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She was then admitted to the intensive coronary care unit &#40;ICCU&#41; and treated with IV inotropes and diuretics&#44; resulting in prompt recovery from aphasia and improvement in congestion&#46; The echocardiogram showed a markedly dilated left ventricle with hypertrabeculation of the apex and of the inferior-inferolateral segments &#40;noncompacted&#47;compacted ratio 2&#58;1&#41;&#44; severely reduced ejection fraction &#40;EF&#41; &#40;22&#37;&#41;&#44; and an apical thrombus&#46; No significant carotid artery disease was found on Doppler echocardiography&#46; She underwent implantation of an implantable cardioverter-defibrillator and was discharged in NYHA class II&#44; under standard heart failure therapy including oral anticoagulation &#40;OAC&#41;&#44; with no evidence of thrombosis &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#46; Twelve months later&#44; due to a major depressive episode&#44; the patient failed to attend the scheduled heart failure clinic &#40;HFC&#41; follow-up and discontinued OAC&#46; Due to recurrent dyspnea and fatigue she presented to the HFC&#44; where an echocardiogram showed a massive LV thrombosis &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#44; so she was admitted to the ICCU and IV UFH was started&#46; After two days the patient complained of chest pain&#59; as the ECG showed marked ST segment elevation in V3-V6 she was referred to the catheterization lab&#46; Coronary angiography revealed a thrombotic occlusion of the mid segment of the left anterior descending artery &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>A&#41;&#59; the clot was aspirated and no significant coronary artery disease &#40;CAD&#41; was found &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>B and C&#41;&#46; A marked increase in plasma troponin I was observed&#44; confirming the diagnosis of acute embolic myocardial infarction &#40;MI&#41;&#46; Her EF fell to 15&#37; and after two days she became hypotensive despite intra-aortic balloon pump and inotropic support&#44; with cardiogenic shock and acute kidney failure&#46; She was considered for a left ventricular assist device&#44; but sepsis and multiorgan failure occurred&#44; and death followed 25 days later&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Discussion</span><p id="par0010" class="elsevierStylePara elsevierViewall">LVNC is associated with HF&#44; arrhythmias and embolism&#46; Cardioembolic events are not uncommon&#44; as trabecular recesses and depressed systolic function predispose to thrombosis&#44; but presentation as an acute coronary syndrome &#40;ACS&#41; is rather unexpected&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">1</span></a> Previous observations suggested that in patients with reported myocardial infarction and LVNC&#44; ischemia is mainly related to CAD and does not appear to be relevant to LVNC&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> However&#44; in the small number of reported cases of ACS in LVNC patients with no evidence of coronary stenosis or LV thrombosis&#44; myocardial infarction was described as a consequence of microvascular dysfunction&#44; as LVNC patients exhibit decreased coronary flow reserve in both compacted and noncompacted LV segments<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> and subendocardial perfusion defects despite normal coronary arteries&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> In a few of them embolism from thrombosis of the LV chamber was suggested&#44; but with no reported evidence of intracavitary thrombus&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a> In our patient&#44; significant angiographic CAD was absent and the evidence of LV thrombosis itself strongly supports embolism as the most likely etiology&#46; Although MI as an embolic complication is relatively infrequent&#44; stroke and&#47;or embolism occur in at least 15&#37; of LVNC patients&#44; mostly in those with advanced HF and AF&#44;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">6</span></a> which implies that OAC is worth starting in the presence of predisposing factors&#46; Nevertheless&#44; in the absence of such conditions&#44; cardioembolic events are rare&#44; and stroke and&#47;or embolism may also have an atherosclerotic cause&#46; Hence&#44; the embolic risk in LVNC patients with systolic dysfunction in sinus rhythm is largely unknown and OAC is mainly an individual therapeutic choice&#44; mandatory in those with evidence of LV thrombosis&#44; or a prudent option in primary prevention for those at the highest risk of embolization&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">7</span></a> In our case OAC was initially prescribed because of a previous transient ischemic attack with LV thrombosis&#44; and paroxysmal AF&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">In conclusion&#44; this case suggests that&#44; although infrequent&#44; ACS is a possible manifestation of LVNC-related embolism&#44; and so an embolic etiology should be kept in mind in differential diagnosis between atherosclerosis in LVNC patients presenting with MI&#46; Careful attention should be paid to embolic risk stratification and the need for OAC in such patients&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Ethical disclosures</span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Protection of human and animal subjects</span><p id="par0020" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this study&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Confidentiality of data</span><p id="par0025" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Right to privacy and informed consent</span><p