[Bacterial endocarditis and Libman-Sacks syndrome].
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Adolescent↗
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Results for “LIBMAN-SACKS DISEASE”
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Cardiovascular lesions in collagen-vascular diseases.
In this review, the cardiac lesions which develop in association with the various collagen-vascular diseases are described. In rheumatoid arthritis, the most frequent lesions are: fibrous obliterative pericarditis, with pericardial deposits of calcium, fibrin, cholesterol, and rheumatoid granulomas; granulomatous or nonspecific myocarditis; valvulitis, vasculitis, and amyloid deposits. In ankylosing spondylitis, the lesions involve mainly the valves (aortic and mitral valves) and the aorta. In systemic lupus erythematosus, the predominant cardiovascular lesions are: pericarditis, Libman-Sacks endocarditis, nonspecific myocarditis, vasculitis with fibrinoid necrosis, and acceleration of atherosclerosis. In scleroderma, the main cardiac lesion is fibrosis with only scanty inflammatory cells; pericarditis and nonbacterial thrombotic endocarditis also occur. In dermatomyositis/polymyositis, fibrous or fibrinous pericarditis can occur, as well as myocarditis with infiltrates of lymphocytes and plasma cells and with degeneration and necrosis of myocytes; valvulitis is uncommon except when the disease is related to mucinous adenocarcinoma. In polyarteritis nodosa, various stages of necrotizing vasculitis involve all layers of the arterial walls; foci of myocardial necrosis of various sizes can occur in association with these lesions; cardiac hypertrophy related to hypertension and pericarditis related to uremia, may also be found. In Wegener's granulomatosis, pericarditis, inflammatory infiltrates, necrotizing granulomas, and vasculitis have been observed in the heart.
Animals↗
Heart disease in systemic lupus erythematosus: diagnosis and management.
Most patients suffering from systemic lupus erythematosus develop secondary heart disease at some time during the course of the primary illness. The most common forms of this type of heart disease are acute fibrinous pericarditis and hypertension. By means of echocardiography, an increased incidence of pericardial effusion has been demonstrated. Although commonly noted at autopsy, myocarditis is often clinically silent. However, endomyocardial biopsy may confirm its presence during life. Libman-Sacks endocarditis, although encountered in 40 to 50% of hearts at autopsy, is rarely diagnosed during life. When significant valve dysfunction such as aortic insufficiency or mitral regurgitation develops during the course of systemic lupus erythematosus, then Libman-Sacks endocarditis should be strongly suspected. Cardiac arrhythmias, first degree AV block, and acquired complete heart block may develop either de novo or in association with lupus pericarditis, myocarditis, vasculitis, etc. Complete congenital heart block has been reported in newborns of mothers with systemic lupus erythematosus, particularly those who have an antibody to a soluble tissue ribonucleoprotein antigen called RO(SS-A). Coronary arteritis and premature coronary atherosclerosis manifesting in either angina pectoris or myocardial infarction in young adults, particularly women suffering from systemic lupus erythematosus, have received attention recently. The development of hypertension and hyperlipidemia while such patients are receiving prolonged corticosteroid therapy has been incriminated as the significant risk factor in premature coronary atherosclerosis. Longstanding hypertension and congestive heart failure have unfavorable prognoses. This report is based on a cumulative review of 50 patients with acute and chronic systemic lupus erythematosus seen at our institution and in private practice during the last 10 years.
Journal Article↗
[Cardiac involvement in systemic autoimmune disease].
Systemic autoimmune diseases form a diverse group which includes: systemic lupus erythematosus (SLE), mixed connective tissue disease (MCTD), scleroderma, dermato-polymyositis, Wegener's granulomatosis, Sjögren syndrome. Although multisystem involvement is the hallmark of these diseases, the heart seems to be less affected than other organ systems. The aim of the study was to study possible cardiac abnormalities in patients with documented systemic autoimmune diseases and to assess whether there was any relation between antiphospholipid, anti-dsDNA antibodies and myocardial dysfunction findings. 76 patients (53 with SLE, 9 with MCTD, 8 with scleroderma, 6 with Wegener's granulomatosis) were subjected to our study, 69% of these patients manifested cardiac involvement, based on two-dimentional echocardiografic examination (36%--post-inflammatory valvular thickening, 20%--pericardial effusions, 15%--valvular regurgitation, 7%--left atrial enlargement, 5%--left ventricular hypertrophy, 4%--left ventricular dysfunction). None of the patients showed characteristic, acute Libman-Sacks endocarditis, which probably can be explained by chronic corticosteroid-treatment. Clinical evidence of cardiac abnormalities has been observed, in as many as 58% of cases with positive echocardiographic findings. The frequency and extend of cardiac pathology positively correlated with the detection of antiphospholipid antibodies. No such relationship was observed in patients with the presence of very high titers of antinuclear antibodies (anti-dsDNA). In conclusion, our results indicate that echocardiography is a useful method for assessment and monitoring cardiac involvement in the systemic autoimmune diseases.
