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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 22-year-old woman with known SLE and chronic hepatitis B developed anginal pain. During this period there was serologic but no other clinical evidence of active SLE. Myocardial perfusion SPECT showed a severe reversible perfusion defect in the posterior wall, and coronary angiography revealed multiple coronary aneurysms in the left anterior descending artery and circumflex artery and total occlusion of the proximal right coronary artery. This case suggests that coronary aneurysms and total occlusion may represent a sequela of arteritis, or of a combination of underlying vasculitis and a recent thrombotic obstruction due to antiphospholipid syndrome.
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PMID:Coexistence of coronary aneurysms and total occlusion of coronary arteries in systemic lupus erythematosus. 984 71

Observational cohort studies in SLE have led to the description of accelerated atherosclerosis as an important cause of mortality and morbidity in this disease. The clinical observation of coronary artery disease occurring in premenopausal females with SLE gave rise to the concept of the bimodal mortality pattern. This pattern was confirmed in autopsy and epidemiological studies. These studies identified hypercholesterolemia and particularly its persistence in the first three years of disease, hypertension, and lupus itself as important risk factors for the development of accelerated atherosclerosis in these patients. It also became evident that corticosteroid therapy plays an important role in the elevation of plasma lipids while antimalarials resulted in a reduction of plasma cholesterol, LDL, and VLDL, especially in steroid-induced hyperlipidemia. Studies of clinical outcomes for atherosclerotic disease (angina, myocardial infarction) have shown a prevalence of 6-12% in a number of SLE cohorts. However, more sensitive investigations including myocardial perfusion imaging and carotid ultrasound have demonstrated a prevalence of atherosclerotic disease in 40% of patients studied. Further studies of SLE disease process, including immunological factors, may more clearly define the pathogenesis of accelerated atherosclerosis in patients with SLE, and may help elucidate mechanisms of atherosclerosis in the general population.
Lupus 2000
PMID:Accelerated atheroma in lupus--background. 1080 81

Coronary artery disease (CAD) is a major cause of morbidity and mortality in SLE, including the Hopkins Lupus Cohort. Currently, 9% of the cohort have had clinical evidence (angina or myocardial infarction) of CAD. In our initial prospective study we found that duration of prednisone, hypertension, hyperlipidemia and obesity were risk factors for later CAD. We can now extend that list to include age, male sex, elevated homocysteine, renal insufficiency and antiphospholipid antibodies. Many of the risk factors are amenable to intervention, but the timing of intervention, and the effectiveness of intervention, must be determined.
Lupus 2000
PMID:Detection of coronary artery disease and the role of traditional risk factors in the Hopkins Lupus Cohort. 1080 83

The description of late-stage mortality and morbidity has been an important contribution to the understanding of systemic lupus erythematosus (SLE) in the past decade. Among the major factors in this clinical spectrum of SLE is the development of accelerated atherosclerosis. This condition has been recognized clinically with the documentation of myocardial infarction and angina in young women with SLE. This accelerated atherosclerosis has also been recognized at postmortem examinations. The exact mechanism for accelerated atherosclerosis remains unclear. However, disease activity with its immunologic events, the anticardiolipin syndrome, and the effect of corticosteroids in promoting hyperlipidemia contribute to its development. It appears that SLE may be a risk factor, in addition to the usual risk factors for the development of atherosclerosis. It has recently been shown that antimalarials may prevent some of the hyperlipidemia caused by corticosteroids. As evidence for the presence of subclinical atherosclerosis in these patients is accumulating, earlier diagnosis and treatment of events may be possible, and preventive measures may be instituted earlier.
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PMID:Atherosclerosis and systemic lupus erythematosus. 1112 35

