Features associated with cardiac abnormalities in systemic lupus erythematosus

Bourré‐Tessier, Josiane; Huynh, Thao; Clarke, AE; Bernatsky, Sasha; Joseph, Lawrence; Bélisle, Patrick; Pineau, CA

doi:10.1177/0961203311420318

Cited by 34 publications

(34 citation statements)

References 23 publications

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“…The deposition of immunoglobulins on the valve leaflets underlies the pathophysiology of Libman-Sacks endocarditis [10]. aPL not only lead to the formation of verrucous vegetations but also can lead to the formation of valve thrombi and consequently serious complications such as cerebral thromboembolism can occur [6][7][8]. This was demonstrated in our patient once.…”

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confidence: 66%

“…Vegetations on the mitral valve generally form on the atrial surface of leaflets [3,6]. Previous reports have also described "kissing lesions" located on the opposing lines of leaflet closure of both the mitral and the aortic valves such as in our case [3,5,6,8]. Decreased leaflet mobility and subvalvular thickening are rarely seen [3].…”

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confidence: 80%

“…Decreased leaflet mobility and subvalvular thickening are rarely seen [3]. Hemodynamically significant valvular stenosis and regurgitation occur in only 3% of cases [3,8,9]. There is a paucity of data documenting the echocardiographic response of APS valve disease to antithrombotic therapy.…”

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confidence: 99%

“…A thrombotic stroke occurring in a young patient with no overt risk factors for cerebrovascular disease is a wellknown clinical setting in which to suspect APS [7]. The heart is an important source of systemic embolization in patients with APS [8]. Valve lesions, especially aortic nodules, are highly associated with the risk of stroke [7].…”

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confidence: 99%

“…This was demonstrated in our patient once. This thromboembolic event is one of the most common manifestations in APS patients with Libman-Sacks endocarditis [6][7][8][9][10].…”

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confidence: 99%

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Primary cardiac involvement of anti-phospholipid syndrome misdiagnosed as infective endocarditis

Çağlar¹,

Bıyık²,

Işıksaçan³

et al. 2017

Arch Med Sci Civil Dis

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Anti-phospholipid syndrome (APS) is defined by thrombosis (venous, arterial, or small vessel) and/or pregnancy morbidity (recurrent miscarriage, fetal loss, or placental insufficiency) occurring in the presence of persistently positive anti-phospholipid antibodies (aPL), lupus anticoagulant (LAC) test, anti-cardiolipin antibodies (aCL), and anti-B2-glycoprotein I antibodies [1]. Anti-phospholipid syndrome can occur as an isolated condition or can be associated with connective tissue diseases, most commonly systemic lupus erythematosus (SLE). Herein we present a patient with aPL syndrome and cardiac involvement, misdiagnosed and treated as infective endocarditis.A 31-year-old woman was admitted to the neurology clinic because of weakness of the left hand. Her clinical history revealed mild weakness of bilateral hands lasting less than 2 h for about 5 years. Cranial contrast magnetic resonance imaging (MRI) showed atrophic gliotic changes and thin strip style gyral hyperintensity in T1 imaging at the superior sylvian fissure. Also gliotic localized atrophic changes were observed at the right posterior horn of the lateral ventricle. The patient was referred to the cardiology department for differential diagnosis. Initial physical examination and electrocardiography were evaluated as normal. Transthoracic and then transesophageal echocardiography revealed a hypodense fibrillated mobile 5 mm mass at the A2 scallop of the anterior mitral valve leaflet and moderate mitral regurgitation (Figures 1-3). Both MRI and transesophageal echocardiography (TEE) findings were consistent with endocarditis, so the patient was admitted to the cardiology department and consulted with rheumatology and infectious diseases. An empiric antibiotic regimen was started after blood culture sampling. Meanwhile her laboratory findings demonstrated all increased positive results of anti-b-2-glycoprotein-1 IgM and IgG, lupus anticoagulant, anti-cardiolipin IgM and IgG and decreased C4 levels. She had no fever and blood cultures were negative, so antibiotherapy was stopped at day 10, with the final diagnosis of primary APS and Libman-Sacks endocarditis. She was discharged with warfarin therapy.The common cardiac manifestations of APS include valvular involvement such as thickening, vegetations and dysfunction, coronary thrombosis, ventricular hypertrophy and dysfunction, intracardiac thrombi and pulmonary hypertension [2]. The most common echocardiographically

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confidence: 66%

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confidence: 80%

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confidence: 99%

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confidence: 99%

“…This was demonstrated in our patient once. This thromboembolic event is one of the most common manifestations in APS patients with Libman-Sacks endocarditis [6][7][8][9][10].…”

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confidence: 99%

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