Adolescent↗
Antiphospholipid syndrome in systemic connective tissue diseases.
Clinical manifestation and immunoserological features of secondary antiphospholipid syndrome (SAPS) were analyzed in this paper in 107 patients with systemic connective tissue diseases. In the group of patients with confirmed systemic lupus erythematosus (SLE), antiphospholipid antibodies (aPL) were positive in 43/93 (46.23%), while in 50/93 (53.76%) they were negative. Among aPL positive patients, 33/43 (76.74%) had clinical manifestations of SAPS, while 10 patients (23.26%) were without any clinical manifestations. The most frequent manifestations of SAPS associated with SLE were: arteriovenous thrombosis in 20/43 (46.51%), thrombocitopenia in 15/43 (34.88%) and autoimmune hemolytic anemia in 7/43 (16.27%). In our patients, rare manifestations of SAPS associated with SLE were recurrent fetal loss (1 case), livedo reticularis (1 case), transversal myelitis (2 cases), neuropathy (2 cases) and aseptic endocarditis (Libman-Sacks) (5 cases). Among 7 patients, with Sjögren's syndrome, clinically manifested SAPS was observed in 2, while in other 5 only increased aPL levels were found, as well as in patients with systemic vasculitis-3, MCTD-2 and Sy. Sjögren with vasculitis-1. One RA patient had thrombosis of v. cava inferior. In majority of patients with clinically present SAPS the levels of both examined immunoglobulin isotypes (IgG + IgM) were decreased-21/40 or 52.5%, while isolated increase of IgG was found in 14 (35%) and isolated increase of IgM in 5 (19.22%) patients. In three out of five patients with Libman-Sacks only LA test was positive. This investigation have shown that arterial and venous thromboses are the most common manifestations of SAPS in SLE. Every blood vessel may be involved (from arteriolae to the aorta and from postcapilar venules to the v. cava).
Antibodies, Antiphospholipid↗
Pancreatitis related to antiphospholipid antibody syndrome in a patient with systemic lupus erythematosus.
A 39-year-old woman was admitted with abdominal pain and dyspnea, and a diagnosis of systemic lupus erythematosus with renal involvement was established. Laboratory tests revealed highly elevated anticardiolipin antibody, thrombocytopenia and false positive VDRL. Generalized thrombus formation and Libman-Sacks endocarditis were found at postmortem examination. The pancreas showed chronic inflammation with thrombi in pancreatic arteries, but no vasculitic change was observed. Lowering of pancreatic blood flow because of arterial thrombi was a possible cause of pancreatitis in this patient. The spectrum of antiphospholipid antibody associated diseases may be extended to include pancreatitis as a thrombotic complication.
Adult↗
Immunopathology of cardiac lesions in fatal systemic lupus erythematosus.
Immunopathologic studies were performed on cardiac tissue obtained at autopsy in 10 patients with severe systemic lupus erythematosus (SLE). The immunopathologic findings were correlated with histopathologic and clinical evidence of cardiac injury, and with clinical and serologic features of SLE. Immune reactants were demonstrated by direct immunofluorescence in nine patients in a granular deposition pattern suggesting immune complex aggregates. Histologic and gross anatomic findings of inflammation were generally more focal than was the distribution of immune reactants. Most of the immune deposits were present in the walls of the blood vessels of myocardium (eight of 10) or pericardium (two of three). In one patient with Libman-Sacks endocarditis, immunoglobulin and complement components were present in the valve stroma and the vegetations. The immune deposits around epicardial nerve fibers in two patients with severe neurologic manifestations contained immunoglobulin E(IgE). In general, the most intense and widespread immune deposits were observed in patients with persistently increased serologic and clinical evidence of activity of their systemic disease. These results suggest a role for immune complex deposition in the pathogenesis of the cardiac lesions of SLE.
Adolescent↗
[Double valve replacement in a 30-year-old man with acute systemic lupus erythematosus].
