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)

The cardiovascular system is often involved during systemic lupus erythematosus (SLE), but only few studies have documented myocardial ischemia and myocardial infarction in young patients. We observed 2 cases of coronary artery disease in young patients with SLE and different clinical presentations. In the first case, a 26-year-old woman, with SLE diagnosed at the age of 12 years, was evaluated for angina (CCS class II). Myocardial scintigraphy revealed a clear reversible thallium-201 apical perfusion defect. During the following 5 years worsening effort angina led to coronary angiography which revealed the presence of a complete obstruction of the left anterior descending coronary artery (LAD) treated with surgical myocardial revascularization (internal mammary artery implantation on the LAD). The second patient had myopericarditis and an acute myocardial infarction 1 year before coming to our observation. Coronary angiography revealed the presence of 100% obstruction of the LAD. On this basis, a diagnosis of SLE was made. Our data constitute two relevant examples of coronary artery disease with different clinical presentation in young SLE patients.
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PMID:Coronary artery disease in young patients with systemic lupus erythematosus: two case reports. 1497 54

Endothelial microparticles (EMP) are small vesicles released from disturbed endothelial cells (EC). Owing to the central importance of EC injury in thrombotic and inflammatory conditions, assay of EMP as a marker of EC disturbance has come under intensive development by several laboratories. The review begins with established markers of EC injury, commonly soluble markers such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, von Willebrand factor (vWF), etc., pointing out that many of these are in fact mixtures of true soluble molecules with membrane-bound forms, for example, EMP. Assays of EMP from different labs are reviewed and standardization of assay is recommended. EMP are heterogeneous: those released in activation vs. apoptosis are distinctive in phenotypic markers and procoagulant properties. Application of EMP phenotype analysis can distinguish EC state of activation from apoptosis. Some EMP carry functional vWF with properties different from soluble vWF. Certain EMP bind to and activate monocytes; EMP-monocyte conjugates were found to be a marker of inflammatory disease such as multiple sclerosis (MS), and to enhance transendothelial migration of leukocytes in vitro. Clinical studies have revealed elevated plasma levels of EMP in lupus anticoagulant (LA), multiple sclerosis (MS), thrombotic thrombocytopenic purpura (TTP), coronary artery disease (CAD), hypertension, preeclampsia, and diabetes. Further refinement of EMP assay could open new windows for evaluating and monitoring endothelial injury in thrombotic and inflammatory disorders.
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PMID:Endothelial microparticles as markers of endothelial dysfunction. 1497 33

Dobutamine stress echocardiography (DSE) is an accurate noninvasive test used for the diagnosis and evaluation of patients with known or suspected coronary artery disease (CAD). The aim of this study was to determine the rate of positive findings in DSE, to define the echocardiographic and clinical characteristics of women with systemic lupus erythematosus (SLE) and to evaluate the safety of DSE in SLE patients. Thirty consecutive SLE patients were enrolled in the study and underwent DSE study. The mean age of patients was 44 years (range 20-76). Mean duration of SLE was 8.1 years and mean SLEDAI was 5.5. None of the DSE tests performed were positive for myocardial ischaemia. A left ventricular outflow gradient (LVOG) was found in 15/28 (54%) patients who completed the test, a result higher than the reported 20% prevalence of this finding in the literature. There were no significant differences in baseline characteristics between patients who developed a gradient and patients in whom a gradient was not found. There were no significant adverse effects during the study. In the general population, LVOG has been reported to be associated with an increased rate of chest discomfort and with a significantly lower prevalence of CAD. Whether this is true for SLE patients requires further study.
Lupus 2004
PMID:Dobutamine stress echocardiography in women with systemic lupus erythematosus: increased occurrence of left ventricular outflow gradient. 1499 2

