LA) was
prolonged at 47 s, and hexagonal phase phospholipid test (HPPL) was positive.
Antibodies for beta glycoprotein (β<sub>2</sub>-GPI) and all anti-cardiolipin (aCL)
isotypes were absent. ANA and anti-ds-DNA were negative, homocysteine levels were
low at 7.6 µmol/L, and other studies for hypercoagulability were unremarkable (<xref rid="table1-2050313X19848597" ref-type="table">Table 1</xref>).</p><table-wrap id="table1-2050313X19848597" orientation="portrait" position="float"><label>Table 1.</label><caption><p>Laboratory results.</p></caption><alternatives><graphic xlink:href="10.1177_2050313X19848597-table1"></graphic><table frame="hsides" rules="groups"><colgroup span="1"><col align="left" span="1"></col><col align="char" char="." span="1"></col><col align="char" char="." span="1"></col><col align="char" char="." span="1"></col></colgroup><thead><tr><th align="left" colspan="4" rowspan="1">Hypercoagulable state work-up studies
at admission</th></tr></thead><tbody><tr><td rowspan="1" colspan="1">Troponin-I (1st)</td><td rowspan="1" colspan="1">0.55 ng/dL</td><td rowspan="1" colspan="1">PTT-LA</td><td rowspan="1" colspan="1">53 s</td></tr><tr><td rowspan="1" colspan="1">Troponin-I (2nd)</td><td rowspan="1" colspan="1">15.0 ng/dL</td><td rowspan="1" colspan="1">dRVTT-LA</td><td rowspan="1" colspan="1">47 s</td></tr><tr><td rowspan="1" colspan="1">NT-Pro-BNP</td><td rowspan="1" colspan="1">371 pg/mL</td><td rowspan="1" colspan="1">HPPL</td><td rowspan="1" colspan="1">Positive</td></tr><tr><td rowspan="1" colspan="1">PT</td><td rowspan="1" colspan="1">13.1 s</td><td rowspan="1" colspan="1">Anti-β2GP1</td><td rowspan="1" colspan="1"><9 SGU</td></tr><tr><td rowspan="1" colspan="1">PTT</td><td rowspan="1" colspan="1">26.4 s</td><td rowspan="1" colspan="1">Anti-cardiolipin</td><td rowspan="1" colspan="1">Negative</td></tr><tr><td rowspan="1" colspan="1">INR</td><td rowspan="1" colspan="1">0.9</td><td rowspan="1" colspan="1">Homocysteine</td><td rowspan="1" colspan="1">7.6 µmol/L</td></tr><tr><td rowspan="1" colspan="1">ANA</td><td rowspan="1" colspan="1">Negative</td><td rowspan="1" colspan="1">Protein C & S</td><td rowspan="1" colspan="1">77%/71%</td></tr><tr><td rowspan="1" colspan="1">Anti-Sm</td><td rowspan="1" colspan="1">Negative</td><td rowspan="1" colspan="1">Antithrombin III</td><td rowspan="1" colspan="1">84%</td></tr><tr><td rowspan="1" colspan="1">Anti-RNP</td><td rowspan="1" colspan="1">Negative</td><td rowspan="1" colspan="1">CRP</td><td rowspan="1" colspan="1">284 mg/L</td></tr><tr><td rowspan="1" colspan="1">Anti-SS-A/Rho</td><td rowspan="1" colspan="1">Negative</td><td rowspan="1" colspan="1">Factor VIII</td><td rowspan="1" colspan="1">79%</td></tr><tr><td rowspan="1" colspan="1">Anti-SS-B/La</td><td rowspan="1" colspan="1">Negative</td><td rowspan="1" colspan="1">Fibrinogen</td><td rowspan="1" colspan="1">422 mg/dL</td></tr><tr><td rowspan="1" colspan="1">Anti-dsDNA</td><td rowspan="1" colspan="1">1 IU/mL</td><td rowspan="1" colspan="1">Amphetamine</td><td rowspan="1" colspan="1">Negative</td></tr><tr><td rowspan="1" colspan="1">C3 and C4</td><td rowspan="1" colspan="1">Normal</td><td rowspan="1" colspan="1">Cocaine</td><td rowspan="1" colspan="1">Negative</td></tr><tr><td rowspan="1" colspan="1">ANCA antibodies</td><td rowspan="1" colspan="1">Negative</td><td rowspan="1" colspan="1">Opioids</td><td rowspan="1" colspan="1">Negative</td></tr><tr><th align="left" colspan="4" rowspan="1">Hypercoagulable state work-up 12 weeks
