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Cardiovasc Res. 2017 Aug 1;113(10):1102-1112. doi: 10.1093/cvr/cvx112.

A role for autoantibodies in atherogenesis.

Author information

Faculty of Medicine and Public Health, The University of Newcastle, Callaghan, NSW 2308, Australia.
Hunter Medical Research Institute, New Lambton Heights, NSW 2305, Australia.
Centre for Brain and Mental Health Research, The University of Newcastle, Callaghan, NSW, Australia.
Brain Behaviour Research Group, School of Science and Technology, University of New England, Armidale, NSW 2351, Australia.
Laboratory of Affective Neuroscience, The University of Newcastle, Callaghan, NSW, Australia.
University of Newcastle, Medical Sciences MS413, Callaghan, NSW 2308, Australia.
Department of General Medicine, John Hunter Hospital, New Lambton Heights, NSW, Australia.


An increased risk of cardiovascular disease (CVD) has long been recognized amongst people with autoimmune disease. It has been unclear whether this is due mainly to the ensuing treatment, particularly steroids, or whether some of this risk is due to the autoimmune process itself with subsequent inflammation. Indeed, a large body of evidence supports a role for chronic inflammation in atherogenesis, and autoantibodies have been identified as mediators in this complex inflammatory environment. Our aim is to carry out a systematic review of existing literature in order to formally establish the strength of the association between autoantibodies and atherosclerosis, amongst individuals without clinical autoimmune disease. An electronic search of five databases to June 2016 was performed by two independent reviewers. Inclusion criteria were analytical studies of adults, with at least two studies per autoantibody. Quality analysis was carried out using the Newcastle-Ottawa scale and the Cochrane Risk of Bias Quality Assessment Tool where appropriate. Where possible, studies were pooled using random effects models. Raised levels of anti-cardiolipin (odds ratio [OR] = 1.30; 95% CI: 1.15-1.49) and anti-oxidized low-density lipoprotein Immunoglobulin (Ig) G (OR = 1.25; 95% CI: 1.11-1.41), unspecified anti-cyclic citrullinated protein (OR = 3.09; 95% CI: 1.49-6.41) and anti-human heat shock protein 60 IgA (OR = 1.57; 95% CI: 1.15-2.16) were observed to increase the risk of cardiovascular outcomes. Alternatively, Anti-phosphorylcholine IgM (OR = 1.31; 95% CI: 1.14-1.50) conferred protection against CVD. Our results support an important role for autoantibodies in mediating cardiovascular events, independent of therapeutic treatments. Future research may focus on the presence of autoantibodies as markers of immune dysregulation and CVD risk.


Atherosclerosis (AS); Autoantibodies; Cardiovascular disease (CVD); Myocardial infarction (MI); Stroke

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