Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 review of 51 patients who died while enrolled in a long-term prospective study of systemic lupus erythematosus (SLE) revealed that active SLE may persist or reappear late in the course of the disease. Vascular events, especially atherosclerotic coronary artery disease, occurred frequently. Moderate to severe atherosclerosis was seen in patients who had died of any cause after a prolonged duration of the disease and often contributed significantly to death. Diffuse proliferative glomerulonephritis, CNS lupus and major infections were indications of poor prognosis particularly early in its course.
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PMID:Mortality in systemic lupus erythematosus: the bimodal pattern revisited. 401 45

One hundred consecutive female patients with active systemic lupus erythematosus (SLE) were studied from the cardiovascular point of view by means of non invasive methods. Seventy percent of the cases presented some type of cardiovascular anomaly. Seventy four percent of the resting electrocardiograms were abnormal as well as 72% of the M mode echocardiograms and 55% of the cardiac X ray series. The most frequent observed complications were: pericarditis and or pericardial effusion (39%), arterial hypertension (22%), ischemic heart disease (16%), myocarditis (14%), congestive heart failure (10%), pulmonary hypertension (9%), valvular heart disease (9%), pleural effusion (7%) and cerebro vascular accident (3%). We analyzed each one of these complications and found of special interest the high incidence of ischemic heart disease which is more frequent than has been hitherto reported. Ischemic heart disease was observed in two types of patients: a) Those with long term steroid therapy. In these, the mechanism seems to be an atherosclerotic disease probably induced by the chronic use of steroids. The management of these cases do not differ from other types of coronary heart disease due to atherosclerosis. b) Those with frank episodes of vasculitis in whom the basic mechanism is an inflammatory process of the coronary arteries and its treatment is fundamentally that of the vasculitis. We consider necessary to study routinely all patients with SLE through non invasive cardiological methods.
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PMID:Cardiovascular manifestations in systemic lupus erythematosus. Prospective study of 100 patients. 402 48

Neuropathologic examination of an autopsy series of 54 patients of various types of CVD revealed a very high frequency of pathologic changes both in brain parenchyma (in 81%) and vessels (in 78%). A broad but continuous spectrum of primary vascular alterations was observed, ranging from fibrinoid deposits in intact or necrotizing vessel walls to fibrohyalinosis and endothelial proliferations. In acute SLE showing LE cells within brain tissues, immune complex deposits were observed for the first time in brain vessels, in addition to similar deposits in the plexus chorioideus and in hematoxylin bodies. Secondary complications are frequently affecting the brain in CVD; they are mainly sequels of systemic atherosclerosis, hypertension, thromboemboli from SLE endocarditis, cardiac, hepatic or renal dysfunctions, or infections and should be clinically differentiated from primary brain involvement in CVD to ensure the appropriate therapeutic measures.
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PMID:Brain pathology in the collagen vascular diseases. 611 36

Four patients with chronic systemic lupus erythematosus (SLE) in whom myocardial infarction occurred at an unusually early age are described. The evidence suggests that the coronary occlusion was due to atherosclerosis. There was no evidence that active arteritis played any role. The only risk factor for atherosclerotic disease was hypertension. All patients had had both central nervous system and renal disease and had been taking corticosteroids for a minimum of 9 years. It is suggested that hypertension aggravated by chronic corticosteroid administration may be an important risk factor for atherosclerosis in patients with SLE.
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PMID:Myocardial infarction in four young patients with SLE. 688 70

A fatal case of systemic lupus erythaematosus complicated by myocardial infarction, papillary muscle dysfunction and mitral incompetence seven months before death is reported. Necropsy examination of the heart revealed that the infarct was due to multiple occlusive thrombi in epicardial branches of the corresponding coronary artery. No evidence of atherosclerosis or previous coronary arteritis was present.
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PMID:Myocardial infarction, papillary muscle dysfunction and mitral valvular incompetence in systemic lupus erythaematosus. 693 Feb 18

