Libman-SacksEndocarditis Involving a Bioprosthesis in the Aortic Valve Position in Systemic Lupus Erythematosus. Described herein is a 39-year-old man with systemic lupus erythematosus not receiving corticosteroid therapy who developed Libman-Sacksendocarditis causing stenosis of a bioprosthesis in the aortic valve position.
Libman-Sacksendocarditis in a Bangladeshi patient suffering from rhupus. Libman-Sacksendocarditis (LSE) is one of the most characteristic cardiac lesions in systemic lupus erythematosus (SLE). Patients may remain asymptomatic, while symptomatic patients often suffer with systemic emboli. These commonly test positive for anti-phospholipid antibody (aPA). The association of LSE with an overlap
Libman-SacksEndocarditis in a Puerpera with Systemic Lupus Erythematosus. Libman-Sacks (LS) endocarditis is rarely seen in the prenatal and puerperal periods and is generally reported as a cardiac manifestation of systemic lupus erythematosus. In this report, we present a rare case of congestive heart failure after vaginal delivery. The patient was diagnosed with systemic lupus erythematosus
Libman-SacksEndocarditis Due to Systemic Lupus Erythematosus Activation After Mitral Valve Plasty. Libman-Sacksendocarditis is a cardiac manifestation of systemic lupus erythematosus (SLE) and antiphospholipid syndrome. We report a case of mitral valve destruction due to Libman-Sacksendocarditis, which was caused by activation of SLE, despite prompt initiation of systemic steroid therapy
Lupus-Negative Libman-SacksEndocarditis Complicated by Catastrophic Antiphospholipid Syndrome Libman-Sacksendocarditis is characterized by sterile and verrucous lesions that predominantly affect the aortic and mitral valves. In most cases, patients do not have significant valvular dysfunction. However, patients with significant valvular dysfunction may present with serious complications such as cardiac failure, arrhythmias, and thromboembolic events. Recently, association of Libman-Sacksendocarditis with antiphospholipid antibody syndrome (APS) has been made. APS is most commonly defined by venous and arterial thrombosis, recurrent pregnancy loss, and thrombocytopenia. While the syndrome can be a primary syndrome, it is usually secondary to systemic lupus erythematosus. Catastrophic
Isolated Tricuspid Valve Libman-SacksEndocarditis in Systemic Lupus Erythematosus with Secondary Antiphospholipid Syndrome Libman-Sacksendocarditis, one of the most prevalent cardiac presentations of systemic lupus erythematosus, typically affects the aortic or mitral valve; tricuspid valve involvement is highly unusual. Secondary antiphospholipid syndrome increases the frequency and severity of cardiac valvular disease in systemic lupus erythematosus. We present the case of a 47-year-old woman with lupus and antiphospholipid syndrome whose massive tricuspid regurgitation was caused by Libman-Sacksendocarditis isolated to the tricuspid valve. In addition, we discuss this rare case in the context of the relevant medical literature.
Antiphospholipid Syndrome and Libman-SacksEndocarditis in a Bioprosthetic Mitral Valve. This report describes one the first cases of antiphospholipid syndrome and Libman-Sacksendocarditis in a bioprosthetic valve. A redo mitral valve replacement was carried out owing to early deterioration of the prior valve. Initially it was considered secondary to rheumatic heart disease; however, pathology analysis and autoimmune workup revealed antiphospholipid syndrome with Libman-Sacksendocarditis. We believe certain populations with mitral valve stenosis may have an underlying antiphospholipid syndrome. As a result, there needs to be a lower threshold for identifying this disease.
Libman-SacksEndocarditis in a Patient With Antiphospholipid Syndrome. Antiphospholipid syndrome is a systemic autoimmune syndrome with cardiac manifestations such as nonbacterial thrombotic endocarditis, also known as Libman-Sacksendocarditis. A 61-year-old female with history of antiphospholipid syndrome presented in acute pulmonary edema. Echocardiography demonstrated mobile vegetations on the free margins of both the anterior and the posterior mitral valve leaflets. Blood cultures and fungal serologies were negative. During mitral valve replacement both the anterior and posterior mitral leaflets were covered with multiple small vegetations with features of nonbacterial thrombotic endocarditis. Though mostly asymptomatic, Libman-Sacksendocarditis may be an indication for valve replacement.
Mitral Valve Perforation in Libman-SacksEndocarditis: A Heart-Wrenching Case of Lupus. Libman-Sacks (LS) endocarditis is one of the most common cardiac manifestations of systemic lupus erythematosus. Rarely, however, it can lead to serious complications, including severe valvular regurgitation or superimposed bacterial endocarditis. We describe the initial diagnostic challenges, clinical course
Aortic valve replacement for Libman-Sacksendocarditis A 24-year-old man with systemic lupus erythematosus and antiphospholipid syndrome complicated by lupus nephritis presented with acute limb ischaemia secondary to an embolus. Following embolectomy, the patient underwent a transthoracic echocardiogram which revealed a large vegetation on all three cusps of the aortic valve. The patient
Diagnosis and surgical treatment for isolated tricuspid libman-sacksendocarditis: a rare case report and literatures review Libman-Sacksendocarditis (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
Libman-Sacksendocarditis and embolic cerebrovascular disease. The aim of this study was to determine whether Libman-Sacksendocarditis is a pathogenic factor for cerebrovascular disease (CVD) in systemic lupus erythematosus (SLE). A cardioembolic pathogenesis of SLE CVD manifested as: 1) neuropsychiatric systemic lupus erythematosus (NPSLE), including stroke and transient ischemic attacks (TIA , microembolism, brain perfusion, neurocognitive dysfunction, and lesion load (all p ≤ 0.04). Finally, patients with vegetations had reduced event-free survival time to stroke/TIA, cognitive disability, or death (p = 0.007). The presence of Libman-Sacksendocarditis in patients with SLE was associated with a higher risk for embolic CVD. This suggests that Libman-Sacksendocarditis may be a source of cerebral
, Ordi-Ros et al suggested that in patients treated with rivaroxaban, the presence of livedo, small vessel, or cardiac valvular disease was associated with an increased risk of recurrent thrombosis. In SLE patients, aPL-positivity is associated with a three-fold increased risk of both heart valve disease (including Libman-Sacksendocarditis) and pulmonary hypertension (including pulmonary arterial