Purpose of review: Genetic, epidemiological, and translational data indicate that Lipoprotein (a) [Lp(a)] is likely in the causal pathway for atherosclerotic cardiovascular diseases as well as calcification of the aortic valves.
Recent findings: Lp(a) is structurally similar to low-density lipoprotein, but in addition to apolipoprotein B-100, it has a glycoprotein apolipoprotein(a) [apo(a)], which is attached to the apolipoprotein B-100. Several distinctive properties of Lp(a) can be attributed to the presence of apo(a). This review discusses the current state of literature on pathophysiological and clinical aspects of Lp(a). After five decades of research, the understanding of Lp(a) structure, biochemistry, and pathophysiology of its cardiovascular manifestations still remains less than fully understood. Universally, Lp(a) elevation may be the most predominant monogenetic lipid disorder with approximate prevalence of Lp(a)>50 mg/dL among estimated >1.4 billion people. This makes a compelling rationale for diagnosing and managing Lp(a)-mediated risk. In addition to discussing various cardiovascular phenotypes of Lp(a) and associated morbidity, we also outline current and emerging therapies aimed at identifying a definitive treatment for elevated Lp(a) levels.
Keywords: Apolipoprotein(a); Cardiovascular diseases; Coronary heart disease; Lipoprotein(a); Lp(a).