Cardiac valve involvement in systemic lupus erythematosus and primary antiphospholipid syndrome: lack of correlation with antiphospholipid antibodies

Gabrielli, Francesco; Alcini, E; Prima, M. A. Di; Mazzacurati, G; Masala, C

doi:10.1016/0167-5273(95)02357-3

Cited by 65 publications

(57 citation statements)

References 35 publications

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“…Our literature search identified 234 publications, of which 23 unique studies were included in the review 13,21,22,[25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44] ( Figure 1). Studies were identified with the use of Embase (nϭ115), MEDLINE (nϭ97), Cochrane Library (nϭ0), and hand search (nϭ22) from August 1987 to December 2010.…”

Section: Literature Flow Chartmentioning

confidence: 99%

Increased Risk for Heart Valve Disease Associated With Antiphospholipid Antibodies in Patients With Systemic Lupus Erythematosus

Zuily¹,

Régnault²,

Selton-Suty³

et al. 2011

Circulation

157

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Background-Heart valve disease (HVD) is frequent in patients with systemic lupus erythematosus (SLE), and the role of antiphospholipid antibodies (aPL) is controversial. Thus, our objective was to estimate the risk of HVD, including Libman-Sacks endocarditis, associated with aPL in patients with SLE. Methods and Results-Studies were selected if they investigated the association between aPL and HVD in SLE patients and if aPL-negative patients were included for comparison. Data sources were MEDLINE, Embase, Cochrane Library, hand search, contact with investigators, and reference lists of studies, without language restrictions. Data on study and patient characteristics, risk estimates, and study quality were independently extracted by 2 investigators. Pooled effect estimates were obtained by using the DerSimonian-Laird method. Of 234 identified abstracts, 23 primary studies (15 cross-sectional, 7 cohort, 1 case-control) met inclusion criteria, including 1656 SLE patients and 508 cases of HVD. Compared with SLE patients without aPL (nϭ988), the overall pooled odds ratios for HVD and Libman-Sacks endocarditis in aPL-positive patients (nϭ668) were 3.13 (95% confidence interval, 2.31 to 4.24) and 3.51 (95% confidence interval, 1.93 to 6.38), respectively. The risk of HVD depending on aPL subtypes was the highest for lupus anticoagulant at 5.

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Section: Literature Flow Chartmentioning

confidence: 99%

Increased Risk for Heart Valve Disease Associated With Antiphospholipid Antibodies in Patients With Systemic Lupus Erythematosus

Zuily¹,

Régnault²,

Selton-Suty³

et al. 2011

Circulation

157

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“…Some authors have supported this association, [5][6][7][8][9] whereas others did not find any correlation between cardiac abnormalities in SLE patients and the aPL antibodies. [10][11][12][13][14][15] An SLE association with anti-Ro/SS-A and anti-La/SS-B antibodies is well established in neonates, 16 and an association between anti-Ro/SS-A and myocarditis or cardiac conduction defects has been described in adults with SLE. 17 Anti-Ro/SS-A and anti-La/SS-B antibodies have been implicated in the initiation of the autoimmune inflammatory process of congenital heart block; in fact, they were the main autoantibodies detected in infants with congenital heart block and their mothers.…”

Section: Introductionmentioning

confidence: 99%

Cardiac involvement in patients with systemic lupus erythematosus and correlation of valvular lesions with anti-Ro/SS-A and anti-La/SS-B antibody levels

Shahin

Hamid

et al. 2004

Mod Rheumatol

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The aim of this study was to evaluate the incidence of morphologic and functional cardiac abnormalities in patients with systemic lupus erythematosus (SLE) and to correlate the findings with levels of anti-Ro/SS-A, anti-La/SS-B, and anti-cardiolipin antibody (aCL). Sixty-two patients with SLE were enrolled in this study. All patients underwent complete history taking, clinical assessment, and standard two-dimensional and Doppler echocardiography. Anti-Ro/SS-A, anti-La/SS-B, and aCL levels were measured using a standardized ELISA test. The patients were subdivided into two subgroups based on the presence or absence of valvular involvement. The two subgroups were then compared. Valvular involvement was present in 19 patients (30.6%), pericardial effusion in 12 patients (19.4%), impaired left ventricular relaxation abnormalities in 2 patients (3.2%), and pulmonary hypertension in 3 patients (4.8%). More patients in the valvular involvement group had positive anti-Ro/SS-A antibodies than in the valvular noninvolvement group (7/19 vs. 4/43). The difference was significant, with P < 0.01. Serum levels of anti-Ro/SS-A levels were significantly higher in the valvular involvement group (33.7 +/- 36.0 vs. 13.7 +/- 25.1; P < 0.01), as were the serum anti-La/SS-B levels (21.9 +/- 23.5 vs. 10.7 +/- 17.8; P < 0.05). The results suggest a causative correlation between anti-Ro/SS-A and anti-La/SS-B antibodies and the pathogenesis of the valvular lesions in SLE patients.