id="par0030" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article&#46;</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Left ventricular noncompaction &#40;LVNC&#41; is characterized by left ventricular &#40;LV&#41; hypertrabeculations and is associated with heart failure&#44; arrhythmias and embolism&#46; We report the case of a 67-year-old LVNC patient&#44; under oral anticoagulation &#40;OAC&#41; therapy for apical thrombosis&#46; After she discontinued OAC&#44; the thrombus involved almost the whole of the left ventricle&#59; in a few months her condition worsened&#44; requiring hospitalization&#44; and despite heparin infusion she experienced myocardial infarction &#40;MI&#41;&#44; caused by embolic occlusion of the left anterior descending artery&#46; Although infrequent as a complication of LVNC&#44; and usually attributable to microvascular dysfunction&#44; in this case MI seems due to coronary thromboembolism from dislodged thrombotic material in the left ventricle&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">A n&#227;o compacta&#231;&#227;o ventricular esquerda &#40;NCVE&#41; &#233; caracterizada por hipertrabecula&#231;&#245;es ventriculares esquerdas &#40;VE&#41; e est&#225; associada &#224; insufici&#234;ncia card&#237;aca&#44; arritmias e embolias&#46; Divulgamos o caso de uma doente de 67 anos com NCVE e em terap&#234;utica de anticoagula&#231;&#227;o oral &#40;ACO&#41; por trombose apical&#46; Como descontinuou a anticoagula&#231;&#227;o oral o trombo envolveu quase todo o VE&#59; em poucos meses a sua situa&#231;&#227;o piorou necessitando internamento e &#8211; apesar da infus&#227;o com heparina &#8211; sofreu um enfarte do mioc&#225;rdio &#40;EM&#41;&#44; causado por oclus&#227;o emb&#243;lica da DAE&#46; Embora seja pouco frequente tal como a complica&#231;&#227;o por NCVE e seja geralmente atribu&#237;vel &#224; disfun&#231;&#227;o microvascular&#44; o EM parece ser&#44; neste caso&#44; devido ao tromboembolismo coron&#225;rio a partir do trombo do VE&#46;</p></span>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#41; Apical 4-chamber view and &#40;B&#41; parasternal short-axis view of mid segments showing intertrabecular recesses filled with blood in the anterolateral segments&#46;</p>"
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Case report
Noncompaction and embolic myocardial infarction: The importance of oral anticoagulation
Não-compactação e enfarte do miocárdio embólico: a importância da anticoagulação oral
Giovanni Pulignanoa,
Autor para correspondência
gipulig@yahoo.it

Corresponding author.
, Maria Denitza Tintia, Stefano Tolonea, Carmine Mustob, Lucia De Lioa, Paolo Giuseppe Pinoa, Giovanni Minardia, Roberto Violinib, Massimo Uguccionia
a Cardiology 1/CCU, S. Camillo Hospital, Rome, Italy
b Interventional Cardiology, S. Camillo Hospital, Rome, Italy
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follow-up and discontinued OAC&#46; Due to recurrent dyspnea and fatigue she presented to the HFC&#44; where an echocardiogram showed a massive LV thrombosis &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#44; so she was admitted to the ICCU and IV UFH was started&#46; After two days the patient complained of chest pain&#59; as the ECG showed marked ST segment elevation in V3-V6 she was referred to the catheterization lab&#46; Coronary angiography revealed a thrombotic occlusion of the mid segment of the left anterior descending artery &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>A&#41;&#59; the clot was aspirated and no significant coronary artery disease &#40;CAD&#41; was found &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>B and C&#41;&#46; A marked increase in plasma troponin I was observed&#44; confirming the diagnosis of acute embolic myocardial infarction &#40;MI&#41;&#46; Her EF fell to 15&#37; and after two days she became hypotensive despite intra-aortic balloon pump and inotropic support&#44; with cardiogenic shock and acute kidney failure&#46; She was considered for a left ventricular assist device&#44; but sepsis and multiorgan failure occurred&#44; and death followed 25 days later&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Discussion</span><p id="par0010" class="elsevierStylePara elsevierViewall">LVNC is associated with HF&#44; arrhythmias and embolism&#46; Cardioembolic events are not uncommon&#44; as trabecular recesses and depressed systolic function predispose to thrombosis&#44; but presentation as an acute coronary syndrome &#40;ACS&#41; is rather unexpected&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">1</span></a> Previous observations suggested that in patients with reported myocardial infarction and LVNC&#44; ischemia is mainly related to CAD and does not appear to be relevant to LVNC&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a> However&#44; in the small number of reported cases of ACS in LVNC patients with no evidence of coronary stenosis or LV thrombosis&#44; myocardial infarction was described as a consequence of microvascular dysfunction&#44; as LVNC patients exhibit decreased coronary flow reserve in both compacted and noncompacted LV segments<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> and subendocardial perfusion defects despite normal coronary arteries&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> In a few of them embolism from thrombosis of the LV chamber was suggested&#44; but with no reported evidence of intracavitary thrombus&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a> In our patient&#44; significant angiographic CAD was absent and the evidence of LV thrombosis itself strongly supports embolism as the most likely etiology&#46; Although MI as an embolic complication is relatively infrequent&#44; stroke and&#47;or embolism occur in at least 15&#37; of LVNC