Key result
The prevalence of anti-beta2-glycoprotein-I IgG antibodies was significantly higher in patients with acute myocardial infarction compared to healthy controls (37.8% vs 10.5%, p=0.003).
Case-Control (n=150)
No
Absolute Event Rate: 37.8% vs 10.5%
p-value: p=0.003
Anti-beta2-glycoprotein-I IgG antibodies are significantly more prevalent in patients with acute myocardial infarction, suggesting a potential autoimmune link to atherosclerosis and acute coronary syndromes.
Anti-β2-GPI IgG was associated with AMI in case-control data; hypothesis-generating for autoimmune role in ACS and requires prospective validation.
Problem statement: Ischemic cardiac manifestations have been reported in a various percentage of patients with anti-phospholipid antibodies. Data concerning the relation between anti-Phospholipid (aPL) antibodies and myocardial infarction in subjects without evidence of overt autoimmune disease are conflicting. Anti-beta2 glycoprotein-I (anti-beta2-GPI) antibody is detected in various diseases like rheumatoid arthritis, systemic lupus erythematosus and anti-phospholipid antibody syndrome. The study of anti-beta2-GPI antibody in Acute Myocardial Infarction (AMI) might shed light on etiologic mechanisms in the pathogenesis of acute coronary syndromes. The purpose of the present study was to determine association of plasma aPL antibodies, namely, anti-beta2-GPI antibodies, with AMI. This study was designed to investigate whether prevalence of anti-beta2-GPI antibodies, in patients who had acute myocardial infarction and to analyze their relationship with traditional cardiovascular risk factors. Approach: We investigated the prevalence of anti-beta2-GPI IgG in a well characterized group of patients with AMI as a case group. Sera from 74 patients with AMI and from 76 healthy subjects, matched for age and sex as a control group. Using ELISA to evaluate the presence of IgG isotype of anti-beta2-GPI autoantibodies in their sera. Results: The prevalence of anti-beta2-GPI IgG in the control group (10.50%) resulted significantly lower than in patients with AMI (37.80%) (p<0.005). There was significant difference between positive anti-2-GPI test in patients with STEMI and those with NSTEMI (66.7% Vs 36.4%), (p = 0.020). Conclusion: Our findings suggest that anti-beta2-GPI IgG antibodies seemed to behave as independent risk factors for myocardial infarction, which may represent a link between autoimmunity and atherosclerosis in patients with acute myocardial infarction. Further studies with bigger patients are needed to explore association of anti-2-GPI IgG with STEMI and NSTEMI.
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Shojaei (2011) conducted a case-control in Acute Myocardial Infarction (n=150). Anti-beta2-Glycoprotein-I (anti-beta2-GPI) IgG antibodies vs. Healthy matched controls was evaluated on Prevalence of positive anti-beta2-GPI IgG antibodies (≥19 U/mL) (p=0.003). The prevalence of anti-beta2-glycoprotein-I IgG antibodies was significantly higher in patients with acute myocardial infarction compared to healthy controls (37.8% vs 10.5%, p=0.003).
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