Abstract 128: Serum Anti-MAA Antibody Titers are Associated with Acute Myocardial Infarction and MMP-9

Introduction Atherosclerotic plaque rupture is the leading cause of acute myocardial infarction (AMI). Malondialdehyde acetaldehyde (MAA) modified proteins have recently been implicated in this process by their ability to initiate inflammatory responses. Matrix metalloproteinase 9 (MMP-9) is increased following AMI and has been associated with the disease due to its ability to degrade the fibrotic cap that forms on some plaques. Objective The purpose of this study was to evaluate the relationship between MMP-9 and anti-MAA antibody isotypes in patients experiencing acute myocardial infarction (AMI). Methods Serum samples from AMI patients (n=10) were collected and tested for the presence of anti-MAA antibody isotypes, peak CK, peak troponin, and MMP-9 levels. Samples were collected at the time of AMI, 24 and 48 hours post event. Data was correlated to determine relationships with antibody isotypes directed against MAA protein antigens. Results MMP-9 increased significantly from the initial presentation at 24 hours post-AMI (p=0.006) and 48 hours post-AMI (p= 0.044). Anti-MAA IgM decreased significantly (p= 0.021) between initial and 24 hours post AMI. A similar significant decrease was observed for anti-MAA IgG (p= 0.006). Anti-MAA IgA levels did not change significantly post-AMI. Significant correlations were demonstrated between peak CK and anti-MAA IgG 24 hours post AMI (r= -0.819, p= 0.013), between peak troponin and anti-MAA IgG 24 hours post AMI (r= -0.860, p= 0.006) and between MMP-9 levels 24 hours post AMI and anti-MAA IgM levels 24 hours post MI ( r= 0.0712, p=0.021). Conclusions The negative correlation of anti-MAA IgG to cardiac enzymes is suggestive that myocardial infarction and tissue necrosis results in the release of the MAA antigen from infarcted myocardium and clearance of anti-MAA antibodies. Additionally, anti-MAA IgM and MMP-9 are positively correlated with each other 24 hours post-AMI, suggesting that anti-MAA IgM titers may correlate to the severity of the AMI and thus CAD. Implications Anti-MAA antibodies might serve as important biomarkers of impending atherosclerotic plaque rupture and subsequent AMI and warrants further investigation in a larger cohort of patients.