To clarify the clinical spectrum of coronary arterial abnormalities in systemic lupus erythematosus, the data were reviewed on six patients who had a diagnosis of lupus at ages 15 to 29 years and who had ischemic heart disease before age 35. Two patients had coronary arteritis diagnosed on postmortem examination. In a third patient alterations in coronary arterial anatomy occurred with angiographic improvement temporally related to the initiation of steroid therapy. The other three patients had severe diffuse atherosclerotic coronary disease that was identified in two at postmortem examination. In the third patient the course of the disease strongly suggested coronary atherosclerosis, and eventually coronary bypass grafting was performed for relief of angina. In summary, clinically important extramural coronary arteritis and atherosclerosis both occur, although rarely, in young patients with lupus. Coronary artery disease may occur with or without coexisting active extracardiac lupus manifestations. Short-term steroid therapy and follow-up angiography for those with angina and in whom coronary arteritis is suspected warrant consideration. When stable coronary arterial anatomy is demonstrated on follow-up angiography, management is determined by the patient's symptoms irrespective of the prior history of lupus and, if indicated, cardiac surgery for symptomatic relief can be safely performed.
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PMID:Ischemic heart disease in systemic lupus erythematosus in the young patient: report of six cases. 697 69

To clarify the etiology of atherosclerosis in collagen disease, the prevalence and quality of coronary arterial lesions was examined histopathologically. The materials consisted of 68 autopsy cases, including 10 of rheumatoid arthritis (RA), 28 of systemic lupus erythematosus (SLE), 8 of progressive systemic sclerosis (PSS), 5 of dermatomyositis (DM) and 17 of miscellaneous collagen disease (MD). As a control group (C), 9 age-matched cases of hematologic disorders were chosen. In order to conduct systematic research on coronary arteries, tissue blocks were taken, according to the method proposed by the "Vascular Lesion of Collagen Disease Research Committee" in Japan. To estimate the narrowing of the coronary arterial lumen quantitatively, the coronary stenosis index (CSI), which was the sum of the grade of three main coronary arterial narrowing scores, were used. Significant coronary stenosis (more than 75% occlusion of the lumen) was observed in 8 cases of SLE, one of PSS, 2 of DM and 4 of MD. Stenosis was due to atherosclerosis except in 3 cases of MD. The degree of stenosis expressed by the CSI was higher in MD, SLE and DM than in C (p less than 0.05). Atherosclerotic lesions in collagen disease tended to have a higher population of cellular components than did those in C. There were no statistical correlations between the CSI and some risk factors (age, hypertension, hypercholesterolemia and long-term corticosteroid administration). In the 12 cases with significant stenosis due to atherosclerosis, only 4 patients received corticosteroid hormone for more than one year. Active vasculitis with prominent inflammatory cell infiltration was observed in 2 cases of RA, 3 of SLE and 9 of MD. In cases of vasculitis in SLE examined by the serial section method, luminal narrowing caused by intimal fibrocellular proliferation seemed to have a close relationship with inflammatory cell infiltration in the media and the adventitia. It was concluded that prolonged stimulation of the injured intima by the common risk factors played an important role in the acceleration of coronary atherosclerosis and this intimal change should be reconsidered as a preceding lesion of coronary atherosclerosis.
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PMID:Atherosclerosis of the coronary arteries in collagen disease and allied disorders, with special reference to vasculitis as a preceding lesion of coronary atherosclerosis. 713 12

In a population sample in whom violent accident was the cause of death, the following prevalence of coronary intimal necrosis, occurring as an independent lesion and as an early step of atherosclerotic involvement, was revealed: 2% of children 6--10 years old, 6% of children and juveniles 11--15 years old, 14% of adolescents 16--20 years old, 32% of young adults 21--25 years old, 56% of young adults 26--30 years old, 72% of mature adults 31--35 years old and 84% of mature adults 36--40 years old. In each age subgroup, the percentage of subjects with coronary intimal necrosis was greater than the percentage of subjects with coronary atherosclerotic plaques. A centrifugal extension with age of intimal necrosis, along the coronary tree in the direction of blood flow, was observed. Histologically, the coronary intimal necrosis exhibited a mucoid form, a swelling form and a dissecting form. Indirect evidence was offered that some areas of coronary intimal necrosis formed an adequate nidus for lipid and fibrin accumulation and also induced the development of a peculiar type of subendothelial connective tissue. These successive changes led to the onset of atheroma-like lesions with a prevalence of lipid deposits, or of intramural thrombi or of a fibro-hyaline cap. The onset, extent and evolution of coronary intimal necrosis was accelerated by the male sex, by some minor deviations from the basal branching anatomical pattern of the coronary arteries, by the main risk factors for coronary heart disease, as well as by some terminal diseases, such as the generalized form of sarcoidosis and the renal complications of systemic lupus erythematosus.
Atherosclerosis 1981 Jul
PMID:Coronary intimal necrosis occurring as an early stage of atherosclerotic involvement. 725 28

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


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