New Treatment Approaches for Dyslipidemia and its Management
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SECONDARY PREVENTION AND INTERVENTION (J FOODY, SECTION EDITOR)
New Treatment Approaches for Dyslipidemia and its Management Matthew Vorsanger & James A. Underberg
Published online: 10 September 2013 # Springer Science+Business Media New York 2013
Abstract The field of lipidology is evolving rapidly. Two novel medications have recently been approved for use in homozygous familial hypercholesterolemia (HoFH); the Apolipoprotein B (Apo B) mRNA antisense oligonucleotide (ASO), mipomersen (Kynamro®) and the microsomal triglyceride transfer protein (MTP) inhibitor, lomitapide (Juxtapid®). Equally important have been the disappointments in cholesterol research; the halting of further investigation into the cholesteryl ester transfer protein (CETP) inhibitor dalcetrapib, yet two others remain in development. The failure of the combination of extended release niacin and laropiprant to show benefit when combined with statin therapy has lead to the discontinuation of this product in Europe. Perhaps one of the most exciting avenues of future research is into the inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9). Keywords Lipidology . Familial hypercholesterolemia . Antisense oligonucleotides . Microsomal triglyceride transfer protein inhibitor . Cholesteryl ester transfer protein inhibitor . Niacin . Laropiprant . Proprotein convertase subtilisin/kexin type 9 inhibitor
Introduction With the advent of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, great strides have been made in the primary and secondary prevention of atherosclerotic disease in patients with both acquired and inborn disorders of lipoprotein metabolism. However, the success of the statin drug class has also served to highlight the remaining J. A. Underberg (*) NYU Center for Prevention of Cardiovascular Disease, NYU School of Medicine, New York, NY, USA e-mail: [email protected] M. Vorsanger Division of General Internal Medicine, NYU School of Medicine, New York, NY, USA
deficiencies in our ability to treat dyslipidemia. Nowhere is this more apparent than in HoFH. The lack of functional lowdensity lipoprotein (LDL) receptors in this disorder leads to not only impaired clearance of LDL from the circulation, but also overproduction of Apo B containing particles in the liver [1]. Thus, the very mechanism of action of HMG-CoA reductase inhibitors, the up-regulation of low-density lipoprotein (LDL) receptors, is undermined by the innate defects of the LDL-receptor that define the disease, resulting in goal LDL levels being achieved in only a subset of patients [2]. It is for this reason that the possibility of diminishing hepatic production of Apo B containing particles becomes so attractive. The need for adjunctive agents is pressing, not only for these patients, but for others who do not meet their goals or cannot tolerate conventional lipid lowering therapy. Recently, medications with novel mechanisms have been approved by the FDA for use in HoFH, the MTP inhibitor, lomitapide and the ApoB ASO, mipomersen. T
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