A 30 year old man presenting with a 10 year history of delayed pressure urticaria had a secondary lupus-induced double mitral and aortic regurgitation which necessitated double valve replacement within 2 years. The anatomical appearances of the valvular lesions were very unusual and suggest a new anatomo-clinical form of the classical Libman-Sacks endocarditis. In addition to infective endocarditis, systemic lupus erythematosus may also lead to valvular lesions necessitating valve replacement. The association of S.L.E. and delayed urticaria is rare, and also merits publication.
Acute Disease↗
Aortic insufficiency and mitral regurgitation in patients with systemic lupus erythematosus and the antiphospholipid syndrome.
PURPOSE, PATIENTS, AND METHODS: Heart disease has not been well characterized in patients with systemic lupus erythematosus (SLE) and the antiphospholipid syndrome. During a prospective study of cerebrovascular disease in autoimmune disease and SLE, 11 lupus patients were identified with an antiphospholipid syndrome characterized by significant cardiac valvular disease in addition to cerebral infarction, deep vein thromboses, and thrombocytopenia. Patients were reviewed for criteria for systemic lupus and underwent echocardiographic studies and measurements of anticardiolipin antibodies, VDRL, and the lupus anticoagulant. RESULTS: Eight of the 11 patients had aortic insufficiency, two of whom had associated mitral regurgitation. Three patients had mitral regurgitation alone. Microscopic analysis of a surgically excised aortic valve indicated typical Libman-Sacks verrucous endocarditis. Infective endocarditis was ruled out in all patients. CONCLUSION: This report expands previous descriptions of antiphospholipid syndromes by describing a subset of lupus patients with significant aortic and mitral valvulitis in addition to circulating antiphospholipid antibodies, thrombocytopenia, and recurrent thromboses.
Adult↗
Aortic stenosis associated with systemic lupus erythematosus.
Hemodynamically significant valvular lesions have been rarely reported sequelae of Libman-Sacks endocarditis complicating systemic lupus erythematosus (SLE). Furthermore, embolic phenomena associated with these vegetations have not been clearly documented. We present a report of critical aortic stenosis associated with SLE in a patient who had received corticosteroid treatment for several years. An embolus, histologically identical with the aortic valve vegetation, was found in the left anterior descending artery at necropsy. There was no evidence of rheumatic heart disease, bacterial endocarditis or a bicuspid aortic valve. Recent reports suggest an increased incidence of significant valvular dysfunction in patients with SLE who have received long-term corticosteroid treatment.
Adult↗
Bioprosthetic valve excision without replacement in the tricuspid position in a patient with Libman-Sacks endocarditis.
A 19 year old girl with Systemic Lupus Erythematosus (SLE), in chronic renal failure and on haemodialysis, underwent tricuspid valve replacement with a Carpentier-Edwards xenograft because of a large calcified mass invading the right side of the heart. The mass caused no symptoms and had been discovered accidentally on a routine chest X-ray. The bioprosthetic valve had subsequently to be removed, having developed functional stenosis, and was not replaced. Despite the absence of a tricuspid valve, the patient remains well five years after the operation.
Adult↗
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.
Antiphospholipid Syndrome↗
Echocardiographic diagnosis of bland thrombus on an aortic valve.
Echocardiography is a valuable modality for imaging thrombi and vegetations. Although patients with systemic lupus erythematosus may develop Libman-Sacks endocarditis, in which punctate verrucous plaques are found histologically on valvular endocardial tissue, these lesions are ordinarily too small for ultrasonic imaging. We describe a patient with systemic lupus erythematosus complicated by systemic embolization, who had a large mobile aortic valve thrombus, which was discovered with the aid of echocardiography and was confirmed by surgical resection.
Adult↗
Mitral valve prolapse in systemic lupus erythematosus.
Despite a low incidence of clinical manifestations, autopsy data suggest endocardial and myocardial disease in about 50% of patients with systemic lupus erythematosus. To investigate whether mitral valve prolapse can be considered a clinical manifestation of cardiac involvement in systemic lupus erythematosus, we carried out an echocardiographic study in 51 affected subjects and 102 normals matched for age and sex. Prevalence of mitral valve prolapse was 25% in patients with systemic lupus erythematosus and 9% in healthy controls with a statistically significant difference (p less than 0.01). Neither pericardial effusion nor prolonged (more than 12 months) treatment with corticosteroids were associated with higher prevalence of mitral valve prolapse. Libman-Sacks verrucae on the mitral valve apparatus as well as focal myocardial scars affecting the papillary muscles and adjacent myocardium could be responsible for the development of the valvular dysfunction. We suggest that mitral valve prolapse can be considered a manifestation of cardiac involvement in patients with systemic lupus erythematosus.
Adolescent↗
Cardiac valve replacement in systemic lupus erythematosus. A review.
