Gissette Reyes-Soffer1. 1. Columbia University Medical Center-College of Physicians and Surgeons, New York, New York, USA.
Abstract
PURPOSE OF REVIEW: Lipoprotein(a) [Lp(a)] is a plasma circulating apoB100 (apoB) containing lipoprotein. It has a unique glycoprotein bound to the apoB100, apolipoprotein(a) [apo(a)]. The majority of the population expresses two apo(a) isoforms, when bound to apoB100 they create two circulating Lp(a) particles. Lp(a) levels are genetically determined and epidemiological studies have established elevated levels of Lp(a) to be a causal risk factor of cardiovascular disease (CVD). Lp(a) levels differ across racial groups and Blacks of Sub-Saharan decent have higher levels when compared to white. In comparison to white populations, studies in minorities are less represented in the published literature. Additionally, there is a lack of standardization in the commercial assays used to measured Lp(a) levels, and hence it is difficult to assess risk based on individual Lp(a) levels, but risk seems to occur in the upper percentiles of the population. RECENT FINDINGS: A recent study using data from the UK biobank highlights the racial differences in Lp(a) levels and the increase risk in CVD amongst all races. SUMMARY: This review will highlight Lp(a) biology and physiology with a focus on available data from racially diverse cohorts. There is a need to perform studies in diverse populations to understand if they are at higher risk than whites are.
PURPOSE OF REVIEW: Lipoprotein(a) [Lp(a)] is a plasma circulating apoB100 (apoB) containing lipoprotein. It has a unique glycoprotein bound to the apoB100, apolipoprotein(a) [apo(a)]. The majority of the population expresses two apo(a) isoforms, when bound to apoB100 they create two circulating Lp(a) particles. Lp(a) levels are genetically determined and epidemiological studies have established elevated levels of Lp(a) to be a causal risk factor of cardiovascular disease (CVD). Lp(a) levels differ across racial groups and Blacks of Sub-Saharan decent have higher levels when compared to white. In comparison to white populations, studies in minorities are less represented in the published literature. Additionally, there is a lack of standardization in the commercial assays used to measured Lp(a) levels, and hence it is difficult to assess risk based on individual Lp(a) levels, but risk seems to occur in the upper percentiles of the population. RECENT FINDINGS: A recent study using data from the UK biobank highlights the racial differences in Lp(a) levels and the increase risk in CVD amongst all races. SUMMARY: This review will highlight Lp(a) biology and physiology with a focus on available data from racially diverse cohorts. There is a need to perform studies in diverse populations to understand if they are at higher risk than whites are.
Authors: Bruce A Warden; Jessica Minnier; Gerald F Watts; Sergio Fazio; Michael D Shapiro Journal: J Clin Lipidol Date: 2019-04-26 Impact factor: 4.766
Authors: Azadeh Beheshtian; Sanyog G Shitole; Alan Z Segal; Dana Leifer; Russell P Tracy; Daniel J Rader; Richard B Devereux; Jorge R Kizer Journal: Atherosclerosis Date: 2016-08-20 Impact factor: 5.162
Authors: Santica M Marcovina; Noémie Clouet-Foraison; Marlys L Koschinsky; Mark S Lowenthal; Allen Orquillas; Michael B Boffa; Andrew N Hoofnagle; Tomáš Vaisar Journal: Clin Chem Date: 2021-03-01 Impact factor: 12.167