Our purpose was to examine prospectively the relationship between systemic hypertension and vascular events in patients with SLE. SLE patients followed in the University of Toronto Lupus Clinic presenting between 1980 and 1988 and within one year of their diagnosis of SLE were identified. Standard definitions were used for hypertension and for all vascular events (MI, angina, CVA, PVD). The presence of traditional CAD risk factors, along with disease- and therapy-related risk factors for the development of vascular disease, were compared in the hypertensive and normotensive group. A multivariate logistic regression was performed to determine the best predictor of a vascular event. One hundred and fifty patients were identified in our inception cohort [75 hypertensive (50%) and 75 (50%) normotensive]. Seventeen hypertensive patients (22.7%) had at least one vascular event as compared to six (8.0%) normotensive patients (p = 0.022). The vascular events included 7 with CAD, 5 with CVA, and 5 with PVD in the hypertensive group while in the normotensive group 3 patients developed CAD, 2 CVA and 1 PVD. Fifteen deaths were recorded in the hypertensive group as compared to eight deaths in the non-hypertensive groups (P = 0.09). The groups were comparable with respect to associated risk factors, except for higher frequency of hypercholesterolemia (P = 0.003), azotemia (P = 0.001) and corticosteroid use (P = 0.038) in the hypertension group. In a multivariate analysis the best predictor of a vascular event was hypercholesterolemia (OR 6.9, 95% CI 2.4-24.8, P < 0.001). We conclude that systemic hypertension is associated with an increased frequency of vascular events in SLE. This is best explained by its association with hypercholesterolemia.
Lupus 2000
PMID:Vascular events in hypertensive patients with systemic lupus erythematosus. 1143 83

The clinical significance of lupus non-inflammatory necrotizing vasculopathy (NINV) is not well established. For example, since lupus renal NINV is usually reported to coexist with proliferative and active glomerulonephritis, it is difficult to demonstrate the role of NINV on renal pathophysiology. Here we report a 16-year-old SLE boy with renal NINV presenting as ischemic glomerulopathy and small vessels-related ischemic heart failure. The renal biopsy demonstrated mild proliferative glomerulonephritis and NINV initially, and one month later repeated renal biopsy showed NINV with ischemic glomerulopathy. These findings established that NINV, but not proliferative glomerulonephritis, was responsive for his acute renal failure (ARF). Another interesting question is about the pathophysiology of his myocardial dysfunction. This patient presented typical angina and congestive heart failure (CHF). Echocardiograms and ventriculography revealed dilatation of four chambers and low ejection fraction. Serial electrocardiograms demonstrated evolutionary ischemic changes. Coronary angiography revealed no abnormality of large vessels. These findings suggested small vascular lesions-induced myocardial ischemia was the underlying mechanism of dilated cardiomyopathy. As myocardial biopsy was not done in our case, we could only speculate, but not prove, that the NINV observed in renal biopsy may also involve in cardiac microvascular beds. Nevertheless, this interesting case emphasized the role of obliterative small vascular lesions in the pathophysiology of ARF and myocardial dysfunction. The patient was treated with high-dose corticosteroid, plasma infusion and hemodialysis. His cardiac function improved gradually, however the renal function did not recover.
Lupus 2002
PMID:Systemic lupus erythematosus presented as non-inflammatory necrotizing vasculopathy-induced ischemic glomerulopathy and small vessels-related ischemic cardiomyopathy. 1219 89

In the United States, systemic lupus erythematosus (SLE) disproportionately affects African Americans. It has become a chronic disease with long-term morbidity including chronic renal disease, osteoporosis, cataracts, psychosocial impairment, and importantly, atherosclerotic vascular disease (ASVD). The latter (myocardial infarction, angina, peripheral vascular disease and stroke) are strikingly accelerated, occurring in subjects who are predominantly premenopausal women at an age when ASVD is rare or unusual. Although much is known about the biology, risk factors, and the prevention of atherosclerosis in normal individuals, little work has been done in SLE. In fact, ASVD in people with SLE may be a different disease. Approximately 1.5% of SLE patients per year will have a myocardial infarction or equivalent; about 0.5% of SLE patients per year will have a stroke. The risk factors for ASVD in SLE are based on small, retrospective, single center studies. These suggest that the risk factors known for the general population (i.e., smoking, obesity, sedentary lifestyle, high LDL cholesterol, etc.) are also observed in SLE. The best study of risk factors shows that even accounting for the known factors, SLE and/or its treatment (glucocorticoids) is by far the most important. Our current management of cardiovascular risk factors in SLE patients with ASVD is substandard and our adherence to national guidelines for prevention is substandard. It is not known whether improving either will prevent these disastrous outcomes. Very little is known about the risk factors in African Americans with SLE, although there is data to suggest that they may not be identical to those seen in Caucasian populations. The study of the best and most effective means to prevent ASVD in SLE and in African Americans with SLE and in African Americans with SLE should be a major priority.
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PMID:Atherosclerotic vascular disease in systemic lupus erythematosus. 1239 45

