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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Case report</span><p id="par0005" class="elsevierStylePara elsevierViewall">A 73-year-old woman with a history of systemic lupus erythematosus &#40;SLE&#41; diagnosed 15 years ago&#44; treated with corticosteroids and hydroxychloroquine&#44; presented to an ophthalmology consultation after a three-hour period of sudden and marked decreased right visual acuity&#46; No other symptoms were reported&#44; including fever or localized weakness&#46; Fundoscopic examination showed a pale retina with a cherry-red macula &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41; and a diagnosis of right central retinal artery occlusion was made&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0010" class="elsevierStylePara elsevierViewall">Transthoracic and transesophageal echocardiography revealed the presence of a mass attached to the ventricular side of the posterior mitral leaflet&#44; with a vibratory motion&#44; a maximum diameter of 13 mm&#44; irregular shape and heterogeneous echogenicity&#44; consistent with vegetation &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; The aortic valve had thickened leaflets &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41; and moderate regurgitation by color Doppler&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Carotid Doppler ultrasound showed no significant atherosclerotic lesions and no other cardioembolic sources were detected&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Inflammatory parameters &#40;white blood cell count 6&#46;9<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>&#47;l&#44; C-reactive protein 1&#46;6 mg&#47;dl and erythrocyte sedimentation rate 44 mm&#47;h&#41; were not suggestive of infection&#46; Blood cultures were negative&#46; Autoimmunity study revealed antinuclear antibodies positive at a titer of 1&#47;320&#44; with no other positive antibodies&#44; including negative antiphospholipid antibodies &#40;APA&#41;&#46; C3 and C4 levels were normal&#46; Thrombophilia tests including C and S protein levels&#44; antithrombin III and resistance to activated protein C were also normal&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">We assumed a diagnosis of Libman-Sacks endocarditis &#40;LSE&#41; and the patient started anticoagulation therapy&#46; A follow-up transesophageal echocardiogram four weeks later showed resolution of the previously described vegetation&#46; There was no recurrence of thromboembolic events&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Discussion</span><p id="par0030" class="elsevierStylePara elsevierViewall">SLE is an autoimmune disease that causes multiorgan inflammatory damage&#46; In recent decades&#44; with increasing survival and advances in diagnostic techniques&#44; particularly in echocardiography&#44; cardiac disease associated with SLE has become more evident&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">Valvular disease is one of the main cardiac manifestations of SLE and can occur in the form of valvular thickening&#44; masses or noninfective vegetations &#40;LSE&#41;&#44; valvular regurgitation and valvular stenosis&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">LSE was first described in 1924 by Libman and Sacks in four patients with SLE and noninfective verrucous vegetations&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Libman-Sacks vegetations develop mainly on the mitral valve&#44; followed by the aortic valve&#44; but may develop on any other valve&#44; on the subvalvular apparatus or on the surface of the endocardium&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> They are usually located on the atrial side of the mitral valve leaflets or the vessel side of the aortic valve leaflets&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">A significant proportion of patients with SLE have LSE detected in autopsy studies &#40;30&#8211;50&#37;&#41;&#46; However&#44; the real prevalence of LSE remains unknown since most patients with Libman-Sacks vegetations have asymptomatic valve abnormalities&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Moyssakis et al&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> studied 342 patients with SLE by echocardiography over four years and found an 11&#37; incidence of LSE and an association with lupus duration&#44; disease activity&#44; presence of anticardiolipin antibody and manifestations of antiphospholipid syndrome&#46; Roldan et al&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> studied 69 patients with SLE by transesophageal echocardiography and found a 43&#37; incidence of LSE&#44; which may be related to the greater accuracy of this modality&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">It has been proposed that LSE is due to the formation of fibrin-platelet thrombi on the injured valve&#44; followed by tissue organization and leading to valvular fibrosis&#44; distortion and subsequent dysfunction&#46; Recent studies have shown deposition of immunoglobulins and complement in the valvular structure which subsequently developed LSE and valvular thickening&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The association of LSE and APA has been widely investigated and has been reported in several studies&#44;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;4&#44;5</span></a> although others have found no connection&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> The role of APA in the pathogenesis of