after initial set</th></tr><tr><td rowspan="1" colspan="1">PT</td><td rowspan="1" colspan="1">12.2 s</td><td rowspan="1" colspan="1">Homocysteine</td><td rowspan="1" colspan="1">9.3 µmol/L</td></tr><tr><td rowspan="1" colspan="1">PTT</td><td rowspan="1" colspan="1">29.2 s</td><td rowspan="1" colspan="1">Protein C & S</td><td rowspan="1" colspan="1">82%/93%</td></tr><tr><td rowspan="1" colspan="1">INR</td><td rowspan="1" colspan="1">3.3</td><td rowspan="1" colspan="1">Antithrombin III</td><td rowspan="1" colspan="1">92%</td></tr><tr><td rowspan="1" colspan="1">PTT-LA</td><td rowspan="1" colspan="1">57 s</td><td rowspan="1" colspan="1">CRP</td><td rowspan="1" colspan="1">40 mg/L</td></tr><tr><td rowspan="1" colspan="1">dRVTT-LA</td><td rowspan="1" colspan="1">44 s</td><td rowspan="1" colspan="1">Factor VIII</td><td rowspan="1" colspan="1">79%</td></tr><tr><td rowspan="1" colspan="1">Hexagonal-LA</td><td rowspan="1" colspan="1">Positive</td><td rowspan="1" colspan="1">Factor V Leiden</td><td rowspan="1" colspan="1">Not sent</td></tr><tr><td rowspan="1" colspan="1">Anti-β2GP1</td><td rowspan="1" colspan="1"><9 SGU</td><td rowspan="1" colspan="1">Fibrinogen</td><td rowspan="1" colspan="1">239 mg/dL</td></tr><tr><td rowspan="1" colspan="1">Anti-cardiolipin</td><td rowspan="1" colspan="1">Negative</td><td rowspan="1" colspan="1">Prothrombin 20210</td><td rowspan="1" colspan="1">No mutation</td></tr><tr><td rowspan="1" colspan="1"></td><td rowspan="1" colspan="1"></td><td rowspan="1" colspan="1">MTHFR gene</td><td rowspan="1" colspan="1">No mutation</td></tr></tbody></table></alternatives><table-wrap-foot><fn id="table-fn1-2050313X19848597"><p>PTT-LA: partial thromboplastin time for lupus anticoagulant antibody;
dRVVT-LA: dilute Russell viper venom; NT-pro-BNP: N-terminal pro b-type
natriuretic peptide; HPPL: hexagonal phase phospholipid; PT: prothrombin
time; PTT: partial thromboplastin time; INR: international normalized
ratio; ANA: antinuclear antibody; Anti-Sm: Anti Smith; Anti-RNP:
anti-ribonucleoprotein; CRP: C-reactive protein; anti-dsDNA:
anti-double-stranded DNA; ANCA: antineutrophil cytoplasmic antibodies;
Anti-β2GP1: anti-beta glycoprotein antibody; MTHFR:
methylenetetrahydrofolate reductase.</p></fn></table-wrap-foot></table-wrap><p>The patient was started on warfarin to target international normalization ratio (INR)
3.0–4.0 as he presented arterial thrombosis. Hydroxychloroquine, high-dose statin,
aspirin, clopidogrel, carvedilol, and enalapril were also prescribed. He was
discharged home with a wearable defibrillator.</p><p>Three months later, repeat PTT-LA was 57 s, dRVTT-LA 44 s, and HPPL was positive.