The objective of this study was to study cardiac valve morphology and function and ventricular function in systemic lupus erythematosus (SLE) patients with and without co-existing cardiovascular disease (CVD) and in population controls. Twenty-six women (52 +/- 8.2 years) with SLE (SLE cases) and a history of CVD (angina pectoris, myocardial infarction, cerebral infarction or intermittent claudication) were compared with 26age-matched women with SLE but without manifest CVD (SLE controls) and 26 age-matched control women (population controls). Echocardiographywas performed to assess valvular abnormalities and manifestations of ischaemic heart disease. Thirteen of the 26 SLE cases but only one of the SLE controls and one of the population controls had cardiac valvular abnormalities. Three of the SLE cases had already undergone valve replacement and another had significant aortic insufficiency; the other nine had thickening of mainly mitral leaflets without hemodynamic significance. Among SLE cases, patients with valvular abnormalities had higher homocysteine (P < 0.001) and triglyceride (P = 0.02) concentrations than patients without valvular disease. In contrast atherosclerosis as determined by IMT, oxidized LDL as measured by the monoclonal antibody E06, autoantibodies against epitopes of OxLDL (aOxLDL) or phospholipids (aPL), disease duration or activity, or acute phase reactants did not differ between SLE cases with or without valvular abnormalities. Valvular abnormalities were not more common in SLE cases with stroke as compared to those with myocardial infarction, angina or claudication. In conclusion, valvular abnormalities are strongly associated with CVD in SLE. Raised levels of homocysteine and triglycerides characterize patients with cardiac valve abnormalities.
Lupus 2002
PMID:Cardiac valvular abnormalities are frequent in systemic lupus erythematosus patients with manifest arterial disease. 1247 5

Cardiac involvement in patients with systemic lupus erythematosus (SLE) is common. The natural history of the cardiovascular manifestations has been altered by systemic corticosteroids used for the treatment of SLE; thus, young patients with SLE may suffer from angina and myocardial infarction. The surgical problems and special requirements in patients with SLE are discussed. CAD is one of the major complications limiting the prognosis of the patient with SLE. In the future, a large number of SLE patients may be candidates for myocardial revascularization. In our opinion, total autogenous arterial bypass grafting is advised and intraoperative biopsies of the LIMA are meaningful in patients with SLE.
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PMID:Coronary artery bypass grafting in patients with systemic lupus erythematosus. 1265 68

The Committee reviewed cardiac involvement in the antiphospholipid antibody syndrome. The Committee's recommendations are: Valve abnormalities: anticoagulation is recommended for symptomatic patients with valvulopathy. Prophylactic antiplatelet therapy may be appropriate for asymptomatic patients (recommended by 13/17 experts in an independent review). Committee members disagreed whether corticosteroid therapy is helpful, but agree that distinguishing among presumptive valvulitis (valve thickening on echocardiogram), valve deformity and vegetations is important, as treatment implications may differ. Occlusive arterial disease (angina, myocardial infarction): the Committee recommends aggressive treatment of all risk factors for atherosclerosis (hypertension, hypercholesterolaemia, smoking) and liberal use of folic acid, B vitamins and cholesterol-lowering drugs (preferably statins). Hydroxychloroquine for cardiac protection in APS patients may be considered. The Committee also recommends warfarin anticoagulation for those who have suffered thrombosis in the absence of atherosclerosis, but recognizes that developing data may support the use of antiplatelet agents instead. Intracardiac thrombi: the Committee recommends intensive warfarin anticoagulation, and consultation with cardiac surgeons when appropriate. Ventricular dysfunction: the Committee has no recommendations on this aspect of cardiac disease. Pulmonary hypertension: the Committee recommends intensive anticoagulation with warfarin and clinical trials of bosentan, epoprostenol and other new agents.
Lupus 2003
PMID:Cardiac disease in the antiphospholipid syndrome: recommendations for treatment. Committee consensus report. 1289 91


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