Antiphospholipid antibodies in acute coronary syndrome

Veres, Katalin; Lakos, Gabriella; Kerényi, Adrienne; Szekanecz, Zoltán; Szegedi, Gyula; Shoenfeld, Yehuda; Soltész, Pál

doi:10.1191/0961203304lu1011oa

Cited by 66 publications

(50 citation statements)

References 21 publications

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“…In a recent study by Veres et al, 42 the authors report that the frequency and titers of anti-␤ 2 -GPI antibodies were significantly higher in patients with acute coronary syndromes than in controls, data that are consistent with previous studies on patients with stable and unstable angina. 43 Building on these observations, de Laat et al 44 developed an assay to discriminate between ␤ 2 -GPI antibody-dependent LA and ␤ 2 -GPI-independent LA activity.…”

Section: Antiphospholipid Antibodiessupporting

confidence: 82%

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Feinbloom

Bauer

2005

ATVB

108

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Abstract-Arterial thrombosis results from endovascular injury and, to a lesser extent, alterations in hemostatic equilibrium. Although multiple hereditary and acquired hemostatic risk factors have been described in the pathophysiology of venous thrombosis, the degree and type of abnormalities that contribute to arterial thrombosis are less well understood. Endothelial cell injury with the elaboration of proinflammatory mediators stimulates the process of arterial thrombosis. Although this is most often the result of endovascular injury attributable to atherosclerotic disease, other disease states can elicit a similar response as well. Similarly, once thrombosis has been initiated, variations in the activity of coagulation proteins and endogenous anticoagulants, as well as the kinetics of platelet aggregation, may alter the effectiveness of thrombus formation. Epidemiological studies have identified several acquired or inherited states that may result in endothelial damage or altered hemostatic equilibrium, thereby predisposing patients to arterial thrombosis. These include hyperhomocysteinemia, elevated C-reactive protein, antiphospholipid antibodies, elevated fibrinogen, Factor VII, plasminogen activator inhibitor-1 (PAI-1), hereditary thrombophilias, and platelet hyper-reactivity. This review explores our present understanding of these risk factors in the development of arterial thrombotic events. At present, the literature supports a role for hyperhomocysteinemia, elevated C-reactive protein, and elevated fibrinogen as risk factors for arterial thrombosis. Similarly, the literature suggests that lupus anticoagulants and, to a lesser extent, elevated titers of cardiolipin IgG antibodies predispose to arterial vascular events. In certain subsets of patients, including those with concomitant cardiac risk factors, Ͻ55 years of age, and women, hereditary thrombophilias such as carriership of the factor V Leiden and the prothrombin G20210A mutations may confer a higher risk of arterial thrombosis. However, the data on Factor VII, PAI-1, and platelet receptor polymorphisms are contradictory or lacking.

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Section: Antiphospholipid Antibodiessupporting

confidence: 82%

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Feinbloom

Bauer

2005

ATVB

108

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“…Moreover, a correlation between serum levels of aCL and anti-␤2GPI antibodies and the incidence and severity of acute coronary syndrome, myocardial infarction, and stroke have been demonstrated previously. 15,16 Early endothelial dysfunction 17 and increased carotid intima-media thickness also have been observed in APS. 18 Various studies have evidenced that oxidative stress is directly involved in the pathophysiology of both APS and SLE.…”