These results established diagnosis of APS as per the modified Sapporo criteria
(<xref rid="table2-2050313X19848597" ref-type="table">Table 2</xref>). A
follow-up echocardiogram revealed a left ventricular ejection fraction of 25%, for
which patient underwent implantation of a cardioverter-defibrillator for primary
prevention of sudden cardiac death. Clopidogrel was discontinued 6 months after
myocardial infarction in order to decrease bleeding risk. The patient has
experienced no further thrombotic events after 1 year of follow-up.</p><table-wrap id="table2-2050313X19848597" orientation="portrait" position="float"><label>Table 2.</label><caption><p>International criteria for the classification of antiphospholipid syndrome.<sup><xref rid="bibr2-2050313X19848597" ref-type="bibr">2</xref></sup></p></caption><alternatives><graphic xlink:href="10.1177_2050313X19848597-table2"></graphic><table frame="hsides" rules="groups"><colgroup span="1"><col align="left" span="1"></col></colgroup><thead><tr><th align="left" rowspan="1" colspan="1">Clinical Criteria</th></tr></thead><tbody><tr><td rowspan="1" colspan="1">1. Vascular thrombosis:<break></break> (a) One or more clinical
episodes of arterial, venous, or small vessel thrombosis
confirmed by appropriate imaging study or histopathological
analysis.<break></break>2. Pregnancy morbidity<break></break> (a) One or more
unexplained death of a morphologically normal fetus at or beyond
the 10th week of gestation.<break></break> (b) One or more premature
births of a morphologically normal neonate at or before the 34th
week of gestation due to preeclampsia, eclampsia, or placental
insufficiency.<break></break> (c) Three or more unexplained consecutive
spontaneous abortions before the 10th week of gestation,
excluding hormonal, anatomical, and progenitor genetical
abnormalities.</td></tr><tr><th align="left" rowspan="1" colspan="1">Laboratory Criteria</th></tr><tr><td rowspan="1" colspan="1">1. LA detection criteria as established by ISTH Scientific and
Standardization Subcommittee for the Standardization of Lupus
Anticoagulant<break></break> (a) Prolongation of screening tests that
are phospholipid-dependent (Hexagonal (II), KCT, dilute
prothrombin time, aPTT or dRVVT)<break></break> (b) Mixing study
demonstrate the presence of inhibitors in platelet-free normal
plasma<break></break> (c) Correction of the prolonged clotting time by
adding excess phospholipids<break></break> (d) Exclusion of other
coagulopathies (heparin or factor VIII inhibitor)<break></break>2.
Anticardiolipin antibody<break></break> (a) Medium or high IgG and/or
IgM isotype titers in the blood (defined as >99th percentile;
>40 GPL or MPL)<break></break>3. Anti-B2-glycoprotein I
antibody<break></break> (a) High IgG and/or IgM isotype titers in blood
(defined as >99th percentile; >40 GPL or MPL).</td></tr></tbody></table></alternatives><table-wrap-foot><fn id="table-fn2-2050313X19848597"><p>LA: lupus anticoagulant antibody; ISTH: International Society on
Thrombosis and Haemostasis; KCT: kaolin clotting time; aPTT: activated
partial thromboplastin time; dRVVT: dilute Russell viper venom time;
GPL: IgG phospholipid units; MPL: IgM phospholipid units; APS:
antiphospholipid syndrome.</p></fn><fn id="table-fn3-2050313X19848597"><p>For APS to be confirmed, positive aPL laboratory tests should be positive
on at least two occasions, and 12 weeks apart.</p></fn></table-wrap-foot></table-wrap></sec><sec sec-type="discussion" id="section3-2050313X19848597"><title>Discussion</title><p>The modified Sapporo criteria require clinical evidence of at least one thrombotic
event in the presence of a positive laboratory test for a known antiphospholipid
antibody and a confirmatory test 12 weeks after the initial positive test.<sup><xref rid="bibr3-2050313X19848597" ref-type="bibr">3</xref></sup> Our patient met these criteria as he had a history of PE and presented an
acute myocardial infarction (AMI) with positive serologic tests for APS on different
occasions.</p><p>The mechanism by which APS induces a hypercoagulable state has not yet been fully
elucidated. It is speculated that it entails inappropriate activation of endothelial
cells, tissue factors, c5a anaphylatoxins, and complement pathways, which ultimately
deregulate the coagulation cascade.<sup><xref rid="bibr4-2050313X19848597" ref-type="bibr">4</xref>,<xref rid="bibr5-2050313X19848597" ref-type="bibr">5</xref></sup></p><p>APS usually presents with deep venous thrombosis, transient ischemic attacks, and
ischemic strokes, but rarely ever myocardial infarction. Even though AMI is uncommon
in patients with APS, Cerveras et al.<sup><xref rid="bibr6-2050313X19848597" ref-type="bibr">6</xref></sup> established AMI as the second most common cause of death in APS patients.
