Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

SLE affects most aspects of cardiac function, and recent studies have reported increasing cardiovascular morbidity and mortality. Pathologically, SLE is characterized by a pancarditis involving pericardium, myocardium, endocardium, and coronary arteries. In autopsy series, pericarditis has been found in 43% to 100% (mean 62%, Table I), and myocarditis was found in 8% to 78% (mean 40%, Table II), but both have been underdiagnosed clinically. Libman-Sacks lesions have been noted in 25% to 100% (mean 43%) and infective endocarditis in 1.1% to 4.9% of clinical and autopsy studies (Table III). Coronary disease may be due to arteritis, which should be treated with high-dose steroids, or it may be due to atherosclerosis, which is amenable to medical or surgical therapy. Valvular disease has been treated surgically, but with a combined surgical mortality as high as 25%. Aortic insufficiency and mitral regurgitation are the most common valvular problems, although aortic and mitral stenosis have also been reported. Hypertension has been noted in 14% to 69%, and heart failure in 5% to 44%. Evidence for a lupus cardiomyopathy, which may be subclinical, is reviewed. While steroids may ameliorate SLE pancarditis, they have also been associated with hypertension, LV hypertrophy, purulent and constrictive pericarditis, mitral regurgitation, and perhaps accelerated atherosclerosis. It remains to be seen if improved diagnosis and treatment of the cardiovascular manifestations of SLE can enhance survival.
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PMID:Cardiovascular manifestations of systemic lupus erythematosus. 390 17

Mitral annulus calcification (MAC), while a relatively frequent autopsy finding in older patients, is rare in childhood. Such calcification has generally been regarded as a degenerative change and of no clinical significance. Recent studies have shown that MAC may be associated with hemodynamically significant lesions including mitral insufficiency, arrhythmias, heart block, and, rarely, mitral stenosis. We have studied a case of massive calcification in the mitral annulus in a 17-year-old girl with juvenile rheumatoid arthritis and systemic lupus erythematosis. In this case, the MAC was considered secondary to the rheumatoid disease. MAC in younger patients with no history of rheumatic fever or bacterial endocarditis suggests an associated connective tissue disorder.
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PMID:Massive calcification of the mitral annulus in a 17-year-old patient with juvenile rheumatoid arthritis and systemic lupus erythematosis. 724 18

The authors had 213 patients under observation with systemic lupus erythematosus. Changes in the heart were revealed in 171 patients, all had affection of the myocardium: myocarditis was found in 66 and myocardial dystrophy in 122. Appraisal of leucocyte migration inhibition with the myocardial antigen (in 23 patients) and detection of antibodies against the myocardium by immunofluorescence (in 33) suggest that disorders in cellular immunity play an important part in the development of lupus myocardial affection. Involvement of the heart in patients with systemic lupus erythematosus was partly associated with renal hypertension, which was conducive, first and foremost, to the development of myocardial hypertrophy and could be attended with increased cardiac ejection and peripheral resistance. A decrease in the cardiac output with a gradual growth in the activity of systemic lupus erythematosus was noted. Steroid myocardial affection was found in 1/4 of patients, which sometimes occurred with cardiac insufficiency and signs of inflammation. Besides mitral valve sclerosis (7%), mitral stenosis was revealed in 3 patients and aortic insufficiency in one. Echocardiography helped to make an early diagnosis of hypertrophy of the heart and pericardial effusion in patients with systemic lupus erythematosus.
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PMID:[Cardiovascular aspects of systemic lupus erythematosus pathology]. 739 79

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

We describe a patient at high surgical risk who was successfully treated with a MitraClip (Abbott Vascular, Menlo Park, CA) without transmitral gradient. She received corticosteroid therapy for systemic lupus erythematosus, and progressive mitral stenosis developed late after MitraClip implantation. It gradually increased and reached 23 mm Hg at 28 months after the procedure; during the same period, her dose of prednisone had to be increased owing to lupus flare. Systemic inflammatory disease has the potential to result in mitral valve inflammation and fibrosis, ultimately causing thickening of the tissue bridge and worsening of the mitral valve obstruction. Preprocedural counseling regarding durability may help in this population.
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PMID:Progressive Mitral Stenosis After MitraClip Implantation in a Patient With Systemic Inflammatory Disease. 2744 66

A 23-year-old African American woman with a past medical history of systemic lupus erythematous (SLE), secondary hypertension, and end stage renal disease (ESRD) on hemodialysis for eight years was stable until she developed symptomatic severe mitral regurgitation with preserved ejection fraction. She underwent a bioprosthetic mitral valve replacement (MVR) at outside hospital. However, within a year of her surgery, she presented to our hospital with NYHA class IV symptoms. She was treated for heart failure but in view of her persistent symptoms and low EF was considered for heart and kidney transplant. This was a challenge in view of her history of lupus. We presumed that her stenosis of bioprosthetic valve was secondary to lupus and renal disease. We hypothesized that her low ejection fraction was secondary to mitral stenosis and potentially reversible. We performed a dobutamine stress echocardiogram, which revealed an improved ejection fraction to more than 50% and confirmed preserved inotropic contractile reserve of her myocardium. Based on this finding, she underwent a metallic mitral valve and tricuspid valve replacement. Following surgery, her symptoms completely resolved. This case highlights the pathophysiology of lupus causing stenosis of prosthetic valves and low ejection cardiomyopathy.
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PMID:Severe Bioprosthetic Mitral Valve Stenosis and Heart Failure in a Young Woman with Systemic Lupus Erythematosus. 2761 Feb 49