The fluoroquinolone antibiotics sparfloxacin, grepafloxacin, gatifloxacin, and levofloxacin have been reported to cause torsades de pointes. Pre-existing risk factors increase vulnerability to this life-threatening arrhythmia. In a 65-year-old woman with a history of hypertension, coronary artery disease, systemic lupus erythematosus, and osteomyelitis, QTc interval prolongation (605 ms) and torsades de pointes developed after the initiation of levofloxacin, 250 mg intravenously once daily. The patient was hypokalemic and mildly hypomagnesemic before the initiation of levofloxacin and at the time of occurrence of torsades de pointes. The QTc interval decreased to 399 ms within hours of discontinuation of the levofloxacin, after which she had no further arrhythmias. In this and the majority of other published cases of fluoroquinolone-associated torsades de pointes, patients had at least 1 risk factor for the arrhythmia, and most had multiple risk factors. Fluoroquinolone antibiotics should be avoided whenever possible in patients with pre-existing risk factors for torsades de pointes.
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PMID:Torsades de pointes associated with fluoroquinolones: importance of concomitant risk factors. 1500 76

Large increases in mortality related to premature atherosclerosis with coronary artery disease have been reported in patients with systemic lupus erythematosus (SLE). The current pathogenic hypothesis for atherosclerosis involves not only the classic factors identified in the Framingham study, but also includes chronic inflammation, corticosteroid therapy, excess of traditional risk factors, autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized low-density lipoproteins, and to endothelial cells), and cytokine-producing activated T cells. Early risk factor intervention and effective control of inflammation should be incorporated into the management of SLE to protect against atherosclerosis.
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PMID:Atherosclerosis and systemic lupus erythematosus. 1531 7

Coronary artery disease remains a major cause of mortality and morbidity with systemic lupus erythematosus (SLE). We report two cases of coronary artery bypass grafting (CABG) associated with SLE. The first patient (a 45-year-old woman) underwent CABG operation for left main and two-vessel coronary disease using cardiopulmonary bypass. Successful CABG was done using off-pump technique in the second patient (a 39-year-old woman) under hemodialysis therapy. Both patients showed good postoperative outcome without complications.
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PMID:Coronary artery bypass grafting in patients with systemic lupus erythematosus. 1538 63

Our objective was to compare brachial artery endothelium dependent and independent vasodilation in lupus patients and healthy females, by means of high-resolution noninvasive brachial artery ultrasound. Endothelially mediated vasodilation was estimated noninvasively by examination of brachial artery responses to postischemic reactive hyperemia and endothelial independent vasodilation from response to sublingual glycerlynitrate (GTN) using high-resolution external vascular ultrasound. Five patients with known coronary artery disease (CAD), five with subclinical CAD, five with no CAD and five control subjects were assessed. Endothelium dependent vasodilation was significantly blunted in lupus patients with CAD as compared with healthy female controls (0.11 versus 11.1%, P = 0.018). Corresponding values for lupus patients with subclinical CAD and no CAD were 11 and 9.6%, respectively. For each subject, endothelium dependent vasodilation (EDV) was related to endothelium independent vasodilation (EIV) to adjust for varying vascular smooth muscle responses to GTN in individual subjects. This ratio was markedly depressed in lupus patients with CAD as compared with control subjects (0.12 versus 1.15). The corresponding EDV/EIV ratios for patients with subclinical CAD and no CAD were similar at 0.69 and 0.65, respectively. The conclusion was that flow mediated vasodilation in lupus patients with coronary artery disease is markedly depressed as compared to healthy subjects.
Lupus 2004
PMID:Impaired brachial artery endothelium dependent flow mediated dilation in systemic lupus erythematosus: preliminary observations. 1546 88

