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CHUYÊN ĐỀ Issue: Số 106 năm 2023

Elevated Lipoprotein(a) as a causual risk factor in atherosclerosis cardiovascular disease: From pathophysiology to clinical pratice

Trương Thanh Hương: Viện Tim mạch Việt Nam, Bệnh viện Bạch Mai;
Published: August 1, 2023
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Abstract

Elevated lipoprotein(a) [Lp(a)] is an causal risk factor for atherosclerosis and is hereditary, which requires attention, because there is no approved medication formally for Lp(a) lowering in clinical pratice; even statins, which are first-line lipid-lowering therapy, do not lower Lp(a). After 50 years of research on Lp(a), in addition to strong evidence for atherogenesis, elevated Lp(a) denifed as >125 nmol/L, is confirmed to be common with 20% of the population. The European Atherosclerosis Society and the European Society of Cardiology recommend Lp(a) testing for individuals with risk of inherited elevated Lp(a) or moderate/high-risk according to risk cardiovascular assessment models. Lp(a)-lowering therapies are being developed; most notably, the HORIZON trial for impact of Lp(a) lowering with pelacarsen, which reduces Lp(a) synthesis through messenger RNA inhibition. Whiles pending their approval decisions formally, individuals with elevated Lp(a) should be controled traditional cardiovascular risk factors closely.

References

1.
Koschinsky ML, Kronenberg F. The long journey of lipoprotein(a) from cardiovascular curiosity to therapeutic target. Atherosclerosis. 2022;349:1-6.
2.
Kronenberg F, Mora S, Stroes ESG, Ference BA, Arsenault BJ, Berglund L, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement European Heart Journal. 2022;43(39):3925-46.
3.
Rawther T, Tabet F. Biology, pathophysiology and current therapies that affect lipoprotein (a) levels. Journal of Molecular and Cellular Cardiology. 2019;131:1-11.
4.
Orsó E, Schmitz G. Lipoprotein(a) and its role in inflammation, atherosclerosis and malignancies. Clinical Research in Cardiology Supplements. 2017;12(1):31-7.
5.
Koschinsky ML, Boffa MB. Oxidized phospholipid modification of lipoprotein(a): Epidemiology, biochemistry and pathophysiology. Atherosclerosis. 2022;349:92-100.
6.
Arsenault BJ, Kamstrup PR. Lipoprotein(a) and cardiovascular and valvular diseases: A genetic epidemiological perspective. Atherosclerosis. 2022;349:7-16.
7.
Langsted A, Kamstrup PR, Nordestgaard BG. High lipoprotein(a) and high risk of mortality. European Heart Journal. 2019;40(33):2760-70.
8.
Khera AV, Everett BM, Caulfield MP, Hantash FM, Wohlgemuth J, Ridker PM, et al. Lipoprotein(a) Concentrations, Rosuvastatin Therapy, and Residual Vascular Risk. Circulation. 2014;129(6):635-42.
9.
Parish S, Hopewell JC, Hill MR, Marcovina S, Valdes-Marquez E, Haynes R, et al. Impact of Apolipoprotein(a) Isoform Size on Lipoprotein(a) Lowering in the HPS2-THRIVE Study. Circulation: Genomic and Precision Medicine. 2018;11(2):e001696.
10.
Tsimikas S, Moriarty PM, Stroes ES. Emerging RNA Therapeutics to Lower Blood Levels of Lp(a): JACC Focus Seminar 2/4. Journal of the American College of Cardiology. 2021;77(12):1576-89.
11.
Nurmohamed NS, Kraaijenhof JM, Stroes ESG. Lp(a): a New Pathway to Target? Current Atherosclerosis Reports. 2022;24(11):831-8.
12.
Tsimikas S, Karwatowska-Prokopczuk E, Gouni-Berthold I, Tardif JC, Baum SJ, Steinhagen-Thiessen E, et al. Lipoprotein(a) Reduction in Persons with Cardiovascular Disease. The New England journal of medicine. 2020;382(3):244-55.

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