Lipoprotein (a) Levels and Abdominal Aortic Aneurysm. A Systematic Review
and Meta-analysis

Oikonomou, Evangelos; Lampsas, Stamatios; Pantelidis, Panteleimon; Theofilis, Panagiotis; Grammatopoulos, Konstantinos; Marathonitis, Anastasios; Vavuranakis, Michael-Andrew; Siasos, Gerasimos; Tousoulis, Dimitris; Vavuranakis, Μanolis

doi:10.2174/1381612829666221124110920

Cited by 11 publications

(1 citation statement)

References 49 publications

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“…Lipoprotein(a) is strongly associated with CVD [12][13][14][15]. A plethora of studies demonstrate that Lp(a) is closely linked to coronary heart disease (CHD) [16], peripheral artery disease (PAD) [17], stroke [18], cardiac valve calcification [19][20][21][22][23] and abdominal aortic aneurysm [24]. Lp(a) is synthesized in hepatocytes, and its structure closely resembles that of LDL-C.…”

Section: Introductionmentioning

confidence: 99%

Novel Pharmacological Therapies for the Management of Hyperlipoproteinemia(a)

Kosmas,

Bousvarou,

Papakonstantinou

et al. 2023

IJMS

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Lipoprotein(a) [Lp(a)] is a well-established risk factor for cardiovascular disease, predisposing to major cardiovascular events, including coronary heart disease, stroke, aortic valve calcification and abdominal aortic aneurysm. Lp(a) is differentiated from other lipoprotein molecules through apolipoprotein(a), which possesses atherogenic and antithrombolytic properties attributed to its structure. Lp(a) levels are mostly genetically predetermined and influenced by the size of LPA gene variants, with smaller isoforms resulting in a greater synthesis rate of apo(a) and, ultimately, elevated Lp(a) levels. As a result, serum Lp(a) levels may highly vary from extremely low to extremely high. Hyperlipoproteinemia(a) is defined as Lp(a) levels > 30 mg/dL in the US and >50 mg/dL in Europe. Because of its association with CVD, Lp(a) levels should be measured at least once a lifetime in adults. The ultimate goal is to identify individuals with increased risk of CVD and intervene accordingly. Traditional pharmacological interventions like niacin, statins, ezetimibe, aspirin, PCSK-9 inhibitors, mipomersen, estrogens and CETP inhibitors have not yet yielded satisfactory results. The mean Lp(a) reduction, if any, is barely 50% for all agents, with statins increasing Lp(a) levels, whereas a reduction of 80–90% appears to be required to achieve a significant decrease in major cardiovascular events. Novel RNA-interfering agents that specifically target hepatocytes are aimed in this direction. Pelacarsen is an antisense oligonucleotide, while olpasiran, LY3819469 and SLN360 are small interfering RNAs, all conjugated with a N-acetylgalactosamine molecule. Their ultimate objective is to genetically silence LPA, reduce apo(a) production and lower serum Lp(a) levels. Evidence thus so far demonstrates that monthly subcutaneous administration of a single dose yields optimal results with persisting substantial reductions in Lp(a) levels, potentially enhancing CVD risk reduction. The Lp(a) reduction achieved with novel RNA agents may exceed 95%. The results of ongoing and future clinical trials are eagerly anticipated, and it is hoped that guidelines for the tailored management of Lp(a) levels with these novel agents may not be far off.

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