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PCSK9 inhibition

Hormone therapy cuts Lp(a) by up to 44% in postmenopausal women, more than niacin or PCSK9 inhibitors, a review of Lp(a) treatment options (Int J Clin Pract 2016)

Original title: Lipoprotein(a) in postmenopausal women: assessment of cardiovascular risk and therapeutic options

Int J Clin Pract · · 6

Anagnostis P, Karras S, Lambrinoudaki I, Stevenson JC, Goulis DG

This narrative review by Anagnostis, Karras, Lambrinoudaki, Stevenson and Goulis examines Lp(a) contribution to cardiovascular risk in postmenopausal women and available treatment strategies, searching literature through November 2015. Hormone replacement therapy, mainly oral estrogens, and tibolone are the only therapies specifically studied in postmenopausal women, reducing Lp(a) by up to 44%, though evidence of a corresponding cardiovascular benefit is lacking. Niacin and the then-emerging PCSK9 inhibitors can reduce Lp(a) by up to 30% as alternatives for women unable or unwilling to take hormonal therapy, while statins have minimal or no effect on Lp(a); other promising therapies including mipomersen, lomitapide, CETP inhibitors and eprotirome have mostly been studied in general high-risk populations rather than postmenopausal women specifically. The authors conclude it remains unproven whether these Lp(a) reductions translate into lower cardiovascular risk in postmenopausal women.

Read the paper (DOI)PubMed

Original abstract

Introduction: Lipoprotein(a) [Lp(a)], a low-density lipoprotein (LDL)-like particle, has been independently associated with increased cardiovascular disease (CVD) risk in various populations, such as postmenopausal women. The purpose of this narrative review is to present current data on the role of Lp(a) in augmenting CVD risk in postmenopausal women and focus on the available therapeutic strategies.

Methods: PubMed was searched for English language publications until November 2015 under the following terms: "therapy" OR "treatment" AND ["lipoprotein (a)" OR "Lp(a)"] AND ("postmenopausal women" OR "menopausal women" OR "menopause").

Results: Only hormone replacement therapy (mainly oral estrogens) and tibolone have been specifically studied in postmenopausal women and can reduce Lp(a) concentrations by up to 44%, although evidence indicating a concomitant reduction in CVD risk associated with Lp(a) is lacking. As alternative treatments for women who cannot, or will not, take hormonal therapies, niacin and the upcoming proprotein convertase subtilisin / kexin type 9 (PCSK-9) inhibitors are effective in reducing Lp(a) concentrations by up to 30%. Statins have minimal or no effect on Lp(a). However, data for these and other promising Lp(a)-lowering therapies including mipomersen, lomitapide, cholesterol-ester-transfer protein inhibitors and eprotirome are derived from studies in the general, mainly high CVD risk, population, and include only subpopulations of postmenopausal women.

Conclusions: Past, present and emerging therapies can reduce Lp(a) concentrations to a varying extent. Overall, it remains to be proven whether the aforementioned reductions in Lp(a) by these therapeutic options are translated into CVD risk reduction in postmenopausal women.

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Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.