Patients with rheumatoid arthritis (RA) have a two to five times increased risk of developing premature cardiovascular disease that shortens life expectancy by 5-10 years. Traditional risk factors known to promote and accelerate the progression of atherosclerotic lesions however, are often absent in patients with RA. Many similarities have emerged between the paradigm of inflammation in the pathogenesis of atherosclerosis and the well-established mechanisms of inflammation in the pathogenesis of RA. Hence it is intriguing to speculate that inflammation in RA is not confined to the joints but also present in the vessel wall. Indeed, low-grade inflammation and endothelial dysfunction play pivotal roles in the initiation, progression and propagation of the atherosclerotic process. While the healthy endothelium prevents adhesion of mononuclear cells, the defence mechanisms cease under the influence of cardiovascular risk factors and inflammation and they express adhesion molecules (selectins, vascular adhesion molecule-([VCAM-]1, intercellular adhesion molecule-[ICAM-]1) that promote the adherence of monocytes. This expression is induced by pro-inflammatory cytokines such as interleukin-(IL-)1beta and tumor necrosis factor-(TNF-)alpha, by C-reactive protein (CRP), and CD40/CD40 ligand interactions. As all of these factors are present at increased levels in the systemic circulation in RA, it appears possible that they might impact the endothelium as well. Further similarities include proteolytic enzymes such as matrix metalloproteinases (MMPs) that play a role in joint destruction as well as in destabilization and rupture of vulnerable atherosclerotic plaques. In addition, coagulation factors such as increased levels of tissue factor (TF), van Willebrand factor (vWF) and plasminogen activator inhibitor-(PAI-)1 are important in both, RA and CAD. Endothelial dysfunction has shown to correlate with cardiovascular prognosis in several studies, which indicates its clinical relevance. Endothelial function measurement is performed in the coronary or peripheral circulation (by venous occlusion plethysmography or flow-mediated dilation). Recent studies have demonstrated impaired endothelial function in patients with RA, already at early stages of the disease. Similar results are found in patients with systemic lupus erythematosus (SLE), indicating that inflammation per se may impair altering vascular function. This and more evidence supports the notion that inflammation plays a pivotal role in vascular dysfunction and may by these mechanisms explain at least part of the excess morbidity and mortality observed in RA and SLE. In light of the growing evidence of increased cardiovascular morbidity and mortality mostly independent of traditional risk factors, treatment strategies in RA should not only aim at relieving symptoms and inhibiting joint destruction but should have a beneficial effect on the vasculature to reduce cardiovascular events. Indeed, an improvement in endothelial function in RA was recently demonstrated by anti-TNF-alpha therapy and statins. Whether and to what degree the effects of anti-inflammatory strategies to improve endothelial function, which although clinically well established is still a surrogate, translate into clinical benefit for our patients with rheumatologic diseases needs to be determined in large-scale clinical trials some of which are now already under way.
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PMID:[Rheumatoid arthritis, inflammation, and atherosclerosis]. 1559 72

Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported during the last few years in patients with systemic lupus erythematosus (SLE). Studies found relative risks of 5 to 7 for myocardial infarction in SLE patients. The traditional risk factors fail to fully account for accelerated atherosclerosis in SLE and APS, in addition prolonged glucocorticoid therapy and long duration of SLE seem to be of importance. The disease SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response, autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), CD40/CD40 ligand interactions, and bacterial or viral infections responsible for an immune response. The determination of classic and new risk factors, together with specific autoantibody titers and the use of Doppler carotid ultrasound, are useful methods to detect early atherosclerosis. Therapeutic strategies, including early risk factor intervention and effective control of inflammation, are essential to reduce morbidity and mortality and should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.
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PMID:[Accelerated atherosclerosis in rheumatic systemic diseases as an example of systemic lupus erythematosus--what is the consequence?]. 1590 83

A significant correlation between autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and premature or accelerated coronary atherosclerosis was found. The objectives of the study were: a) evaluate myocardial perfusion in patients with rheumatic diseases by means of contrast echocardiography (CE) and to establish its usefulness as compared to the results obtained by nuclear medicine (NM) (reference method). b) evaluate the prevalence of alterations in subclinical myocardial perfusion in autoimmune diseases and to establish a strategy to evaluate the cardiovascular changes in this disease. Myocardial perfusion in 37 outpatients of the rheumatology department was evaluated by CE at rest and with pharmacological stress (dobutamine) and NM. The prevalence of alterations in the myocardial perfusion in autoimmune diseases by CE and NM, when these methods were analyzed independently or when both methods were used was 27%. The positive predictive value (PPV) and negative predictive value (NPV) of both tests was 80% and 93%, respectively, the sensitivity was 80% and the specificity was 93%. The prevalence of alterations of perfusion in the primary antiphospholipid syndrome (PAPS) was of 30%. In this patients it was found that when both diagnostic tests are performed, NM reaches a sensitivity of 100% if the CE is positive and an specificity of 100% when the CE is negative. We can conclude that it is important to determine the presence of subclinic coronary artery disease in patients with autoimmune disease by noninvasive studies such as Sestamibi SPECT and/or CE for assessment of myocardial perfusion in order to plan an adequate treatment and follow-up.
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PMID:[Analysis of the ulsefulnes of contrast echocardiography and nuclear medicine in cardiovascular affection due to autoimmune diseases]. 1590 39


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