Serum Lp(a) and diabetes mellitus increase the risk of cardiovascular diseases (CVD). However, the relationship between serum Lp(a) and diabetes is poorly characterized, and it is a subject of debate as to whether they are independently or causally associated (1).
One of the atherogenic mechanisms in hyperglycemia is based on enhanced inflammation. Diabetes is associated with increased vascular production of reactive oxygen species (ROS), which causes premature cell apoptosis via reduction of endothelial nitric oxide (NO), resulting in decreased smooth muscle relaxation and antiatherogenic properties, including decreased platelet aggregation and adhesion inhibition (1).
