ACP1 and ADA1 Genetic Polymorphisms and Coronary Artery Disease. Effects on Age at Onset of Clinical Manifestations

Previous studies have shown an association of Coronary Artery Disease (CAD) with Acid Phosphatase locus 1 (ACP1 ) and Adenosine Deaminase locus 1 (ADA1 ) genetic polymorphisms. Both systems are involved in immune reactions and several studies point to a significant autoimmune component in the pathogenesis of CAD. In the present note we have investigated the role of the two polymorphisms on age of onset of the disease. Hundred and thirty patients admitted to Valmontone Hospital for the first episode of CAD have been studied. Informed consent was obtained by the patients to participate in the study that was approved by the Sanitary Direction of the Hospital. In patients at the first episode of CAD, ACP1 genotype was determined in 130 subjects and ADA1 genotype in 126 subjects by DNA analysis. SPSS programs performed statistical analyses. The age at onset of CAD is lower in subjects with low ACP1 activity genotypes and in those with low ADA1 activity genotypes. The association is stronger in females than in males. The effects of the two systems appears additive with a lower age of onset in subjects carrying the two factors associated with lower age at onset and a higher age in subjects with no factor. The pattern is stronger in females than in males. Gender differences in autoimmunity are well documented: women with low ACP1 activity and/or ADA1 genotype seem to have a high risk of early clinical manifestations as compared to women carrying genotypes with high activity. These differences support the hypothesis of significant autoimmune component in the pathogenesis of CAD.