Title:Lipoprotein(a) as a Predictive Biomarker and Therapeutic Target for Acute
Coronary Syndromes
Volume: 29
Issue: 23
Author(s): Yannis Dimitroglou*, Constantina Aggeli, Panagiotis Theofilis, Panagiotis Tsioufis, Evangelos Oikonomou, Konstantinos Tsioufis and Dimitris Tousoulis
Affiliation:
- 1st Cardiology Clinic, ‘Hippokration’ General Hospital, School of Medicine, National and Kapodistrian University of Athens,
Athens, Greece
Keywords:
Lipoproteins, cardiovascular disease, myocardial infarction, antisense oligonucleotides, siRNA, CAD.
Abstract: Coronary artery disease (CAD) is the leading cause of morbidity and mortality in Western societies,
despite the significant advances that have improved primary and secondary prevention. Hence, several novel
biomarkers have been identified as potential diagnostic and therapeutic targets which could improve outcomes
even when traditional risk factors are well-controlled. Lipoprotein (a) [Lp(a)] has pro-atherogenic, pro-thrombotic,
and pro-inflammatory properties, and its levels are relatively constant and genetically predetermined. Several
epidemiological studies have associated high Lp(a) with increased risk for acute coronary syndromes (ACS)
even when other CAD risk factors are included in the multivariate analysis. However, until recently, specific
therapeutic options targeting Lp(a) were not associated, and thus, Lp(a) is currently used as a risk and treatment
modifying biomarker with guidelines suggesting the intensified treatment of low-density lipoprotein in intermediate-
to-high-risk patients with increased Lp(a) levels. Lately, specific treatment options targeting Lp(a) have
become available and include antisense oligonucleotides and small-interfering RNA, which induce a robust reduction
of Lp(a). Results of ongoing phase-3 trials will answer whether Lp(a) will become a biomarker specifically
treated to reduce the burden of cardiovascular mortality. The scope of this review article is to present the
current evidence regarding the use of Lp(a) as a biomarker, predictive of increased CAD risk, and to discuss the
future perspectives on pharmaceutical reduction of Lp(a) as a therapeutic target in high-risk patients.