Lipoprotein(a). The bad cholesterol

Abstract

The aim of this review is to highlight the role of lipoprotein(a) [Lp(a)] in atherogenesis and coronary artery disease. After 40 years from discovery, Lp(a) still remains an enigma and we are still far in understanding the pathophysiological role of Lp(a). Based on its peculiar structure, Lp(a) has both atherogenic and thrombogenic potentials as it is internalized by macrophages and has structural similarity with plasminogen. The results of the prospective studies performed over the past decade have also shown that Lp(a) is a predictor of coronary artery disease (CAD), even though some of the studies have failed to show a statistically significant difference in Lp(a) levels on subjects that subsequently developed CAD and those that did not. Within the population, the plasma levels can vary from <0.5 mg/dl to >200 mg/dl. There is currently no safe drug for long term treatment of patients with high levels of Lp(a). However, it has been proposed that there is a possibility of interfering with apolipoprotein(a) (apoA) translation by using adenovirus mediated antisense RNA technology. Despite more than 3 decades of intense scientific research, the physiopathological role of Lp(a) is still poorly understood and the extent to which Lp(a) levels should be assessed in clinical practice remain controversial until now.