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Diagnosis and surgical treatment for isolated tricuspid libman-sacks endocarditis: a rare case report and literatures review

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      Abstract

      Libman-Sacks endocarditis (LSE), characterized by verrucous vegetations formation, is a typical cardiac manifestation of autoimmune diseases such as systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). It primarily leads to lesions of cardiac valves and mostly involved valves are mitral and aortic, but isolated tricuspid valve involvement is exceptional. Here we reported a 20-years-old female with past SLE history suffered from acute right heart failure caused by multiple tricuspid vegetations and valve regurgitation. The patient recovered following tricuspid valve replacement with a bioprosthesis. Transesophageal echocardiography(TEE), especially real time 3-dimensional (RT3D) TEE provide a better imaging modality for assessing cardiac valvular involvement of LSE. For patients with active SLE/APS course, uncontrolled systemic inflammation may made it difficult for surgical exposure and suture. The durability of bioprosthesis for this patient and the prosthesis selection for tricuspid LSE both need further follow-up and more clinical investigation.

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      Most cited references 21

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      ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC.

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        Libman-Sacks endocarditis in systemic lupus erythematosus: prevalence, associations, and evolution.

        We evaluated the prevalence and progression of Libman-Sacks endocarditis in patients with systemic lupus erythematosus and any association between this valvulopathy and their clinical and laboratory characteristics. Doppler echocardiography was performed in 342 consecutive patients with systemic lupus erythematosus (297 females and 45 males). The clinical and laboratory data were recorded. Patients were reevaluated after a follow-up period of 4 years. Libman-Sacks endocarditis was found in 38 patients (11%). In 24 of 38 patients, mitral valve involvement was found, resulting in regurgitation in all (mild in 18, moderate in 4, and severe in 2), whereas stenosis co-occurred with regurgitation in 9 patients (mild in 6 and moderate in 3). Thirteen (34%) of 38 patients had aortic valve involvement; 11 had regurgitation (mild) and 8 had stenosis (mild), coexistent with regurgitation in 6 of them. One patient had mild tricuspid regurgitation. A significant association was found between Libman-Sacks endocarditis and disease duration and activity, thromboses, stroke, thrombocytopenia, anticardiolipin antibodies, and antiphospholipid syndrome. During the follow-up period, 252 of 342 patients were reevaluated echocardiographically. Among the 38 patients with Libman-Sacks vegetations, 5 with mild mitral regurgitation at the beginning developed moderate (n=4) and severe mitral regurgitation (n=1), 2 patients with mitral stenosis (mild in 1 and moderate in 1) developed severe mitral regurgitation, and 2 patients with mild aortic regurgitation developed moderate and severe mitral regurgitation, whereas a significant deterioration of aortic stenosis was found. Two patients who were candidates for surgery died. Among the 213 patients without vegetations at the beginning, 8 developed new Libman-Sacks lesions. Libman-Sacks vegetations can be found in approximately 1 of 10 patients with systemic lupus erythematosus, and they are associated with lupus duration, disease activity, anticardiolipin antibodies, and antiphospholipid syndrome manifestations. A progression of valve lesions may occur during long-term follow-up.
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          Heart valve involvement (Libman-Sacks endocarditis) in the antiphospholipid syndrome.

          The antiphospholipid syndrome (APS) is defined by the presence of anti-phospholipid antibodies (aPLs) and venous or arterial thrombosis, recurrent pregnancy loss, or thrombocytopenia. The syndrome can be either primary or secondary to an underlying condition, most commonly systemic lupus erythematosus (SLE). Echocardiographic studies have disclosed heart valve abnormalities in about a third of patients with primary APS. SLE patients with aPLs have a higher prevalence of valvular involvement than those without these antibodies. Valvular lesions associated with aPLs occur as valve masses (nonbacterial vegetations) or thickening. These two morphological alterations can be combined and are thought to reflect the same pathological process. Both can be associated with valve dysfunction, although such association is much more common with the latter alteration. The predominant functional abnormality is regurgitation; stenosis is rare. The mitral valve is mainly affected, followed by the aortic valve. Valvular involvement usually does not cause clinical valvular disease. The presence of aPLs seems to further increase the risk for thromboembolic complications, mainly cerebrovascular, posed by valve lesions. Superadded bacterial endocarditis is rare but may be difficult to distinguish from pseudoinfective endocarditis. The current therapeutic guidelines are those for APS in general. Secondary antithrombotic prevention with long-term, high-intensity oral anticoagulation is advised. The efficacy of aspirin, either alone or in combination, is yet to be assessed. Corticosteroids are not beneficial and may even facilitate valve damage. Immunosuppressive agents should only be used for the treatment of an underlying condition. Current data suggest a role for aPLs in the pathogenesis of valvular lesions. aPLs may promote the formation of valve thrombi. These antibodies may also act by another mechanism, as indicated by the finding of subendothelial deposits of immunoglobulins, including anticardiolipin antibodies, and of colocalized complement components in deformed valves from patients with APS.
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            Author and article information

            Affiliations
            Department of Cardiovascular Surgery, West China Hospital, Sichuan University, 37 Guoxue Xiang St., Chengdu, Sichuan China
            Contributors
            zhixuan.bai@foxmail.com
            Houjl@126.com
            815624967@qq.com
            drguoyq@hotmail.com
            Journal
            J Cardiothorac Surg
            J Cardiothorac Surg
            Journal of Cardiothoracic Surgery
            BioMed Central (London )
            1749-8090
            8 July 2015
            8 July 2015
            2015
            : 10
            4494164 302 10.1186/s13019-015-0302-1
            © Zhixuan et al. 2015

            This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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            © The Author(s) 2015

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