Abstract
Malondialdehyde-acetaldehyde adducts (MAA) have been implicated in atherosclerosis. The purpose of this study was to investigate the role of MAA in atherosclerotic disease. Serum samples from controls (n = 82) and patients with; non-obstructive coronary artery disease (CAD), (n = 40), acute myocardial infarction (AMI) (n = 42), or coronary artery bypass graft (CABG) surgery due to obstructive multi-vessel CAD (n = 72), were collected and tested for antibody isotypes to MAA-modifed human serum albumin (MAA-HSA). CAD patients had elevated relative levels of IgG and IgA anti-MAA, compared to control patients (p<0.001). AMI patients had a significantly increased relative levels of circulating IgG anti-MAA-HSA antibodies as compared to stable angina (p<0.03) or CABG patients (p<0.003). CABG patients had significantly increased relative levels of circulating IgA anti-MAA-HSA antibodies as compared to non-obstructive CAD (p<0.001) and AMI patients (p<0.001). Additionally, MAA-modified proteins were detected in the tissue of human AMI lesions. In conclusion, the IgM, IgG and IgA anti-MAA-HSA antibody isotypes are differentially and significantly associated with non-obstructive CAD, AMI, or obstructive multi-vessel CAD and may serve as biomarkers of atherosclerotic disease.
Highlights
Inflammation is thought to be central in the pathogenesis of atherosclerosis [1,2] and acute myocardial infarction (AMI) [3]
Evaluation and comparison of 4 patient groups were undertaken and this study cohort is presented in the Table 1. These four groups included; 1) ‘‘Controls’’ – Patients without any history of coronary artery disease (CAD); 2) ‘‘Non-Obstructive CAD’’ - Patients that presented for cardiac catheterization with chest pain and CAD, but no evidence of an AMI; 3) ‘‘Acute MI’’ - Patients with CAD who presented with an AMI; and, 4) ‘‘Multi-Vessel Obstructive CAD’’ - Patients with severe CAD who presented for coronary artery bypass graft (CABG) surgery
Non-Obstructive CAD and Acute MI patients who were diagnosed with CAD at the time of catheterization, have a lower incidence of ACE inhibitor and statin use compared to patients with known CAD presenting for CABG surgery
Summary
Inflammation is thought to be central in the pathogenesis of atherosclerosis [1,2] and acute myocardial infarction (AMI) [3]. The driving mechanism(s) of cardiovascular inflammation is/are uncertain Modification of proteins, such as lipoproteins and the formation of protein-adducts, is one mechanism that has been associated with the development and/or progression of atherosclerotic disease [5,6,7,8,9]. These modified proteins have been found in the circulation [10,11] and in atherosclerotic lesions of patients with atherosclerotic disease [5,8,12,13,14]. The exact direct and/or indirect mechanism(s) by which modified proteins result in cellular dysfunction, [14] immune sensitization, [15,16,17,18,19] tissue inflammation, and atherosclerotic plaque formation and rupture is not fully known
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