Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A women who developed mitral stenosis from Libman-Sacks endocarditis is described. The mitral valve was replaced by a Starr-Edwards prosthesis. One year later, despite her being maintained on steroids and azathioprine, the verrucous endocarditis progressed to cause sudden, severe dysfunction of the prosthetic valve.
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PMID:Mitral valve replacement for mitral stenosis caused by Libman-Sacks endocarditis. 46 48

A patient who developed a multisystem involvement of systemic lupus erythematosus (SLE) after 9 years of procainamide therapy, during which time he ingested enormous amounts of the drug, is described. The patient first suffered from recurrent episodes of pleuritis and arthritis, after which he developed a characteristic SLE nephritis associated with a high level of antinative DNA antibodies and a low level of complement. He finally died from a complication of a nonbacterial endocarditis. Autopsy showed polyserositis and typical deposits of electron-dense material on the glomerular basement membrane, and confirmed the clinical diagnosis of Libman-Sacks endocarditis. The possibility that procainamide-induced SLE might have all the clinical, immunological, and pathological features of spontaneous SLE, especially in patients exposed to large doses of the drug for many years, is discussed.
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PMID:Clinicopathological study of a patient with procainamide-induced systemic lupus erythematosus. 94 76

The purpose of this study was to evaluate the spectrum of morphologic and functional cardiac involvement in a selected population of patients with systemic lupus erythematosus (SLE) by means of echocardiography. Thirteen patients (2 male and 11 female) affected by SLE, mean age 41.9 years (range, 21-64), underwent M-Mode, two-dimensional and Doppler echocardiography. Eleven patients had renal disease and 3 of them were undergoing dialysis. One patient had findings of active disease. Six patients had systemic hypertension. None had a history suggestive of rheumatic fever or infective endocarditis. At echocardiographic study nine patients demonstrated findings of valvular involvement. These alterations were defined, according to the echocardiographic features, in two types: vegetation (verrucous Libman-Sacks endocarditis) and thickening. Vegetations were present in 6 patients, involving the mitral valve in all six and the aortic valve in three. The mitral valve vegetations were more frequent on the subannular portion of the posterior leaflet. Seven patients had valvular thickening: involvement of both mitral and aortic valve was present in five, and isolated mitral or aortic valve lesions in the remaining two patients. Combined valvular vegetation and thickening were observed in 4 patients. Eight patients had mild valvular dysfunction on Doppler examination: five isolated mitral regurgitation, two combined mitral and aortic regurgitation and one combined mitral stenosis and regurgitation. In agreement with previous reports, our study shows that valvular involvement in SLE is relatively frequent. Echocardiography can identify additional patterns of valvular lesions different from the known "verrucous Libman-Sacks endocarditis". The degree of valvular dysfunction is not important.
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PMID:[Heart valve involvement in systemic lupus erythematosus: an echocardiographic study]. 129 16

A 38-year-old female was admitted to our hospital because she was suffered from severe dyspnea on effort. She had a history of nasal bleeding, endocarditis, fever, proteinuria, and alopecia at the age of 16, and was diagnosed as SLE. She was suffered from recurrent cerebral infarctions at the age of 35 and 38, and then mitral regurgitation was pointed out. Preoperative examination revealed non-active phase of SLE and UCG showed massive mitral regurgitation. Operative findings showed thrombosed verrucca circumferentially on the mitral valve. Mitral valve replacement (B-S #27) was done with using a felt strip in order to reinforce the mitral annular tissues. Histological findings of the verrucca showed Libman-Sacks endocarditis. Postoperative course was uneventful. Surgical treatment for Libman-Sacks endocarditis is extremely rare.
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PMID:[A case of mitral valve replacement for Libman-Sacks endocarditis]. 156 50

