Lipoprotein(a) in postmenopausal women: assessment of cardiovascular risk and therapeutic options. Issue 12 (December 2016)

• Record Type: Journal Article
• Authors: Anagnostis, Panagiotis; Karras, Spyridon; Lambrinoudaki, Irene; Stevenson, John C.; Goulis, Dimitrios G.
• Is Part Of: International journal of clinical practice. Volume 70:Issue 12(2016)
• Page Start: 967
• Page End: 977
• Publication Date: 2016-12
• Subjects: Lipoprotein(a) -- Menopause -- postmenopausal women -- cardiovascular risk; Clinical medicine -- Periodicals; Medicine -- Periodicals; 610.5
• DOI: 10.1111/ijcp.12903
• Languages: English
• ISSNs: 1368-5031

Abstract

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.