The role of lipoprotein(a) [Lp(a)] in atherogenesis has been the target of many studies that have demonstrated that this lipoprotein is an independent risk factor for coronary artery disease (CAD). Due to the structural likeness with plasminogen, Lp(a) can compete with binding sites, reducing the plasmin generation and inhibiting fibrinolysis. Thrombus formed due to ruptured atherosclerotic plaque trigger most ischemic cardiovascular events. As the thrombus are dissolved by the fibrinolytic system, the hypothesis that a decrease in fibrinolytic activity might be a risk factor for ischemic events has been suggested. However, some studies have not demonstrated any correlation between Lp(a) and CAD while others attribute the real predictive value to a subpopulation of Lp(a) with high affinity for fibrin. This hypothesis suggests that some Lp(a) phenotypes are not associated with atherothrombosis. Furthermore, research on Lp(a) and CAD is controversial and highly dependent on the studied population. In the Brazilian population, which presents heterogeneity of the ethnic groups, studies of this type are rare. Based on the controversies, it is expected that a contribution of the present review will motivate investigators to develop studies involving the measurement of Lp(a) in patients with CAD in the Brazilian population. The accumulated knowledge on the association between Lp(a) and CAD was obtained through foreign studies. Thus, such studies must be performed in our setting in order to bring a better understanding for a more adequate management of CAD.
Lipoprotein(a); fibrinolysis; coronary artery disease
