Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial infarction is an underestimated complication of disseminated lupus erythematosus (DLE). Its features, treatment and prognosis are poorly understood. From June 1988 to December 2002, out of 1572 consecutive patients admitted during the first hours of acute myocardial infarction with ST elevation, 7 (5 women, aged 38 +/- 7 years) had DLE. The commonest risk factor was smoking (N = 4). There was a higher incidence of anterior infarction (N = 5). The infarct occurred 7 +/- 5 years after diagnosis of DLE. There were other complications of DLE in all cases. Three patients had antiphospholipid syndromes. The culprit artery was usually the left anterior descending (N = 5). The lesions included stenosing atheroma (N = 5) and extensive thrombosis (N = 5). The coronary disease was usually limited to a single vessel (N = 5). Revascularisation procedures include pre-hospital thrombolysis (N = 3) followed by immediate angioplasty (N = 2) or primary angioplasty (N = 4). TIMI grade 3 flow was obtained in all cases, 278 +/- 162 min after the onset of symptoms. The clinical course was characterised by acute reocclusion in 3 patients, recurrent in 2 patients with an antiphospholipid syndrome, and death in 1 case. Acute myocardial infarction occurs in already complicated cases of DLE, in young patients, associating atherosclerosis and extensive thrombosis. The risk of early reocclusion after reperfusion is high, especially in cases with the antiphospholipid syndrome.
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PMID:[Myocardial infarction and disseminated lupus erythematosus]. 1503 12

We present a case of a 32-year-old male survivor of two myocardial infarctions, without any classic risk factor of atherosclerosis. Laboratory and genetic diagnostic tests revealed primary antiphospholipid syndrome, mutation in blood coagulation factor V (Leiden) and mild hyperhomocysteinemia, which could be predisposing factors for coronary artery occlusions and should especially be considered in a young patient without apparent cardiovascular risk factors. Additional anticoagulation and substitutional treatment of the folic acid, vitamin B6 and B12 are effective and the continues to do well at home 3 years after discharge.
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PMID:[Myocardial infarction as an initial symptom of antiphospholipid syndrome, factor V Leiden mutation, and hyperhomocysteinemia]. 1508 23

Stroke in young adults has been related to mechanisms different to those found in older individuals. Cardiogenic embolism, arteritis, atherosclerosis, fibromuscular dysplasia, pregnancy-related angiopathy, migrainous stroke, anaemia, antiphospholipid syndrome, arterial dissection, the consumption of toxic substances and head trauma have been described. We present a young man with a case history of tobacco and cocaine abuse who suffered a mild head trauma, with normal neurological examination, and a computed tomography scan image of a right anterior cerebral infarction. Serum biochemistry showed no alterations according to the diagnosis protocol for stroke in young patients. Various mechanisms have been involved, such as vasospasm, increasing arterial pressure and embolism. Considering the cocaine abuse and the mild head trauma, in our patient vasospasm was thought to be the mechanism involved in the cerebral infarction, which proved a challenge to diagnose in the emergency room.
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PMID:Stroke in young patients: a diagnostic challenge in the emergency room. 1516 83

Antiphospholipid antibodies (APA) are present in a variety of autoimmune disorders, including systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS). Increasing evidence suggests that a subset of APA can also be detected in patients with atherosclerosis. In this review, we discuss the specificities of the autoantibodies that are present during both APS and atherosclerosis. A critical and unresolved question is whether these APA are specific for epitopes that result from lipid oxidation. Despite the fact that APA are present in patients with systemic autoimmunity and that they may participate in the pathogenesis of APS, recent studies have paradoxically proposed a beneficial role for some APA in atherosclerosis. We review the evidence that some APA specificities may be protective against plaque formation, and we discuss the putative mechanisms by which some APA could be useful in the prevention of atherosclerosis.
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PMID:Antiphospholipid antibodies and atherosclerosis. 1524 Jan 62

The oxidative modification of low-density lipoprotein (LDL) in the intima of arteries contributes to the initiation and progression of atherosclerotic lesions. We have previously reported that oxidized LDL (oxLDL) interacts with an endogenous plasma protein, beta2-glycoprotein I (beta2GPI), to form complexes and that the interaction is mediated by oxLDL specific ligands. We have also demonstrated the presence of oxLDL/beta2GPI complexes in the blood stream of patients with systemic inflammatory and autoimmune diseases. These findings implicate that oxLDL/beta2GPI complexes are possible atherogenic autoantigens. Autoantibodies to oxLDL/beta2GPI complexes have been associated with arterial thrombosis. Further, circulating IgG immune complexes containing oxLDL and beta2GPI were also detected in patients with systemic lupus erythematosus (SLE) and/or antiphospholipid syndrome (APS). Although many unanswered questions remain about the exact pathogenic mechanism(s) involved, oxLDL/beta2GPI complexes may be described as metabolic products relevant in atherogenesis and as significant participants in autoimmune-mediated atherosclerosis.
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PMID:Are oxidized LDL/beta2-glycoprotein I complexes pathogenic antigens in autoimmune-mediated atherosclerosis? 1533 Apr 45

