Emerging Pharmacotherapy to Reduce Elevated Lipoprotein(a) Plasma Levels
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LEADING ARTICLE
Emerging Pharmacotherapy to Reduce Elevated Lipoprotein(a) Plasma Levels Nathaniel Eraikhuemen1 · Dovena Lazaridis2 · Matthew T. Dutton3
© Springer Nature Switzerland AG 2020
Abstract Lipoprotein(a) is a unique form of low-density lipoprotein. It is associated with a high incidence of premature atherosclerotic disease such as coronary artery disease, myocardial infarction, and stroke. Plasma levels of this lipoprotein and its activities are highly variable. This is because of a wide variability in the size of the apolipoprotein A moiety, which is determined by the number of repeats of cysteine-rich domains known as “kringles.” Although the exact mechanism of lipoprotein(a)induced atherogenicity is unknown, the lipoprotein has been found in the arterial walls of atherosclerotic plaques. It has been implicated in the formation of foam cells and lipid deposition in these plaques. Pharmacologic management of elevated levels of lipoprotein(a) with statins, fibrates, or bile acid sequestrants is ineffective. The newer and emerging lipid-lowering agents, such as the second-generation antisense oligonucleotides, cholesteryl ester transfer protein inhibitors, and proprotein convertase subtilisin/kexin type 9 inhibitors offer the most effective pharmacologic therapy. Key Points Lipoprotein(a) is associated with a high incidence of premature atherosclerotic disease such as coronary artery disease, myocardial infarction, and stroke. Pharmacologic management of elevated levels of lipoprotein(a) with statins, fibrates, or bile acid sequestrants is ineffective. The newer and emerging lipid-lowering agents, such as the second-generation antisense oligonucleotides, cholesteryl ester transfer protein inhibitors, and proprotein convertase subtilisin/kexin type 9 inhibitors, offer the most effective pharmacologic therapy. * Dovena Lazaridis [email protected] Nathaniel Eraikhuemen [email protected] Matthew T. Dutton [email protected] 1
College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University, Davie, FL 33324, USA
2
Memorial Regional Hospital-Department of Pharmacy, 3501 Johnson Street, Hollywood, FL 32301, USA
3
College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health, Florida A&M University, Tallahassee, FL, USA
1 Introduction Significant advances have been made in the treatment of dyslipidemia. However, many patients continue to experience clinical manifestations of atherosclerotic vascular diseases, such as myocardial infarction (MI), cerebrovascular diseases, and peripheral vascular disease [1]. Clinical dyslipidemias fall into four broad categories: high levels of low-density lipoprotein cholesterol (LDL-C), low levels of high-density lipoprotein cholesterol (HDL-C), elevated triglycerides, and elevated lipoprotein(a) [Lp(a)] [2]. Over time, more emphasis has been placed on pharmacologic and nonpharmacologic reduction of LDL-C as a method of reducing atherosclerotic vascular diseases. In addition, lifestyle modificat
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