scholarly journals Anticardiolipin antibody levels in diabetic subjects with and without coronary artery disease.

1989 ◽  
Vol 65 (761) ◽  
pp. 140-143 ◽  
Author(s):  
T. J. Hendra ◽  
E. Baguley ◽  
E. N. Harris ◽  
M. H. Khamashta ◽  
R. C. Trembath ◽  
...  
1988 ◽  
Vol 74 (s18) ◽  
pp. 25P-25P
Author(s):  
TJ Hendra ◽  
EN Harris ◽  
RC Trembath ◽  
GRV Hughes ◽  
JS Yudkin

2011 ◽  
Vol 3 (2) ◽  
pp. 17 ◽  
Author(s):  
Stuart P. Adler ◽  
Al M. Best ◽  
Beth Marshall ◽  
George W. Vetrovec

Over 90% of the world’s population acquires a cytomegalovirus (CMV) infection. This infection, although asymptomatic or self-limiting, is a major burden to the immune system. For this reason, and because CMV immunization is possible, determining whether CMV can cause reduced longevity, particularly among those with coronary artery disease, is important and previous reports have been conflicting. Thus our objective was to assess the association between CMV infection as defined serologically and antibody levels against CMV and longterm survival (18 years). We completed a prospective observational cohort study of 915 consecutive patients (mean age 58 years) undergoing coronary angiography. CMV immunoglobulin levels were measured at baseline using either a whole cell CMV antigen or a purified protein antigen (gB). After adjustment for potentially confounding variables (age, race, gender, body mass index, the presence or absence of coronary artery disease, the number of diseased vessels, diabetes, renal disease, hypertension, dialysis, congestive heart failure, and the maximum percent reduction in luminal diameter), Cox’s proportional hazards models showed no association between CMV seropositivity or levels of antibodies against CMV by either assay and longevity for both patients with or without coronary artery disease (CAD) nor for those under or over 70 years of age at baseline. Our observations suggest that universal immunization against CMV may not improve longevity.


Heart ◽  
2007 ◽  
Vol 93 (11) ◽  
pp. 1412-1413
Author(s):  
I. Ikonomidis ◽  
J. Lekakis ◽  
G. Vamvakou ◽  
S. Loizou ◽  
I. Revela ◽  
...  

2005 ◽  
Vol 38 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Dilek Bilgen ◽  
Hüseyin Sönmez ◽  
Hakan Ekmekçi ◽  
Turgut Ulutin ◽  
Zeynep Öztürk ◽  
...  

2017 ◽  
Vol 52 (5) ◽  
pp. 930-935 ◽  
Author(s):  
V. L. Berquist ◽  
A. C. Hearps ◽  
P. Ford ◽  
A. Jaworowski ◽  
S. J. Leishman ◽  
...  

2015 ◽  
Vol 24 (5) ◽  
pp. 424-431 ◽  
Author(s):  
Amir Ali Rahsepar ◽  
Asadollah Mirzaee ◽  
Fatemeh Moodi ◽  
Mohsen Moohebati ◽  
Shima Tavallaie ◽  
...  

2012 ◽  
Vol 3 (2) ◽  
pp. 15
Author(s):  
Mahadev D. Dixit ◽  
Kishore G. Bhat ◽  
Aruneshwari Dayal

The role of chronic infections in causing coronary artery disease (CAD) has been investigated for the past several years. Among them, the role of Helicobacter pylori has stimulated keen interest. Though initial results were conflicting, there are growing data to support the role of H. pylori in CAD. The main mechanism of endothelial damage is hypothesized to be through molecular mimicry involving heat shock proteins. This study was designed to determine the prevalence of H.pylori and cytotoxin associated gene A (cagA) positive H.pylori infection in patients undergoing coronary artery bypass grafting (CABG) and the potential role of anti-H. pylori specific heat shock protein-60 (Hp-HSP-60) antibody response in these patients, for cardiac events. One hundred patients undergoing CABG and 100 controls were studied. The H.pylori infection and cagA status were determined serologically by enzyme-linked immunosorbent assay (ELISA). Hp-HSP-60 Immunoglobulin G (IgG) antibodies were estimated by using an in house ELISA. Although there was no difference in the prevalence of H.pylori infection in patients and controls (74% vs 70%), 58% of patients were infected with cagA positive H.pylori compared to 36% of controls (P=0.002). Mean systemic levels of Hp-HSP-60 IgG were also higher in patients than in controls (27.9 vs 18.7, P=0.0001). These antibody levels were also significantly higher in H.pylori positive patients (P=0.0001). There was a strong correlation between Hp-HSP-60 antibody levels and occurrence of myocardial infarction (P=0.003). CagA positive H.pylori infection may be associated with the development of CAD. High levels of Hp-HSP-60 antibodies may constitute a marker and/or concomitant pathogenic factor of the disease.


2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  

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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