The antiphospholipid syndrome (APS) with its typical clinical manifestations of recurrent thrombosis and fetal loss is biochemically defined by the presence of circulating antiphospholipid antibodies (aPL). The disease pattern has raised special interest as a possible link between autoimmunity and atherosclerosis. aPL, oxidized low density lipoproteins (oxLDL), and antibodies to oxLDL (Anti-oxLDL) are suggested to play an important role in atherogenesis. In the present study we compared the serum levels of oxLDL and Anti-oxLDL in APS patients (20 subjects with primary APS; 14 subjects with secondary APS) and nonAPS subjects (24 phenotypically healthy controls samples and 12 patients with systemic lupus erythematosus [SLE]) and investigated associations of the above mentioned parameters with the intima-media thickness (IMT), a clinical surrogate parameter of atherosclerosis.SLE patients with and without APS showed significantly increased levels of Anti-oxLDL as compared to the controls group (p = 0.038 and p = 0.007, respectively). In contrast, oxLDL levels were not significantly different between the controls group and patients. The Anti-oxLDL levels correlated significantly with anticardiolipin (p = 0.002) and beta(2)-glycoprotein I antibodies (p < 0.048), both from IgG isotype. Only SLE patients without APS revealed a significantly elevated production of reactive oxygen species indicating an increased proatherogenic oxidative stress in the circulation (p < 0.002). In the patient groups, the circulating levels of oxLDL and Anti-oxLDL showed no association with atherosclerosis as estimated by IMT. In conclusion, our experimental data do not support the concept of oxidative stress-induced accelerated atherosclerosis in APS patients.
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PMID:[Oxidatively modified lipoproteins and their antibodies in patients with antiphospholipid syndromeand systemic lupus erythematosus]. 1533 57

Atherosclerosis has been considered an inflammatory disease based on the finding that atherosclerotic lesion contains activated T lymphocytes reacting with oxidized low-density lipoproteins (oxLDL) and heat shock proteins (HSP); it also contains autoantigens like beta2GPI, a target of antibodies occurring in an immune-mediated thrombophilia called antiphospholipid syndrome (APS). Further support to this hypothesis comes from the cross-reactivity, which occurs between antiphospholipid antibodies (aPL) and antibodies to oxLDL. Animal experiments have shown that aPL are associated with atheroma. In addition, accelerated atherosclerosis has been detected in patients with a prototype systemic autoimmune disease, such as systemic lupus erythematosus (SLE). However, the association of APS or aPL with atherosclerosis is a matter of debate due to the small numbers of patients studied, and the fact that traditional risk factors for atherosclerosis coexist. The prevalence of APS ranges from 1.7% to 6%, and that of aPL reaches to 14% among patients with peripheral vascular disease defined on the basis of clinical outcomes. On the other hand, the prevalence of asymptomatic atherosclerosis, defined in terms of plaques in ultrasonography, reaches to 15% of patients with APS compared to 9% of SLE patients and 3% of normal controls. Among SLE patients with aPL, the prevalence of plaques ranges from 6% in premenopausal women to 31% in unselected patients. Less than 10% of APS patients express premature atherosclerosis in the absence of other risk factors. Which APS patient will develop atherosclerosis is unpredictable.
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PMID:Peripheral vascular disease in antiphospholipid syndrome. 1550 85

Anti-apolipoprotein A-1 (Apo A-1) autoantibodies were described in autoimmune disorders such as systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) and might be involved in the genesis of arterial and venous thrombotic events. To investigate the presence of these autoantibodies in patients with acute coronary syndrome (ACS) without other features of autoimmunity, we set up an enzyme-linked immunosorbent assay (ELISA) for anti-Apo A-1 antibodies. We used it to investigate their prevalence in ACS as compared to SLE and APS and correlated them to plasma Apo A-1 and serum amyloid A protein (SAA) concentrations. The prevalence of anti-Apo A-1 autoantibodies in the healthy control group was 1% (1/92), but was significantly higher in other groups: 21% (11/53) in ACS group (P=0.001), 13% (12/92) in SLE and/or APS group (P=0.005). Multiple linear regression revealed a significant correlation between plasma Apo A-1 (r=-0.72, P=0.013), plasma SAA concentration (r=0.76, P=0.0066) and anti-Apo A-1 IgG titre in ACS patients. The presence of anti-Apo A-1 autoantibodies in patients with ACS highlights an additional link between autoimmunity, inflammation and atherosclerosis.
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PMID:Presence of autoantibodies to apolipoprotein A-1 in patients with acute coronary syndrome further links autoimmunity to cardiovascular disease. 1557 29

Antiphospholipid syndrome (APS) is characterized by arterial and/or venous thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). Beta2-glycoprotein I (beta2-GPI) and prothrombin are representative autoantigens, the former more extensively investigated. Anti-beta2-GPI antibodies are not only markers of APS, but also are considered to be pathogenic. Possible roles of anti-beta2-GPI antibodies are, 1) enhancement the binding of beta2-GPI to anionic phospholipid and inhibition of protein C activation/activated protein C, 2) to form anti-beta2-GPI antibody-beta2-GPI-oxidized LDL complex and to promote uptake by sub-endothelial macrophage, resulting in atherosclerosis, 3) to dimerize beta2-GPI on the surface of platelets and to activate platelets via apoE receptor 2 and subsequent signal transduction, 4) stimulation of monocytes via p38 MAP kinase pathway and induction of tissue factor production. In pregnancy morbidity, activation of complement cascade plays an important role. These findings may provide a novel target in the management of APS.
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PMID:[Pathogenic roles of anti-beta2-GPI antibody in patients with antiphospholipid syndrome]. 1567 90

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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