Three cases of cardiac valve replacement for Libman-Sacks endocarditis and their long-term follow-up are described. From the review of the literature, an additional nine patients who required cardiac valve replacement are studied. Steroids probably increase the incidence of valve incompetence, but most patients presumably die of other associated organ involvement before undergoing a cardiac operation. Operation is indicated because of change in the intensity or character of the murmur, and a new murmur with resultant, resistant congestive cardiac failure. Both the aortic and mitral valves should be explored. Valve reconstruction in these young patients, with the expectation of avoiding prosthetic valve dysfunction and repeat operation, is not possible. Bioprosthetic valve replacement may be preferable, since it eliminates the need for anticoagulation during steroid treatment. Overall mortality was 25%.
Adolescent↗
[Extensive fibrous endocarditis as first manifestation of systemic lupus erythematosus].
BACKGROUND: Cardiac abnormalities, such as myocarditis, pericarditis or verrucous endocarditis (Libman-Sacks endocarditis) occur in about one third of patients with systemic lupus erythematosus. This study describes an unusual aspect of endocardial involvement. CASE REPORTS: Case no. 1: A 14 year-old girl was admitted 3 months after acute hemichorea because of heart failure plus biological inflammatory findings. Echocardiography showed mitral insufficiency with enlargement of the left atrium and ventricle. There was some infiltration involving the endocardium of the left ventricle, the chordae tendinae and the mitral valve. The titres of anti-DNA and anti-nuclear antibodies were elevated while the serum hemolytic complement was depressed. Skin biopsy showed IgG, IgM and C1q deposits along the dermoepidermal junction. Corticosteroids, diuretics and vasodilator drugs failed to completely cure the heart failure; the mitral insufficiency required mitral valve replacement 21 months later. Pathological examination showed extended fibrotic changes of the endocardium. Case no. 2: A 4 year-old boy was admitted for acute heart failure due to mitral insufficiency, associated with biological inflammatory findings. Echocardiography showed mitral insufficiency and enlarged left atrium and ventricle. Anti-DNA and anti-nuclear antibody titres were elevated. The patient was given antibiotics followed by corticosteroids and immunosuppressive drugs. The persistence of the mitral insufficiency required mitral valve replacement 7 months later. Pathological examination showed fibrotic changes of the endocardium. Exacerbation of the inflammatory process was seen 2 months after surgery, with development of diffuse proliferative lupus nephritis. The patient died of kidney failure and neurological complications, 44 months after cardiac surgery. CONCLUSION: In both patients, the systemic lupus erythematosus was revealed by endocardial involvement, a complication that is usually seen later. The endocardium changes responsible for mitral insufficiency and requiring valve replacement in these two cases were different from those described as verrucous endocarditis in classical forms of the disease.
Adolescent↗
Prevalence of infective endocarditis in patients with systemic lupus erythematosus.
BACKGROUND: Compared with the general population, patients with systemic lupus erythematosus, or SLE, have an increased prevalence of functionally impaired cardiac valves due to the presence of Libman-Sacks lesions. These lesions may place patients with SLE at risk of developing infective endocarditis, or IE. METHODS: The authors performed a retrospective chart review to determine the association between SLE with valvulopathy and IE. They reviewed the records of 361 patients from two health care facilities who had the diagnostic code of SLE. RESULTS: Of the 275 records that met the 1982 revised American Rheumatism Association criteria for SLE, 51 (18.5 percent) were for patients who had a clinically detectable heart murmur that resulted in echocardiography being performed. Nine (3.3 percent) of the 275 patients had a clinically significant valvular abnormality, three (1.1 percent) had a potentially significant valvular abnormality, and one (0.4 percent) had a history of IE that was diagnosed two years before her diagnosis of SLE was made. CONCLUSIONS: The findings suggest that 18.5 percent of this cohort of patients with SLE had a clinically detectable heart murmur that would require further investigation to determine its significance. Furthermore, between 3.3 and 4.4 percent of the study population had cardiac valve abnormalities that potentially required antibiotic prophylaxis before certain dental procedures. However, the authors identified no cases that demonstrated an association between IE and diagnosed SLE. CLINICAL IMPLICATIONS: Dentists should query their patients with SLE about their cardiac status and consult with the patient's physician if the cardiac status is unknown. Patients with confirmed valvular abnormalities should receive antibiotic prophylaxis for designated bacteremia-producing dental procedures.
Adolescent↗
Cardiovascular manifestations of systemic lupus erythematosus: current perspective.
Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
Adrenal Cortex Hormones↗