scholarly journals Lp(A): When and how to measure it

2020 ◽  
pp. 000456322096847
Author(s):  
Jaimini Cegla ◽  
Michael France ◽  
Santica M Marcovina ◽  
R Dermot G Neely
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Lipoprotein A ◽  
Clinical Laboratories ◽  
Considerable Work ◽  
The Uk ◽  
Size Heterogeneity ◽  
Eqa Schemes

Lipoprotein(a) has long been regarded as a risk factor for cardiovascular disease; however, its routine use in clinical practice has been hampered by difficulties inherent in the measurement of this complex lipoprotein. The major challenges relate to its size heterogeneity and related issues including (1) use of appropriate calibrators (2) standardization of calibration protocols (3) traceability and (4) reporting units. In the UK, results from the current EQA schemes for lipoprotein(a) suggest that there is considerable work required to standardize lipoprotein(a) measurement. This is becoming increasingly pertinent with the increasing recognition of lipoprotein(a) as an independent risk factor for cardiovascular disease in international guidelines and the emergence of novel antisense therapies to effectively reduce lipoprotein(a). This article raises awareness of the importance of measurement of lipoprotein(a) for the assessment of cardiovascular disease risk and gives guidance to clinical laboratories regarding choice of appropriate assays.

scholarly journals Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association

2021 ◽  
Author(s):  
Gissette Reyes-Soffer ◽  
Henry N. Ginsberg ◽  
Lars Berglund ◽  
P. Barton Duell ◽  
Sean P. Heffron ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Density Lipoprotein ◽  
Major Protein ◽  
Atherosclerotic Cardiovascular Disease ◽  
Lipoprotein A ◽  
Scientific Statement ◽  
Genetically Determined

High levels of lipoprotein(a) [Lp(a)], an apoB100-containing lipoprotein, are an independent and causal risk factor for atherosclerotic cardiovascular diseases through mechanisms associated with increased atherogenesis, inflammation, and thrombosis. Lp(a) is predominantly a monogenic cardiovascular risk determinant, with ≈70% to ≥90% of interindividual heterogeneity in levels being genetically determined. The 2 major protein components of Lp(a) particles are apoB100 and apolipoprotein(a). Lp(a) remains a risk factor for cardiovascular disease development even in the setting of effective reduction of plasma low-density lipoprotein cholesterol and apoB100. Despite its demonstrated contribution to atherosclerotic cardiovascular disease burden, we presently lack standardization and harmonization of assays, universal guidelines for diagnosing and providing risk assessment, and targeted treatments to lower Lp(a). There is a clinical need to understand the genetic and biological basis for variation in Lp(a) levels and its relationship to disease in different ancestry groups. This scientific statement capitalizes on the expertise of a diverse basic science and clinical workgroup to highlight the history, biology, pathophysiology, and emerging clinical evidence in the Lp(a) field. Herein, we address key knowledge gaps and future directions required to mitigate the atherosclerotic cardiovascular disease risk attributable to elevated Lp(a) levels.

scholarly journals Molecular, Population, and Clinical Aspects of Lipoprotein(a): A Bridge Too Far?

2019 ◽  
Vol 8 (12) ◽  
pp. 2073 ◽  
Author(s):  
Natalie C. Ward ◽  
Karam M. Kostner ◽  
David R. Sullivan ◽  
Paul Nestel ◽  
Gerald F. Watts
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Outcome Data ◽  
Clinical Aspects ◽  
Cardiovascular Disease Risk Factor ◽  
Atherosclerotic Cardiovascular Disease ◽  
Lipoprotein A ◽  
Risk Reclassification

There is now significant evidence to support an independent causal role for lipoprotein(a) (Lp(a)) as a risk factor for atherosclerotic cardiovascular disease. Plasma Lp(a) concentrations are predominantly determined by genetic factors. However, research into Lp(a) has been hampered by incomplete understanding of its metabolism and proatherogeneic properties and by a lack of suitable animal models. Furthermore, a lack of standardized assays to measure Lp(a) and no universal consensus on optimal plasma levels remain significant obstacles. In addition, there are currently no approved specific therapies that target and lower elevated plasma Lp(a), although there are recent but limited clinical outcome data suggesting benefits of such reduction. Despite this, international guidelines now recognize elevated Lp(a) as a risk enhancing factor for risk reclassification. This review summarises the current literature on Lp(a), including its discovery and recognition as an atherosclerotic cardiovascular disease risk factor, attempts to standardise analytical measurement, interpopulation studies, and emerging therapies for lowering elevated Lp(a) levels.

Parental history and cardiovascular disease risk factor variables in children

1981 ◽  
Vol 10 (1) ◽  
pp. 25-37 ◽  
Author(s):  
Caroline V. Blonde ◽  
Larry S. Webber ◽  
Theda A. Foster ◽  
Gerald S. Berenson
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cardiovascular Disease Risk Factor ◽  
Parental History ◽  
Disease Risk Factor

scholarly journals Identification of Endothelial Proteins in Plasma Associated With Cardiovascular Risk Factors

2021 ◽  
Author(s):  
Maria J. Iglesias ◽  
Larissa D. Kruse ◽  
Laura Sanchez-Rivera ◽  
Linnea Enge ◽  
Philip Dusart ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Body Mass Index ◽  
Risk Factor ◽  
Total Cholesterol ◽  
Body Mass ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Cardiovascular Disease Risk Factor ◽  
Venous Disease

Objective: Endothelial cell (EC) dysfunction is a well-established response to cardiovascular disease risk factors, such as smoking and obesity. Risk factor exposure can modify EC signaling and behavior, leading to arterial and venous disease development. Here, we aimed to identify biomarker panels for the assessment of EC dysfunction, which could be useful for risk stratification or to monitor treatment response. Approach and Results: We used affinity proteomics to identify EC proteins circulating in plasma that were associated with cardiovascular disease risk factor exposure. Two hundred sixteen proteins, which we previously predicted to be EC-enriched across vascular beds, were measured in plasma samples (n=1005) from the population-based SCAPIS (Swedish Cardiopulmonary Bioimage Study) pilot. Thirty-eight of these proteins were associated with body mass index, total cholesterol, low-density lipoprotein, smoking, hypertension, or diabetes. Sex-specific analysis revealed that associations predominantly observed in female- or male-only samples were most frequently with the risk factors body mass index, or total cholesterol and smoking, respectively. We show a relationship between individual cardiovascular disease risk, calculated with the Framingham risk score, and the corresponding biomarker profiles. Conclusions: EC proteins in plasma could reflect vascular health status.

Sign in / Sign up

Export Citation Format

Share Document