Autoantibodies to Cardiolipin and Beta-2-Glycoprotein-I in Coronary Artery Disease Patients with and without Hypertension

Aim. To compare parameters of prothrombotic activity in patients with myocardial infarction (MI) with obstructive (MICAD) and non-obstructive coronary artery disease (MINOCA).Material and methods. The study included 40 patients with MI, which were divided into experimental (n=19) and control group (n=21). Three patients (15,7%) with acute myocarditis were excluded from the analysis. Hemostasiological and hematological blood tests were studied upon admission, on the 2nd, 4th, 7th days from hospitalization. Blood samples for protein C, antithrombin, von Willebrand factor (VWF), plasminogen, homocysteine were performed on 4th±1 day from hospitalization. To determine the IgG/IgM anticardiolipin (aCL) and anti-beta 2 glycoprotein I (β2-GPI) antibodies in order to diagnose antiphospholipid syndrome (APS), the ORGENTEC Anti- β2-Glycoprotein I IgG/IgM ELISA enzyme immunoassay was used. Blood tests for lupus anticoagulant were performed using an ACL-Top 700 analyzer (Werfen) with HemosIL SynthASil dRVVT screen/dRVVT confirm and with a SCT screen/SCT confirm quartz activator.Results. According to the data obtained, it was found that patients with MINOCA had a significantly lower level of plasminogen (p=0,007), as well as a higher level of homocysteine (p=0,03). For such indicators as protein C, antithrombin, ejection fraction, differences between the groups were not revealed (p<0,05). At the same time, protein C deficiency was detected in 2 (12,5%) patients with MINOCA and in 1 (5,3%) patient in the control group. Antithrombin deficiency was detected in 2 (12,5%) patients with MINOCA and in 2 (9,5%) patients with MICAD. An increase in the level of ejection fraction was found in 6 (37,5%) patients in the study group and in 7 (33,3%) patients in the control group. There were no differences in levels of lupus anticoagulant, aCL and β2-GPI antibodies (p>0,05). There was a higher platelet count in patients with MINOCA on the 2nd and 4th days of acute MI (p=0,46 and p=0,01, respectively). However, the hemoglobin level in patients with MINOCA was significantly lower on admission, 4th and 7th day of MI (p=0,02, p=0,03 and p=0,04, respectively).Conclusion. According to the study results, in patients with MINOCA and MICAD, differences in blood thrombotic activity were revealed. A higher level of homocysteine and a lower level of plasminogen were determined in patients with MINOCA. For such parameters as protein C, antithrombin, VWF, aCL and β2-GPI antibodies, differences between the groups were not determined. According to laboratory data, patients with MINOCA showed higher platelet count, but lower levels of hemoglobin and hematocrit in the early postinfarction period.

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Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

Clinical Science ◽

10.1042/cs20190999 ◽

2019 ◽

Vol 133 (22) ◽

pp. 2283-2299

Author(s):

Apabrita Ayan Das ◽

Devasmita Chakravarty ◽

Debmalya Bhunia ◽

Surajit Ghosh ◽

Prakash C. Mandal ◽

...

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Chronic Inflammation ◽

Ex Vivo ◽

Human Subjects ◽

Critical Role ◽

Atherosclerotic Cardiovascular Disease ◽

Tnf Α ◽

Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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