valvular disease is thought to be by promoting thrombus formation on injured valve endothelium and inflammatory changes&#44; rather than a more direct pathogenic role&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Further&#44; the observation that there is a significantly higher prevalence of valvular lesions in patients with antiphospholipid syndrome &#40;APS&#41; secondary to SLE than in those with primary APS may mean that there are SLE-related factors that promote endocardial damage and contribute to this difference&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;4</span></a> APA were not detected in our patient&#44; which is in agreement with this theory&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">One recognized complication of LSE is the development of secondary infectious endocarditis<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> which increases the complexity of differential diagnosis in a patient with SLE who presents with a valve mass&#46; Infective endocarditis lesions are usually located at the leaflet&#39;s line of closure&#44; are homogeneous in echogenicity and may show a vibratory or rotatory motion&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> In contrast&#44; LSE lesions are usually located at the base&#44; middle or tip of the leaflets and are variable in shape and size and heterogeneous in echogenicity&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Thus it is imperative to differentiate between these two clinical identities&#44; since management and treatment are quite different&#46; Our patient had no fever&#44; her leukocyte count was normal and blood cultures were negative&#44; which enabled us to reach a diagnosis of LSE and to initiate anticoagulation therapy&#46; Follow-up transesophageal echocardiography provided an assessment of disease progression&#44; revealing the regression of the previously observed vegetation&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">The main clinical impact of LSE is related to the probability of lesion progression to valvular dysfunction and the tendency to thromboembolic events&#44; especially stroke or transient ischemic attack&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;3&#44;4</span></a> The incidence of thromboembolic cerebrovascular events in patients with LSE has been reported as 10&#8211;20&#37;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;3</span></a> and a cardioembolic origin was assumed in most cases&#46; In our search of the literature we found several case reports of distal embolization from LSE&#44; the majority reporting cerebral embolization&#44; but none with retinal embolization&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">In the present case&#44; there was an occlusion of the right central retinal artery&#44; which originates from the ophthalmic artery&#44; the first intracranial branch of the internal carotid artery&#46; Given the temporal relationship between the onset of right blindness and the echocardiographic finding of a mass adhering to the mitral valve&#44; it was assumed that the retinal artery occlusion was cardioembolic in origin&#46; The patient was started on anticoagulation therapy for secondary thromboprophylaxis and remission of the previously detected vegetation was achieved&#46; To date she has had no new thromboembolic events&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">With this case report we highlight the importance of awareness of this entity&#44; 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Case report
Retinal artery embolization complicating Libman-Sacks endocarditis in a systemic lupus erythematosus patient
Endocardite de Libman-Sacks complicada por embolização da artéria da retina num doente com LES
Liliana Martaa,
Corresponding author
liliana.marta@gmail.com

Corresponding author.
, Maria Luz Pittaa, Marisa Peresa, Vítor Ferreirab, Maria Clotilde Pugab, Davide Severinoa, Graça Ferreira da Silvaa
a Serviço de Cardiologia, Hospital de Santarém, Santarém, Portugal
b Departamento de Oftalmologia, Hospital de Santarém, Santarém, Portugal
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Transesophageal echocardiogram showing vegetation &#40;Veg&#46;&#41; on the ventricular side of the posterior mitral leaflet &#40;PML&#41; and aortic valve &#40;AoV&#41; with thickened leaflets&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Case report</span><p id="par0005" class="elsevierStylePara elsevierViewall">A 73-year-old woman with a history of systemic lupus erythematosus &#40;SLE&#41; diagnosed 15 years ago&#44; treated with corticosteroids and hydroxychloroquine&#44; presented to an ophthalmology consultation after a three-hour period of sudden and marked decreased right visual acuity&#46; No other symptoms were reported&#44; including fever or localized weakness&#46; Fundoscopic examination showed a pale retina with a cherry-red macula &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41; and a diagnosis of right central retinal artery occlusion was made&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0010" class="elsevierStylePara elsevierViewall">Transthoracic and transesophageal echocardiography revealed the presence of a mass attached to the ventricular side of the posterior mitral leaflet&#44; with a vibratory motion&#44; a maximum diameter of 13 mm&#44; irregular shape and heterogeneous echogenicity&#44; consistent with vegetation &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; The aortic valve had thickened leaflets &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41; and moderate regurgitation by color Doppler&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Carotid Doppler ultrasound showed no significant atherosclerotic lesions and no other cardioembolic sources were detected&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Inflammatory parameters &#40;white blood cell count 6&#46;9<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>10<span class="elsevierStyleSup">9</span>&#47;l&#44; C-reactive protein 1&#46;6 mg&#47;dl and erythrocyte sedimentation rate 44 mm&#47;h&#41; were not suggestive of infection&#46; Blood cultures were negative&#46; Autoimmunity study revealed antinuclear antibodies positive at a titer of 1&#47;320&#44; with no other positive antibodies&#44; including negative antiphospholipid antibodies &#40;APA&#41;&#46; C3 and C4 levels were normal&#46; Thrombophilia tests including C and S protein levels&#44; antithrombin III and resistance to activated protein C were also normal&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">We assumed a diagnosis of Libman-Sacks endocarditis &#40;LSE&#41; and the patient started anticoagulation therapy&#46; A follow-up transesophageal echocardiogram four weeks later showed resolution of the previously described vegetation&#46; There was no recurrence of thromboembolic events&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Discussion</span><p id="par0030" class="elsevierStylePara elsevierViewall">SLE is an autoimmune disease that causes multiorgan inflammatory damage&#46; In recent decades&#44; with increasing survival and advances in diagnostic techniques&#44; particularly in echocardiography&#44; cardiac disease associated with SLE has become more evident&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">Valvular disease is one of the main cardiac manifestations of SLE and can occur in the form of valvular thickening&#44; masses or noninfective vegetations &#40;LSE&#41;&#44; valvular regurgitation and valvular stenosis&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">LSE was first described in 1924 by Libman and Sacks in four patients with SLE and noninfective verrucous vegetations&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Libman-Sacks vegetations develop mainly on the mitral valve&#44; followed by the aortic valve&#44; but may develop on any other valve&#44; on the subvalvular apparatus or on the surface of the endocardium&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> They are usually located on the atrial side of the mitral valve leaflets or the vessel side of the aortic valve leaflets&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">A significant proportion of patients with SLE have LSE detected in autopsy studies &#40;30&#8211;50&#37;&#41;&#46; However&#44; the real prevalence of LSE remains unknown since most patients with Libman-Sacks vegetations have asymptomatic valve abnormalities&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Moyssakis et al&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> studied 342 patients with SLE by echocardiography over four years and found an 11&#37; incidence of LSE and an association with lupus duration&#44; disease activity&#44; presence of anticardiolipin antibody and manifestations of antiphospholipid syndrome&#46; Roldan et al&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> studied 69 patients with SLE by transesophageal echocardiography and found a 43&#37; incidence of LSE&#44; which may be related to the greater accuracy of this modality&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">It has been proposed that LSE is due to the formation of fibrin-platelet thrombi on the injured valve&#44; followed by tissue organization and leading to valvular fibrosis&#44; distortion and subsequent dysfunction&#46; Recent studies have shown deposition of immunoglobulins and complement in the valvular structure which subsequently developed LSE and valvular thickening&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The association of LSE and APA has been widely investigated and has been reported in several studies&#44;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;4&#44;5</span></a> although others have found no connection&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> The role of APA in the pathogenesis of valvular disease is thought to be by promoting thrombus formation on injured valve endothelium and inflammatory changes&#44; rather than a more direct pathogenic role&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Further&#44; the observation that there is a significantly higher prevalence of valvular lesions in patients with antiphospholipid syndrome &#40;APS&#41; secondary to SLE than in those with primary APS may mean that there are SLE-related factors that promote endocardial damage and contribute to this difference&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;4</span></a> APA were not detected in our patient&#44; which is in agreement with this theory&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">One recognized complication of LSE is the development of secondary infectious endocarditis<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> which increases the complexity of differential diagnosis in a patient with SLE who presents with a valve mass&#46; Infective endocarditis lesions are usually located at the leaflet&#39;s line of closure&#44; are homogeneous in echogenicity and may show a vibratory or rotatory motion&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> In