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“…Of the patients who have cardiac involvement, valves are involved in as many as 40%, with the tricuspid valve much less likely to be involved than the left-sided valves (18,19). The valvular pathology in lupus includes immune deposition, mononuclear infiltration, fibrous plaque, calcinosis and particularly with the IgG antiphospholipid antibody syndrome, thrombi or Libman-Sacks verrucous endocarditis.…”

Section: Lupusmentioning

confidence: 99%

Non-functional tricuspid valve disease

Adler¹

2017

Ann. Cardiothorac. Surg.

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Only 75% of severe tricuspid regurgitation is classified as functional, or related primarily to pulmonary hypertension, right ventricular dysfunction, or a combination of both. Non-functional tricuspid regurgitation occurs when there is damage to the tricuspid leaflets, chordae, papillary muscles, or annulus, independent of right ventricular dysfunction or pulmonary hypertension. The entities that cause non-functional tricuspid regurgitation include rheumatic and myxomatous disease, acquired and genetic connective tissue disorders, endocarditis, sarcoid, pacing, RV biopsy, blunt trauma, radiation, carcinoid, ergot alkaloids, dopamine agonists, fenfluramine, cardiac tumors, atrial fibrillation, and congenital malformations. Over time, severe tricuspid regurgitation that is initially non-functional, can blend into functional tricuspid regurgitation, related to progressive right ventricular dysfunction. Symptoms and signs, including a falling right ventricular ejection fraction, cardiac cirrhosis, ascites, esophageal varices, and anasarca, may occur insidiously and late, but are associated with substantial morbidity and mortality. Attempted valve repair or replacement at late stages carries a high mortality. Crucial to following patients with severe non-functional tricuspid regurgitation is attention to echo quantification of the tricuspid regurgitation and right ventricular function, patient symptoms, and the physical examination. Keynote Lecture Series Review of non-functional tricuspid regurgitationMore than 75% of severe tricuspid regurgitation is classified as functional or related to pulmonary hypertension or right ventricular dysfunction or dilatation, rather than independent abnormalities of the tricuspid valve components: leaflets, annulus, chordal attachments, and papillary muscles. An understanding of non-functional tricuspid regurgitation mandates an appreciation of functional tricuspid regurgitation because the former may ultimately be worsened by some of the same forces that propel the latter (1,2).The anatomy of the tricuspid valve lends itself to functional impairment. Unlike the dense, separate, fibrous structure, with two fibrous trigones, that surrounds the mitral valve, the tricuspid annulus, with only a right fibrous trigone, blends into the right atrial fibro fatty structures and is more susceptible to dilate or not reduce appropriately in size during systole, with either right atrial or right ventricular dilatation. Only two papillary muscles, albeit with an additional posterior commissural chord, supply three leaflets. The chordal attachments to the anterior leaflet arise largely from the anterolateral papillary muscle, not both papillary muscles, and there is a reliance on attachments to the moderator band and free wall. The smallest leaflet, the septal leaflet, is relatively fixed. Right ventricular expansion can readily tether or restrict the anterior leaflet. The posterior leaflet can become restricted via an interesting mechanism: the posteroseptal portion of the valve is more apically ...

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Cardiac valve involvement in systemic lupus erythematosus and primary antiphospholipid syndrome: lack of correlation with antiphospholipid antibodies

Cited by 65 publications

References 35 publications

Increased Risk for Heart Valve Disease Associated With Antiphospholipid Antibodies in Patients With Systemic Lupus Erythematosus

Increased Risk for Heart Valve Disease Associated With Antiphospholipid Antibodies in Patients With Systemic Lupus Erythematosus

Cardiac involvement in patients with systemic lupus erythematosus and correlation of valvular lesions with anti-Ro/SS-A and anti-La/SS-B antibody levels

Non-functional tricuspid valve disease

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