Cardiac manifestations of APS include accelerated coronary atherosclerosis, valvular
abnormalities, early bypass graft failure, pulmonary hypertension, intracardiac
thrombi, myocardial microthrombi formation, and non-inflammatory microvasculopathies.<sup><xref rid="bibr7-2050313X19848597" ref-type="bibr">7</xref></sup> Circulating antiphospholipid antibody (aPL) are thought to bind to cardiac
tissue, including the valvular endothelium, leading to superficial damage.</p><p>Lupus anticoagulant antibody (LAA) is the most common antiphospholipid in APS, and it
is considered a risk factor for both venous and arterial thrombosis. A positive LAA,
as in our patient, increases the risk of AMI by 5.5%, and the risk for angina
pectoris by 2.7%.<sup><xref rid="bibr8-2050313X19848597" ref-type="bibr">8</xref>,<xref rid="bibr9-2050313X19848597" ref-type="bibr">9</xref></sup>Similarly, the IgG isotype of anticardiolipin (aCL) is strongly atherogenic and
associated with worse cardiovascular outcomes, although this antibody was not
present in our patient. In the end, all individual aPLs increase the risk for
thrombosis and atherosclerosis. However, the more aPLs present in an individual, the
worse the outcomes and the higher the risk of thrombosis in APS patients,
irrespective of their anticoagulation status and known conventional risk
factors.<sup><xref rid="bibr10-2050313X19848597" ref-type="bibr">10</xref>,<xref rid="bibr11-2050313X19848597" ref-type="bibr">11</xref></sup></p><p>It is rare for young individuals to suffer AMI as their vascular endothelium is not
yet significantly affected by atherosclerosis. Nevertheless, AMI in APS is likely
due to thrombus formation rather than of premature atherosclerosis. This case
illustrates that ACS is possible in a patient with primary APS without traditional
risk factors for atherosclerosis or pre-existing structural heart disease. Thus, a
hypercoagulable state should be suspected in young individuals who present ACS.</p><p>Primary PCI and thromboaspiration, if needed, are the treatment of choice in young
patients with STEMI and APS. Patients with APS still have significant morbidity and
mortality despite PCI and anticoagulation treatment. Optimal management is still
debatable, as patients have worse long-term clinical outcome due to higher rates of
need for target lesion revascularization. Our patient presented with stent
thrombosis, which has an incidence of 0.8% in the general population.<sup><xref rid="bibr12-2050313X19848597" ref-type="bibr">12</xref></sup> However, due to the rarity of APS and stent thrombosis, there is not enough
data to establish a direct link between the two. There are some documented cases of
recurrent stent thrombosis that make a case for APS as a risk for stent thrombosis.<sup><xref rid="bibr13-2050313X19848597" ref-type="bibr">13</xref></sup> Interestingly, recurrent stent thrombosis has occurred in APS patients on
optimal anticoagulation therapy, suggesting the presence of unforeseen variables at
play.</p><p>The combination of a hypercoagulable state in APS patients, along with increased
blood stasis due to ventricular wall akinesia, and endothelial injury from the
infarcted tissue increase the likelihood of apical thrombus. Risk factors for
developing intracardiac thrombi are associated with significant size AMI, anterior
wall location, ejection fraction of ⩽40%, severe apical akinesia, or a left
ventricular aneurysm. All of these factors were present in our patient. Prashanth et al.<sup><xref rid="bibr14-2050313X19848597" ref-type="bibr">14</xref></sup> previously published a similar case of an APS patient developing intracardiac
thrombi in the setting of an anterior wall MI. The incidence of intracardiac thrombi
in APS is unknown.</p><p>Patients with definite APS and a first venous thrombosis event should be treated with
anticoagulation with a vitamin K antagonist (VKA) to a target INR of 2.0–3.0 for at
least 3–6 months. In patients who present with arterial thrombosis, the
high-intensity VKA therapy with target INR of 3.0–4.0 is recommended. However, there
is much controversy regarding this approach as clinical trials regarding
high-intensity VKA therapy have yielded mixed results with an increased risk of bleeding.<sup><xref rid="bibr15-2050313X19848597" ref-type="bibr">15</xref></sup> Also, there are several reports of thrombotic recurrence in the presence of
high-intensity VKA.<sup><xref rid="bibr16-2050313X19848597" ref-type="bibr">16</xref></sup> Prospective cohort studies are needed to clarify the appropriate timing of
and selection criteria for high-intensity VKA therapy. For primary
thromboprophylaxis, a low-dose aspirin therapy has been shown to be effective in
decreasing first thrombotic event among SLE patients and asymptomatic aPL patients.
