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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four cases of endocarditis due to Kingella kingae are described in compromised patients. All had primary heart disease, and two had systemic lupus erythematosis and congenital heart defect respectively, in addition. Confirmation of Kingella kingae was made in one case at autopsy. The literature on 11 cases of endocarditis, 2 bacteremia, 4 osteomyelitis, 5 septic arthritis and 1 intervertebral disc infection, all caused by Kingella kingae, is reviewed. Our findings confirm that the organism is of low pathogenicity. Children may be predisposed to infection with Kingella kingae.
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PMID:Endocarditis due to Kingella kingae. 646 70

To evaluate the diagnostic help afforded by immune determinations in feverish valvular patients, we prospectively determined: total hemolytic complement, cryoglobulin, rheumatoid factor, circulating immune complexes and direct skin immunofluorescence. Twenty patients entered the study, twelve with bacterial endocarditis, six without any bacteremia and two septicemic patients without endocarditis. We detected at least one immune abnormality in 10/12 endocarditis patients: - in 7/11 (64 p. cent) circulating immune complexes; - in 3/12 rheumatoid factor; - in 3/12 positive fluorescence in dermal vessels (IgM-C3); - and in one patient an IgG lupus-like band in the membrane basal zone. We also found circulating immune complexes in 3/4 patients without bacteremia and in 1/2 septicemic patients. We conclude that, in our small prospective study, immune abnormalities are frequent in bacterial endocarditis patients but their diagnostic values is rather limited : their absence do not rule out endocarditis and they can be present in many other febrile disorders.
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PMID:[Bacterial endocarditis : lack of diagnostic value of immunological investigations (author's transl)]. 708 72

A retrospective study of 112 cases of lupus erythematosus, 103 acute disseminated lupus erythematosus (ADLE) and 9 chronic discoid lupus (CDL), was conducted to determine the incidence of disorders of conduction (DC), and to study their prognosis and discuss their pathogenicity. The mean age of the group was 38 +/- 16 years, and the mean follow-up period after discovery of the DC was 53 months. Cardiac lesions were present in 49.5 p. cent of the 103 patients with ADLE : pericarditis in 27 p. cent, murmur from lupus endocarditis or cardiomyopathy in 23 p. cent, heart failure in 4.8 p. cent, and hypertension in 17 p. cent. Disorders of conduction were present in 18 (17.5 p. cent) of the 112 patients studied. These included 5 partial right bundle-branch blocks (no complete right bundle-branch block), 2 complete and 3 partial left bundle-branch blocks, 5 complete, 2 first degree, and 1 second degree atrioventricular blocks (AVB). The atrioventricular blocks were usually located in the truncal or fascicular regions, but in 2 cases they were nodal in origin. The 5 complete AVB were associated with ADLE in two cases and CDL in the three other cases. The AVB in the ADLE cases appeared 9 to 20 years after the onset of the lupus, these two patients developing pericardiomyocarditis unaccompanied by disorders of conduction. The three complete AVB occurring during CDL were detected 9 to 18 months after the diagnosis. A fatal outcome was noted in 13 (12.5 p. cent) of the ADLE patients and one of the 9 cases of CDL. Ten-year survival curves showed no difference in prognosis for the groups with or without disorders of conduction, but mortality increased in patients with DC after 10 years. As disorders of conduction were more frequently observed in patients with lupus than in a control population, they can be attributed to either a lupus myocarditis or prolonged administration of synthetic antimalarial agents. Disorders of conduction, and particularly complete AVB are, in fact, observed in patients without pericardiomyocardial lesions, and when they exist usually develop a long time after the onset of the cardiac lesion. All patients had been treated with antimalarials, however, and the onset of the DC was associated with a chloroquine myopathy in some of them. Three of the five complete AVB were observed during the course of CDL in patients without cardiac lesions, this being a supplementary argument for implicating synthetic antimalarials.
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PMID:[Disorders of conduction in lupus erythematosus : frequency and incidence in a group of 112 patients (author's transl)]. 730 72

This case involves a 41-year-old woman with SLE. The patient began having symptoms of arthralgia in 1978 and developed fever, pleuritis and lupus psychosis in 1986. Laboratory exams showed positive antinuclear-antibody, LE-cell phenomenon, hypocomplementemia and lupus anticoagulant. Echo cardiography demonstrated mitral regurgitation and stenosis. She was treated with 50 mg of prednisolone and these manifestations subsided. In 1989, she developed dyspnea on exertion and echo cardiography revealed severe mitral stenosis. Pulmonary infarction was detected by MAA lung scintigraphy. At this time, she was diagnosed as SLE associated with antiphospholipid syndrome (APS). A mitral valvular replacement operation was performed in 1991. Pathological studies of mitral valve demonstrated Libman Sacks endocarditis. APS is known occasionally to complicate with left-sided valvular diseases, mitral stenosis is quite rare in both SLE and APS. This patient reveals a rare case of SLE associated with APS and mitral stenosis. It is suggested that this patient developed mitral stenosis with Libman Sacks endocarditis, associated with the presence of antibody against phospholipids.
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PMID:[A case of SLE associated with antiphospholipid syndrome and mitral stenosis]. 755 44