contrast&#44; LSE lesions are usually located at the base&#44; middle or tip of the leaflets and are variable in shape and size and heterogeneous in echogenicity&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Thus it is imperative to differentiate between these two clinical identities&#44; since management and treatment are quite different&#46; Our patient had no fever&#44; her leukocyte count was normal and blood cultures were negative&#44; which enabled us to reach a diagnosis of LSE and to initiate anticoagulation therapy&#46; Follow-up transesophageal echocardiography provided an assessment of disease progression&#44; revealing the regression of the previously observed vegetation&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">The main clinical impact of LSE is related to the probability of lesion progression to valvular dysfunction and the tendency to thromboembolic events&#44; especially stroke or transient ischemic attack&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;3&#44;4</span></a> The incidence of thromboembolic cerebrovascular events in patients with LSE has been reported as 10&#8211;20&#37;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;3</span></a> and a cardioembolic origin was assumed in most cases&#46; In our search of the literature we found several case reports of distal embolization from LSE&#44; the majority reporting cerebral embolization&#44; but none with retinal embolization&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">In the present case&#44; there was an occlusion of the right central retinal artery&#44; which originates from the ophthalmic artery&#44; the first intracranial branch of the internal carotid artery&#46; Given the temporal relationship between the onset of right blindness and the echocardiographic finding of a mass adhering to the mitral valve&#44; it was assumed that the retinal artery occlusion was cardioembolic in origin&#46; The patient was started on anticoagulation therapy for secondary thromboprophylaxis and remission of the previously detected vegetation was achieved&#46; To date she has had no new thromboembolic events&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">With this case report we highlight the importance of awareness of this entity&#44; allowing rapid referral for cardiovascular examination and thus enabling early diagnosis and appropriate intervention&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">Given that most patients with SLE and valvular disease have no cardiac symptoms&#44; a careful cardiovascular examination should be made periodically&#46; Since strokes in patients with SLE are frequent and&#44; on the other hand&#44; valvular thickening and vegetations are common and can act as substrates for cardioembolism&#44; prophylactic therapy with anticoagulation may be an appropriate approach to these patients&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Ethical disclosures</span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Protection of human and animal subjects</span><p id="par0085" 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">Confidentiality of data</span><p id="par0090" 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">Right to privacy and informed consent</span><p id="par0095" 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">Conflicts of interest</span><p id="par0100" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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        "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Libman-Sacks endocarditis &#40;LSE&#41; is the most characteristic cardiac manifestation of systemic lupus erythematosus &#40;SLE&#41;&#46; It is usually clinically silent but heart failure due to valvular dysfunction&#44; secondary infective endocarditis and embolic phenomena can complicate valvular abnormalities&#46; We present a patient with SLE and blindness due to right central retinal artery occlusion&#46; Echocardiographic examination revealed a verrucous vegetation on the posterior mitral valve leaflet consistent with LSE&#46; Anticoagulation therapy was started&#46; Echocardiographic regression of the vegetation was observed and there has been no recurrence of thromboembolic events to date&#46;</p>"
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        "resumen" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">A endocardite de Libman-Sacks &#233; a manifesta&#231;&#227;o card&#237;aca mais caracter&#237;stica do LES&#46; &#201; habitualmente clinicamente silenciosa&#44; mas a insufici&#234;ncia card&#237;aca por disfun&#231;&#227;o valvular&#44; a endocardite infecciosa secund&#225;ria e os fen&#243;menos emb&#243;licos podem complicar as altera&#231;&#245;es valvulares&#46; Apresentamos um caso cl&#237;nico de uma doente com LES e amaurose &#224; direita por trombose da art&#233;ria central da retina&#46; O ecocardiograma mostrou uma vegeta&#231;&#227;o verrucosa no folheto posterior da v&#225;lvula mitral&#44; compat&#237;vel com endocardite de Libman-Sacks&#46; A doente iniciou terap&#234;utica com anticoagula&#231;&#227;o&#44; verificou-se regress&#227;o da vegeta&#231;&#227;o descrita e n&#227;o teve recorr&#234;ncia de eventos tromboemb&#243;licos at&#233; &#224; data&#46;</p>"
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Article information
ISSN: 21742049
Original language: English
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Idiomas
Revista Portuguesa de Cardiologia (English edition)
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