In subjects with single positive aPL test results, aspirin has been shown to be
equally effective for preventing recurrence of thrombotic events.<sup><xref rid="bibr17-2050313X19848597" ref-type="bibr">17</xref></sup> Similarly, statin therapy has been shown to reduce prothrombotic biomarkers.<sup><xref rid="bibr18-2050313X19848597" ref-type="bibr">18</xref></sup></p></sec><sec sec-type="conclusions" id="section4-2050313X19848597"><title>Conclusion</title><p>APS should be suspected in young individuals with unexplained thrombotic events,
including AMI. Proper immunological work-up should be performed promptly, as an
early diagnosis can decrease disease burden. Careful history taking should be
undertaken with emphasis on prior thrombotic events, such as PE or deep venous
thrombosis. Percutaneous transluminal coronary angioplasty (PTCA) is the treatment
of choice for APS patients who present with STEMI. This strategy has resulted in
satisfactory long-term results with low complication rates. Once APS is confirmed,
long-term anticoagulation should be continued and maintained at the appropriate INR
range. Just as for patients without APS, secondary preventive measures for coronary
artery disease should be provided in order to decrease morbidity and mortality in
these patients.</p></sec></body><back><fn-group><fn fn-type="COI-statement"><p><bold>Declaration of conflicting interests:</bold> The author(s) declared the following potential conflicts of interest with respect
to the research, authorship, and/or publication of this article: The content is
solely the responsibility of the authors and does not necessarily represent the
official views of the National Institutes of Health or The National Heart, Lung,
and Blood Institute.</p></fn><fn fn-type="other"><p><bold>Ethical approval:</bold> Our institution does not require ethical approval for reporting individual cases
or case series.</p></fn><fn fn-type="financial-disclosure"><p><bold>Funding:</bold> The author(s) disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: The National Institute
of Health partially supported this case report (Award Number: HCTRECD
R25MD007607) from the National Institute on Minority Health and Health
Disparities. This article was also funded by The National Heart, Lung, and Blood
Institute (NHLBI grant #SC1 HL123911).</p></fn><fn fn-type="other"><p><bold>Informed consent:</bold> Written informed consent was obtained from the patient(s) for their anonymized
information to be published in this article.</p></fn><fn fn-type="other"><p><bold>ORCID iD:</bold> Ariel Gonzalez-Cordero <inline-graphic xlink:href="10.1177_2050313X19848597-img1.jpg"></inline-graphic><ext-link ext-link-type="uri" xlink:href="https://orcid.org/0000-0001-9185-9635">https://orcid.org/0000-0001-9185-9635</ext-link></p></fn></fn-group><ref-list><title>References</title><ref id="bibr1-2050313X19848597"><label>1</label><mixed-citation publication-type="web"><collab>Antiphospholipid Syndrome</collab>, <day>20</day><month>12</month>, <year>2018</year>, <ext-link ext-link-type="uri" xlink:href="https://emedicine.medscape.com/article/333221-overview">https://emedicine.medscape.com/article/333221-overview</ext-link></mixed-citation></ref><ref id="bibr2-2050313X19848597"><label>2</label><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ortel</surname><given-names>TL.</given-names></name></person-group><article-title>Antiphospholipid syndrome: laboratory testing and diagnostic
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