Section: Introductionmentioning

confidence: 96%

Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q10 treatment

Pérez-Sánchez

Ruiz-Limón

Aguirre

et al. 2012

Blood

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The exact mechanisms underlying the role of oxidative stress in the pathogenesis and the prothrombotic or proinflammatory status of antiphospholipid syndrome (APS) remain unknown. Here, we investigate the role of oxidative stress and mitochondrial dysfunction in the proatherothrombotic status of APS patients induced by IgG-antiphospholipid antibodies and the beneficial effects of supplementing cells with coenzyme Q 10 (CoQ 10 ). A significant increase in relevant prothrombotic and inflammatory parameters in 43 APS patients was found compared with 38 healthy donors. Increased peroxide production, nuclear abundance of Nrf2, antioxidant enzymatic activity, decreased intracellular glutathione, and altered mitochondrial membrane potential were found in monocytes and neutrophils from APS patients. Accelerated atherosclerosis in APS patients was found associated with their inflammatory or oxidative status. CoQ 10 preincubation of healthy monocytes before IgG-antiphospholipid antibody treatment decreased oxidative stress, the percentage of cells with altered mitochondrial membrane potential, and the induced expression of tissue factor, VEGF, and Flt1. In addition, CoQ 10 significantly improved the ultrastructural preservation of mitochondria and prevented IgG-APS-induced fission mediated by Drp-1 and Fis-1 proteins. In conclusion, the oxidative perturbation in APS patient leukocytes, which is directly related to an inflammatory and proatherothrombotic status, relies on alterations in mitochondrial dynamics and metabolism that may be prevented, reverted, or both by treatment with CoQ 10 .

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“…COPE-Ab = circulating anti-coatomer protein complex subunit epsilon autoantibody, HD = healthy volunteer donor, OSA = obstructive sleep apnea. According to recent studies, circulating autoantibodies exist in the sera of patients with atherosclerosis, including autoantibodies against phospholipids in patients with acute coronary syndrome, 17,18 apolipoprotein A-1 in patients exhibiting atherosclerotic plaque vulnerability, 19 and oxidized low-density lipoprotein, which is associated with plaque formation and coronary risk in some patients with systemic lupus Figure 2-Associations between COPE-Ab levels and clinical parameters other than OSA severity in patients with OSA.…”

Section: Discussionmentioning

confidence: 99%

Circulating Anti-Coatomer Protein Complex Subunit Epsilon (COPE) Autoantibodies as a Potential Biomarker for Cardiovascular and Cerebrovascular Events in Patients with Obstructive Sleep Apnea

Matsumura

Terada

Kinoshita

et al. 2017

Journal of Clinical Sleep Medicine

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Study Objectives: Although moderate to severe obstructive sleep apnea (OSA) is an independent risk factor for severe arteriosclerotic diseases such as cardiovascular disease (CVD) and stroke, the development of atherosclerosis-related diseases cannot yet be predicted in patients with OSA. In a pilot study, we identified autoantibodies against the coatomer protein complex, subunit epsilon [circulating anti-coatomer protein complex subunit epsilon autoantibody (COPE-Ab)], a cytosolic complex that mediates protein transport in the Golgi compartment, as a potential novel biomarker of atherosclerosis. This study aimed to evaluate whether COPE-Ab levels had an association with cardiovascular and cerebrovascular events in patients with OSA. Methods: Eighty-two adult patients with a diagnosis of OSA via polysomnography and 64 healthy donors were studied. Serum COPE-Ab levels were measured using an amplified luminescence proximity homogeneous assay. Then, clinical factors related to atherosclerosis were evaluated with respect to COPE-Ab levels. Results: Significant differences in COPE-Ab levels were observed in terms of OSA severity. COPE-Ab levels were significantly higher in patients with OSA and also CVD and/or stroke, hypertension, and a high body mass index. Univariate and multivariate logistic regression analyses of patients with OSA identified elevated COPE-Ab level as a significant predictor of CVD and/or stroke. Conclusions: An elevated COPE-Ab level may be a potential predictor of the risks of cardiovascular and cerebrovascular events in patients with OSA. Therefore, patients with higher COPE-Ab levels may require more careful and intensive treatment. Commentary: A commentary on this article appears in this issue on page 361.

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Antiphospholipid antibodies in acute coronary syndrome

Cited by 66 publications

References 21 publications

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Assessment of Hemostatic Risk Factors in Predicting Arterial Thrombotic Events

Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q10 treatment

Circulating Anti-Coatomer Protein Complex Subunit Epsilon (COPE) Autoantibodies as a Potential Biomarker for Cardiovascular and Cerebrovascular Events in Patients with Obstructive Sleep Apnea

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