SLE is an inflammatory disease of unknown etiology with the potential of affecting virtually all organ systems. Cardiovascular involvement occurs frequently, although it is often mild enough not to cause clinical concern. Pericarditis is most commonly subclinical, noted only on echocardiogram. Pericardial fluid, which can accumulate rapidly enough to cause tamponade, is inflammatory in nature and can totally mimic infection. The occurrence of Libman-Sacks endocarditis, usually a pathological diagnosis of little clinical significance, has little if any correlation with the presence of audible murmurs. However, valve replacement is occasionally necessary secondary to sterile destruction. These valvular lesions can also embolize or become infected. The incidence of ischemic coronary disease is increased, both secondary to premature atherosclerosis and, rarely, coronary arteritis. Conduction disease and arrhythmias are infrequently reported in adult patients, but congenital CHB has been noted in children born to mothers who have circulating anti-Ro antibody. Evidence is accumulating that suggests there is a mild cardiomyopathy associated with SLE that may be due to thrombotic or inflammatory microvascular coronary disease. Acute clinical myocarditis also rarely occurs. Therapeutically, at present, a reasonable course would seem to be to limit all known possible contributing factors to premature coronary artery and myocardial disease (hypertension, hypercholesterolemia, smoking, steroid therapy, etc), to be vigilant about recognizing the rarer complications associated with SLE (infectious pericarditis and endocarditis, coronary arteritis, pericardial tamponade, clinical myocarditis), and to remember that these uncommon complications are indeed uncommon. The importance of vigorously treating systemic hypertension cannot be overstressed.
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PMID:Cardiovascular involvement in systemic lupus erythematosus. 333 84

We performed echocardiography prospectively 4.9 +/- 0.7 years apart (mean +/- SD), in 74 patients with systemic lupus erythematosus. On the basis of the first study, the patients were distributed in four groups according to the type of valvular involvement: 7 patients had vegetations (Libman-Sacks endocarditis; group 1); 6 patients had rigid and thickened valves with stenosis, regurgitation, or both (group 2); 5 patients had miscellaneous forms of valvular involvement without valvular dysfunction (group 3), as did the 60 controls; and 56 patients had no valvular disease (group 4). The overall prevalence of clinically important valvular disease (groups 1 and 2) was 18 percent. Patients in group 1 were younger than those in group 2 (33.5 +/- 16.7 vs. 47.8 +/- 17.6 years; P less than 0.05), had a shorter mean duration of lupus (4.8 +/- 2.2 vs. 10.7 +/- 6.4 years; P less than 0.001), and had received a smaller cumulative dose of steroids (21.5 +/- 13.1 vs. 79.5 +/- 63.4 g of methylprednisolone or its equivalent; P less than 0.05). During the five-year follow-up, one patient in group 1 and five in group 2 required valve surgery, no patient in group 3 had valvular dysfunction, and five patients in group 4 had mild valvular lesions. We conclude that clinically important valvular involvement in systemic lupus is relatively frequent and sometimes requires surgery. Echocardiography can identify a subset of lesions (valvular thickening and dysfunction), other than verrucous (Libman-Sacks) endocarditis, that are prone to hemodynamic deterioration.
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PMID:Prevalence, morphologic types, and evolution of cardiac valvular disease in systemic lupus erythematosus. 341 13

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.
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PMID:[Double valve replacement in a 30-year-old man with acute systemic lupus erythematosus]. 357 90

This is a report of abnormal endocardial structures on the left ventricular wall as visualized by two-dimensional echocardiography (2-D echo) in patients with systemic lupus erythematosus. Abnormal endocardial structures, arising from the left ventricular endocardium and appearing to proliferate into the cavity, were found in 11 (20%) of 54 patients. The most frequently involved site was posterobasal left ventricular wall in the parasternal long-axis view, and the posterolateral segment of the left ventricle including the anterior and posterior papillary muscles in the parasternal short-axis view. M-mode echocardiograms, simultaneously recorded with 2-D echo, revealed abnormal structures of increased intensity adjacent to the endocardium with thicknesses of 4 approximately 7 mm. Most of the abnormal endocardial structures were observed in patients in the active phase by 2-D echo, and they appeared to regress with steroid therapy. In one autopsy case, fibrous endocardial thickening suggesting healed endocarditis was present in the anterior papillary muscle as observed by 2-D echo. Their location and response to steroid therapy suggests that these abnormal echoes could represent Libman-Sacks endocarditis.
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PMID:[Abnormal left ventricular endocardial structures detected by two-dimensional echocardiography in systemic lupus erythematosus]. 384 91

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.
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PMID:Cardiovascular lesions in collagen-vascular diseases. 391 76

A case of aortic infective endocarditis due to Hemophilus paraphrophilus in a patient with previous Libman-Sacks endocarditis is presented. Suggestions regarding antibiotic prophylaxis are made concerning patients with systemic lupus erythematosus.
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PMID:Clinical considerations regarding infective Libman-Sacks endocarditis. 398 75


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