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

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

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

The authors present the cases of two young patients, a man and a woman, who presented with myocardial infarction, in the absence of ischemic heart disease or stenosis of the coronary arteries. The woman was known to have systemic lupus erythematosus (SLE) for the past 3 years (the immunoglobulin M [IgM] anticardiolipins antibodies were positive), without a history of coronary risk factors. Suddenly she presented with acute chest pain on rest that lasted 4 hours and culminated in anterior wall myocardial infarction. She was admitted to the coronary care unit, where no thrombolysis was given. She did not have echocardiographic evidence of Libman-Sacks endocarditis, but myocardial infarction was evident at the electrocardiogram (ECG). The young man had SLE (the IgM anticardiolipins were absent, but he was positive for lupus anticoagulant antibodies), he was hyperlipidemic, was a moderate smoker and moderately obese, and had no history of ischemic heart disease. He suddenly presented with an acute myocardial infarction documented by ECG, enzymes, and gammagraphy. In both patients, coronary angiography findings were normal and myocardial biopsy did not show evidence of arteritis. The relevance of these cases is the rare association of ischemic heart disease in SLE, with normal coronary arteries and without evidence of arteritis or verrucous endocarditis.
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PMID:Myocardial infarction in patients with systemic lupus erythematosus with normal findings from coronary arteriography and without coronary vasculitis--case reports. 1008 5

Many patients with systemic lupus erythematosus (SLE) develop cardiac manifestations during the course of their disease. Pericarditis is most commonly seen, with a reported prevalence of 60%. Myocardial involvement is present in only a minority of patients. In recent years, due to better noninvasive diagnostic techniques, valvular abnormalities can be demonstrated in an increasing number of patients. Depending on the technique used, valvulopathy can be demonstrated in up to 77% of SLE patients. Although most of the valvular lesions will be present without any symptoms, valve incompetence can result in congestive heart failure. Valvular lesions are associated with IgG anticardiolipin antibodies (aCL) and disease duration. We present a patient with SLE and secondary antiphospholipid syndrome (APS) who developed acute congestive heart failure due to pancarditis. Endocarditis, together with left ventricular dysfunction and pericardial effusion, were present. The endocarditis caused hemodynamically significant mitral valve insufficiency due to thickening of the mitral cusps. Just two weeks prior to the occurrence of congestive heart failure echocardiography had been normal. Treatment with high dose corticosteroids resulted in a gradual, almost complete recovery. Literature concerning cardiac manifestations in lupus is reviewed.
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PMID:Cardiac abnormalities in SLE: pancarditis. 1086 93

Out of 242 patients treated for systemic lupus erythematosus (SLE) in Novosibirsk for 15 years, valvular lesions and endocarditis were diagnosed in 41(16.9%) patients. Combination of Libman-Sax endocarditis (LSE) with infectious endocarditis (IE) was observed in three patients (two women, one man, age 18-40 year). SLE ran a subacute course in one woman, an acute one--in the other. LSE emerged early in SLE in two patients. All the patients had polyorganic lupus pathology, lupus nephritis with nephrotic syndrome (morphological class IV). Two patients had mitral valve disease, one patient--mitral-aortic disease. The rise of secondary IE was seen after massive immunosuppressive therapy. The diagnosis of secondary IE was made after SLE duration for 10-36 months. At IE diagnosis, all the patients had high titers of blood antiphospholipid antibodies. IE was of staphylococcal origin in two patients and candidosis-induced in one patient. In SLE with IE there was thromboembolic syndrome. LSE and IE have related aspects which should be regarded in clinical practice: possible "IE mask" in LSE, risk of secondary IE in about 10% of LSE patients, prophylactic measures necessary to prevent IE in hemodynamically prominent forms of LSE.
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PMID:[Combination of Libman-Sacks endocarditis with infectious endocarditis]. 1198 Jan 54

Over the last 10 years we have seen 31 children with systemic lupus: 10 (32%) of these have died. The commonest primary determinant of mortality was uncontrolled disease activity (60%), possibly contributed to by late referrals leading to delays in diagnosis and the institution of therapy. Thromboembolic disease was responsible for two deaths and tuberculosis for one. The major contributory factors were nephritis in two patients and myocarditis, endocarditis, lupus pneumonia and CNS disease in one patient each. Concomitant infections, predominantly nosocomial, occurred in a significant proportion of patients (40%) but were only cofactors in mortality. Autopsies were done in three cases. These patterns of death are significantly different from those seen in the developed world, where disease activity has ceased to be an important factor owing to early recognition of cases. Avoiding late referrals and delays in diagnosis can reduce mortality in childhood-onset lupus.
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PMID:Mortality patterns in childhood lupus--10 years' experience in a developing country. 1244 28


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