Evolution of cardiac dysfunction in patients with antiphospholipid antibodies and/or antiphospholipid syndrome: A 10-year follow-up study

Kampolis, Christos; Tektonidou, Maria G.; Moyssakis, Ioannis; Tzelepis, George E.; Moutsopoulos, Haralampos Μ.; Vlachoyiannopoulos, Panayiotis G.

doi:10.1016/j.semarthrit.2013.07.016

Cited by 38 publications

(22 citation statements)

References 47 publications

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“…In another study evaluating patients with antiphospholid syndrome (APS), pulmonary hypertension was the most common finding in APS and was associated with thromboembolic disease; in contrary left ventricular disease and cardiac thrombi were rare [10] . Furthermore, in APS and SLE (with or without aPL), SLE/APS and disease duration were independent predictors for valvular disease progression and ventricular diastolic dysfunction in a 10-year follow-up echocardiographic evaluation [11] . In a metaanalysis, the presence of aPL in SLE was associated with high risk for heart valvular disease, including Libman-Sacks endocarditis.…”

Section: Echocardiographymentioning

confidence: 90%

“…Therefore, systematic echocardiography evaluation in SLE with aPL should be always scheduled [12] . Echocardiography has been successfully used in both antiphospholipid syndrome [11,12] and asymptomatic patients with juvenile-onset SLE, who presented evidence of declining ventricular diastolic function with time [13] . Rexhepaj et al [14] found significant differences in early diastolic flow velocity (E), atrial flow velocity (A) and E/A ratios in rheumatoid arthritis (RA) compared with normals, suggesting that a subclinical lesion of left and right ventricular function is present in RA patients, although left ventricular parameters were still normal.…”

Section: Echocardiographymentioning

confidence: 99%

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“How many times must a man look up before he can really see the sky?” Rheumatic cardiovascular disease in the era of multimodality imaging

Mavrogeni

Markousis‐Mavrogenis

Heutemann

et al. 2015

WJM

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Cardiovascular involvement in rheumatic diseases (RD) is the result of various pathophysiologic mechanisms including inflammation, accelerated atherosclerosis, myocardial ischemia, due to micro-or macro-vascular lesions and fibrosis. Noninvasive cardiovascular imaging, including echocardiography, nuclear techniques, cardiovascular computed tomography and cardiovascular magnetic resonance, represents the main diagnostic tool for early, non-invasive diagnosis of heart disease in RD. However, in the era of multimodality imaging and financial crisis there is an imperative need for rational use of imaging techniques in order to obtain the maximum benefit at the lowest possible cost for the health insurance system. The oligo-asymptomatic cardiovascular presentation and the high cardiovascular mortality of RD necessitate a reliable and reproducible diagnostic approach to catch early cardiovascular involvement. Echocardiography remains the routine cornerstone of cardiovascular evaluation. However, a normal echocardiogram can not always exclude cardiac involvement and/or identify heart disease acuity and pathophysiology. Therefore, cardiovascular magnetic resonance is a necessary adjunct complementary to echocardiography, especially in new onset heart failure and when there are conflicting data from clinical, electrocardiographic and echocardiographic evaluation of RD patients.

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Section: Echocardiographymentioning

confidence: 90%

Section: Echocardiographymentioning

confidence: 99%

“How many times must a man look up before he can really see the sky?” Rheumatic cardiovascular disease in the era of multimodality imaging

Mavrogeni

Markousis‐Mavrogenis

Heutemann

et al. 2015

WJM

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“…Valve lesions, especially aortic nodules, are highly associated with the risk of stroke [7]. If routine transthoracic echocardiography is normal, transesophageal echocardiography may be indicated to assess for vegetations due to nonbacterial endocarditis [4,9]. The deposition of immunoglobulins on the valve leaflets underlies the pathophysiology of Libman-Sacks endocarditis [10].…”

mentioning

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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Non-classification Criteria

Gerosa

Rovelli

2014

Antiphospholipid Antibody Syndrome

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Evolution of cardiac dysfunction in patients with antiphospholipid antibodies and/or antiphospholipid syndrome: A 10-year follow-up study

Cited by 38 publications

References 47 publications

“How many times must a man look up before he can really see the sky?” Rheumatic cardiovascular disease in the era of multimodality imaging

“How many times must a man look up before he can really see the sky?” Rheumatic cardiovascular disease in the era of multimodality imaging

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

Non-classification Criteria

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