Newer antiphospholipid antibodies predict adverse outcomes in patients with acute coronary syndrome.
ABSTRACT Antiphospholipid antibodies (aPLs) have been implicated in atherogenesis. We studied 344 patients with acute coronary syndromes; approximately 40% were aPL+ in 1 or more tests and 60% aPL-. In 215 patients, coronary artery disease (CAD) was angiographically documented, with 43.7% positive for aPL vs 34.9% of patients without CAD positive for aPLs. Anti-beta(2)-glycoprotein I (beta2GPI; 54%) and anti-oxidized low-density lipoprotein (oxLDL)/beta2GPI (48%) were most frequent, accounting for 87% of all aPL+ CAD cases. aPLs correlated with severity of CAD (P = .012). Adverse events occurred in 16.7% of patients with CAD, more frequently in patients who were aPL+ (P = .0006; relative risk, 2.9; 95% confidence interval, 1.5-5.6). Patients who were aPL+ with severe CAD had more adverse events than patients who were aPL- with severe CAD (P = .005) and aPL+ patients undergoing revascularization procedures (P = .001). Vascular events occurred in 21.7% of aPL+ patients compared with 7.1% of aPL- patients (P = .005). Anti-beta2GPI and anti-oxLDL/beta2GPI were associated with CAD severity and adverse outcomes.
SourceAvailable from: Abdolreza Sotoodeh jahromi[Show abstract] [Hide abstract]
ABSTRACT: Problem statement: Ischemic cardiac manifestations have been reported in a various percentage of patients with anti-phospholipid antibodies. Data concerning the relation between anti-Phospholipid (aPL) antibodies and myocardial infarction in subjects without evidence of overt autoimmune disease are conflicting. Anti-beta2 glycoprotein-I (anti-beta2-GPI) antibody is detected in various diseases like rheumatoid arthritis, systemic lupus erythematosus and anti-phospholipid antibody syndrome. The study of anti-beta2-GPI antibody in Acute Myocardial Infarction (AMI) might shed light on etiologic mechanisms in the pathogenesis of acute coronary syndromes. The purpose of the present study was to determine association of plasma aPL antibodies, namely, anti-beta2-GPI antibodies, with AMI. This study was designed to investigate whether prevalence of anti-beta2-GPI antibodies, in patients who had acute myocardial infarction and to analyze their relationship with traditional cardiovascular risk factors. Approach: We investigated the prevalence of anti-beta2-GPI IgG in a well characterized group of patients with AMI as a case group. Sera from 74 patients with AMI and from 76 healthy subjects, matched for age and sex as a control group. Using ELISA to evaluate the presence of IgG isotype of anti-beta2-GPI autoantibodies in their sera. Results: The prevalence of anti-beta2-GPI IgG in the control group (10.50%) resulted significantly lower than in patients with AMI (37.80%) (p<0.005). There was significant difference between positive anti-β2-GPI test in patients with STEMI and those with NSTEMI (66.7% Vs 36.4%), (p = 0.020). Conclusion: Our findings suggest that anti-beta2-GPI IgG antibodies seemed to behave as independent risk factors for myocardial infarction, which may represent a link between autoimmunity and atherosclerosis in patients with acute myocardial infarction. Further studies with bigger patients are needed to explore association of anti-β2-GPI IgG with STEMI and NSTEMI.
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ABSTRACT: Antiphospholipid syndrome is a rare autoimmune disease characterized by a high tendency of developing thrombotic events. It is diagnosed in the presence of specific laboratory criteria (positivity for lupus anticoagulant, and the presence of anticardiolipin and aβ2GPI antibodies) and clinical criteria such as thrombosis in any district (arterial or venous) and pregnancy morbidity. Being a multisystem disease, the heart is commonly affected by direct (autoimmune mediated action) or indirect (thrombosis) pathological mechanisms. Heart valve lesions are the most frequent manifestations; however, the haemodynamic significance is quite uncommon but when it occurs it may require surgery that further complicates the picture due to the high risk of thrombosis. Coronary arteries and myocardium are also affected leading to ischaemic heart disease and left ventricular dysfunction. Other findings include chronic thromboembolic pulmonary hypertension and accelerated atherosclerosis. The consequences of heart involvement may be significant in overt disease. The treatment of cardiac complications is challenging and requires an in-depth knowledge of the disease.Autoimmunity Reviews 11/2014; 14(3). DOI:10.1016/j.autrev.2014.11.003 · 7.10 Impact Factor
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ABSTRACT: OxLDL/β2GPI complexes have been implicated in the initiation and progression of atherosclerosis and associated with disease severity and adverse outcomes. We investigate the significance of anti-oxLDL/β2GPI antibodies and oxLDL/β2GPI complexes in patients with arterial and idiopathic venous disease. A cohort of 61 arterial disease patients, 32 idiopathic venous disease patients, and 53 healthy controls was studied. Because statins influence oxLDL/β2GPI, these complexes were analyzed on subjects not taking statins. Arterial and venous groups expressed higher levels of IgG anti-oxLDL/β2GPI antibodies than controls without any other significant clinical association. OxLDL/β2GPI complexes were significantly elevated in arterial (0.69 U/mL, P = 0.004) and venous disease (0.54 U/mL, P = 0.025) than controls (0.39 U/mL). Among arterial diseases, oxLDL/β2GPI was 0.85 U/mL for carotid artery disease, 0.72 U/mL for peripheral artery disease, and 0.52 U/mL for abdominal aortic aneurysm. There was a significant association with male gender, age, hypertension, and history of thrombosis. Subjects with oxLDL/β2GPI above the median (0.25 U/mL) were more likely to have arterial (OR 4.5, P = 0.004) or venous disease (OR 4.1, P = 0.008). Multivariate regression indicated that males (P = 0.021), high cholesterol (P = 0.011), and carotid disease (P = 0.023) were significant predictors of oxLDL/β2GPI. The coexistence of oxLDL/β2GPI in arterial and venous disease may suggest a common oxidative mechanism that independently predicts carotid artery disease.Research Journal of Immunology 01/2014; 2014:234316. DOI:10.1155/2014/234316