patients&#44; mostly in those with advanced HF and AF&#44;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">6</span></a> which implies that OAC is worth starting in the presence of predisposing factors&#46; Nevertheless&#44; in the absence of such conditions&#44; cardioembolic events are rare&#44; and stroke and&#47;or embolism may also have an atherosclerotic cause&#46; Hence&#44; the embolic risk in LVNC patients with systolic dysfunction in sinus rhythm is largely unknown and OAC is mainly an individual therapeutic choice&#44; mandatory in those with evidence of LV thrombosis&#44; or a prudent option in primary prevention for those at the highest risk of embolization&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">7</span></a> In our case OAC was initially prescribed because of a previous transient ischemic attack with LV thrombosis&#44; and paroxysmal AF&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">In conclusion&#44; this case suggests that&#44; although infrequent&#44; ACS is a possible manifestation of LVNC-related embolism&#44; and so an embolic etiology should be kept in mind in differential diagnosis between atherosclerosis in LVNC patients presenting with MI&#46; Careful attention should be paid to embolic risk stratification and the need for OAC in such patients&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Ethical disclosures</span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Protection of human and animal subjects</span><p id="par0020" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this study&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Confidentiality of data</span><p id="par0025" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Right to privacy and informed consent</span><p id="par0030" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article&#46;</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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            0 => "Left ventricular noncompaction"
            1 => "Embolism"
            2 => "Heart failure"
            3 => "Myocardial infarction"
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            0 => "N&#227;o compacta&#231;&#227;o ventricular esquerda"
            1 => "Embolia"
            2 => "Insufici&#234;ncia card&#237;aca"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Left ventricular noncompaction &#40;LVNC&#41; is characterized by left ventricular &#40;LV&#41; hypertrabeculations and is associated with heart failure&#44; arrhythmias and embolism&#46; We report the case of a 67-year-old LVNC patient&#44; under oral anticoagulation &#40;OAC&#41; therapy for apical thrombosis&#46; After she discontinued OAC&#44; the thrombus involved almost the whole of the left ventricle&#59; in a few months her condition worsened&#44; requiring hospitalization&#44; and despite heparin infusion she experienced myocardial infarction &#40;MI&#41;&#44; caused by embolic occlusion of the left anterior descending artery&#46; Although infrequent as a complication of LVNC&#44; and usually attributable to microvascular dysfunction&#44; in this case MI seems due to coronary thromboembolism from dislodged thrombotic material in the left ventricle&#46;</p></span>"
      ]
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">A n&#227;o compacta&#231;&#227;o ventricular esquerda &#40;NCVE&#41; &#233; caracterizada por hipertrabecula&#231;&#245;es ventriculares esquerdas &#40;VE&#41; e est&#225; associada &#224; insufici&#234;ncia card&#237;aca&#44; arritmias e embolias&#46; Divulgamos o caso de uma doente de 67 anos com NCVE e em terap&#234;utica de anticoagula&#231;&#227;o oral &#40;ACO&#41; por trombose apical&#46; Como descontinuou a anticoagula&#231;&#227;o oral o trombo envolveu quase todo o VE&#59; em poucos meses a sua situa&#231;&#227;o piorou necessitando internamento e &#8211; apesar da infus&#227;o com heparina &#8211; sofreu um enfarte do mioc&#225;rdio &#40;EM&#41;&#44; causado por oclus&#227;o emb&#243;lica da DAE&#46; Embora seja pouco frequente tal como a complica&#231;&#227;o por NCVE e seja geralmente atribu&#237;vel &#224; disfun&#231;&#227;o microvascular&#44; o EM parece ser&#44; neste caso&#44; devido ao tromboembolismo coron&#225;rio a partir do trombo do VE&#46;</p></span>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#41; Apical 4-chamber view and &#40;B&#41; parasternal short-axis view of mid segments showing intertrabecular recesses filled with blood in the anterolateral segments&#46;</p>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#41; Parasternal short-axis view of the mid segments&#46; Two-layered structure of the thickened myocardium&#44; with deep trabecular recesses in inferior&#44; inferolateral and anterolateral segments&#59; &#40;B&#41; apical 5-chamber view showing a floating thrombotic mass&#59; &#40;C&#41; parasternal short-axis view showing thrombotic masses in the basal and mid segments of the anterior wall of the left ventricle&#46;</p>"
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Informação do artigo
ISSN: 08702551
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2017 Julho 25 13 38
2017 Junho 40 12 52
2017 Maio 34 6 40
2017 Abril 27 7 34
2017 Maro 27 14 41
2017 Fevereiro 22 7 29
2017 Janeiro 27 7 34
2016 Dezembro 25 4 29
2016 Novembro 19 7 26
2016 Outubro 36 5 41
2016 Setembro 32 6 38
2016 Agosto 19 3 22
2016 Julho 6 4 10
2016 Junho 2 7 9
2016 Maio 30 10 40
2016 Abril 23 2 25
2016 Maro 21 8 29
2016 Fevereiro 43 20 63
2016 Janeiro 16 9 25
2015 Dezembro 29 11 40
2015 Novembro 34 13 47
2015 Outubro 34 22 56
2015 Setembro 107 23 130
2015 Agosto 216 107 323
2015 Julho 17 13 30
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Revista Portuguesa de Cardiologia
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