To assess the cardiological status of patients with long-term lupus nephritis we evaluated 30 patients (mean age 43 +/- 11 years) with lupus nephritis lasting from at least 10 years (mean 15 +/- 5 years). At the time of cardiological evaluation the mean plasma creatinine was 132.6 +/- 11.1 mumol/l and in 28 patients lupus had been quiescent for at least 3 years. Fourteen patients (46.6%) showed one or more cardiac abnormalities: 10 had valvular lesions (1 verrucous endocarditis, 9 thickening and stiffness of one or more valves)--4 patients had regional myocardial akinesis as a consequence of a previous cardiac infarct (one had valvular abnormalities too). One patient had pulmonary hypertension probably secondary to pulmonary vasculitis. No patient had pericarditis. These cardiac abnormalities proved to be statistically correlated with the number of ARA criteria (p = 0.045), the number of lupus flares (p = 0.004), the serum levels of cholesterol (p = 0.04) and of triglycerides (p = 0.025) as well as the duration of hypercholesterolemia (p = 0.005) and of hypertriglyceridemia (p = 0.007). In conclusion, in patients with long-term lupus nephritis cardiac lesions are frequent. The main lesions are non-verrucous valvulopathy (probably a consequence of healing verrucous endocarditis) and cardiac infarct (caused by an accelerated atherosclerosis). On the contrary cardiac lesions caused by active lupus as pericarditis, myocarditis and verrucous endocarditis are rare.
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PMID:Cardiologic abnormalities in patients with long-term lupus nephritis. 769 32

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant aortic valves. Part I discusses stenotic aortic valves and Part II will discuss causes of purely regurgitant aortic valves. In over 95% of stenotic aortic valves, the etiology is one of three types: congenital (primarily bicuspid), degenerative, or rheumatic. Other rare causes of stenotic aortic valves include active infective endocarditis, homozygous type II hyperlipoproteinemia, and systemic lupus erythematosis. The causes of pure aortic regurgitation are multiple but can be separated into diseases affecting the valve (normal aorta) (infective endocarditis, congenital bicuspid, rheumatic, floppy), diseases affecting the walls of aorta (normal valve) (syphilis, Marfan's, dissection), disease affecting both aorta and valve (abnormal aorta, abnormal valve) (ankylosing spondylitis), and diseases affecting neither aorta nor valve (normal aorta, normal valve) (ventricular septal defect, systemic hypertension). Diseases affecting the aortic valve alone are the most common subgroup of conditions producing pure aortic valve regurgitation.
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PMID:Pathology of aortic valve stenosis and pure aortic regurgitation. A clinical morphologic assessment--Part I. 816 31

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant aortic valves. Part I discussed stenotic aortic valves and Part II discusses causes of purely regurgitant aortic valves. In over 95% of stenotic aortic valves, the etiology is one of three types: congenital (primarily bicuspid), degenerative, and rheumatic. Other rare causes included active infective endocarditis, homozygous type II hyperlipoproteinemia, and systemic lupus erythematosis. The causes of pure aortic regurgitation are multiple but can be separated into diseases affecting the valve (normal aorta) (infective endocarditis, congenital bicuspid, rheumatic, floppy), diseases affecting the walls of aorta (normal valve) (syphilis, Marfan's dissection), disease affecting both aorta and valve (abnormal aorta, abnormal valve) (ankylosing spondylitis), and disease affecting neither aorta nor valve (normal aorta, normal valve) (ventricular septal defect, systemic hypertension). Diseases affecting the aortic valve alone are the most common subgroup of conditions producing purely regurgitant aortic valves.
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PMID:Pathology of aortic valve stenosis and pure aortic regurgitation: a clinical morphologic assessment--Part II. 816 82

A case of systemic lupus erythematosus (SLE) associated with fever, heart failure, and left ventricular (LV) aneurysm is reported. A diagnosis of SLE was suspected owing to the presence of active lymphocytic myocarditis and fibrinous endocarditis at LV endomyocardial biopsy and was confirmed by identification of 4 of the 11 criteria proposed by the American Rheumatism Association for the definition of SLE. A 2-month period of steroid therapy was followed by a remarkable recovery of LV function and progression of endomyocarditis to a healed phase at control LV biopsy. The LV aneurysm disappeared, likely because thrombosis occurred as a result of the hypercoagulable state accompanying the presence of anticardiolipin antibodies. This is the first reported case of LV aneurysm induced by SLE and is a rare clinicohistologic documentation of the effectiveness of steroid treatment on lupus endomyocarditis.
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PMID:Acute myocarditis and left ventricular aneurysm as presentations of systemic lupus erythematosus. 854 1

We report a case of neonatal lupus erythematosus (NLE) with congenital heart block and severe myocardial failure, which was followed from the 25th week of gestation because of fetal bradycardia. The child was delivered at the 37th week of gestation by elective cesarean section because of echocardiographically documented heart enlargement, pericardial effusion and moderate insufficiency of the mitral and tricuspid valves. In spite of immediate pacing, intubation and supportive treatment, the newborn developed progressive heart failure. Echocardiography showed endocarditis of the mitral valve and diffuse myocarditis. The heart failure resolved under steroid treatment. Our experience supports the early use of steroids in treating myocarditis due to NLE. Intrauterine steroid treatment in the presence of fetal hydrops and congenital heart block is discussed.
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PMID:Neonatal lupus erythematosus with congenital heart block and severe heart failure due to myocarditis and endocardititis of the mitral valve. 879 3

Early diagnosis and greatly improved treatment have markedly altered the clinical evolution of systemic lupus erythematosus; the pattern of cardiac involvement in lupus has also changed. To illustrate this, a young woman who died from severe mitral valve disease, including a coronary embolus from verrucous endocarditis, is presented. Mitral valve involvement in lupus is no longer limited to the small benign lesions described by Libman and Sacks.
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PMID:Lupus-related mitral valve disease: embolic coronary occlusion as a unique cause of myocardial infarction. 934 38


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