August 2024 Br J Cardiol 2024;31(suppl 1):S3 doi:10.5837/bjc.2024.s01
Tina Z Khan
As with all health conditions, effective communication between the healthcare professional and patient is a key component of management. It is important that patients understand that raised Lp(a) is predominantly genetically inherited (>90%)2; therefore, other family members should be screened for the condition5 and made aware of the associated risks. Intensive treatment and management of other cardiovascular risk factors, such as low-density lipoprotein-cholesterol, blood glucose and blood pressure, is recommended. Patients should be mindful of other conditions that might affect their Lp(a) levels, such as chronic kidney disease.5 Lastly
August 2024 Br J Cardiol 2024;31(suppl 1):S4–S9 doi:10.5837/bjc.2024.s02
Paul Durrington
Introduction Lipoprotein(a) (Lp[a]) was discovered in 1963 as an antigen causing rare blood transfusion reactions.1 The antigen was found to be present in the lipoprotein fraction of plasma, hence the name lipoprotein(antigen). As methods for its measurement improved, researchers realised that Lp(a) had a continuous population frequency distribution, which in people of European descent, was markedly positively skewed.2,3 It was also reported that in those with higher concentrations, the prevalence of coronary heart disease was increased. Furthermore, higher levels were inherited; the concentration of Lp(a) was twice as much in men who had ex
August 2024 Br J Cardiol 2024;31(suppl 1):S10–S15 doi:10.5837/bjc.2024.s03
Saleem Ansari, Jaimini Cegla
Why should lipoprotein(a) be measured? The cardiovascular risk conferred by serum lipoprotein(a) (Lp(a)) in large noteworthy epidemiological studies1,2 over two decades ago was inconsistent and often underestimated owing to poor standardisation of the commercially available Lp(a) immunoassays. During the last decade, however, genome-wide association and Mendelian randomisation studies have identified Lp(a) as a new risk factor for calcific aortic stenosis and as a causal risk factor for atherosclerotic cardiovascular disease (ASCVD) across ethnicities.3,4 Elevated Lp(a) is associated with accelerated progression of low-attenuation plaque for
August 2024 Br J Cardiol 2024;31(suppl 1):S16–S20 doi:10.5837/bjc.2024.s04
Pyotr Telyuk, David Austin, Paul Williams, Ahai Luvai, Azfar Zaman
Introduction Lipoprotein(a) (figure 1) has emerged as an independent and causal risk factor for cardiovascular diseases (CVDs) and cerebrovascular diseases with prospective epidemiological studies demonstrating a link between elevated Lp(a) levels and increased incidence of ischaemic heart disease (IHD) and myocardial infarction (MI).1 The value of this association is that it was seen to be independent of traditional cardiovascular (CV) risk factors including diabetes, hypertension and smoking.1 Moreover, Lp(a) levels greater than 50 mg/dL were associated with a threefold increase in acute coronary syndrome (ACS) in younger patient cohorts (
August 2018 Br J Cardiol 2018;25:95
Jaqui Walker
Professor Klaus Parhofer Lipoprotein (a) The role of lipoprotein (a) [Lp(a)] was explored by Professor Klaus Parhofer (Ludwig Maximilians University, Munich, Germany). This is an independent risk factor in cardiovascular disease (CVD), with a causal link to atherosclerosis, myocardial infarction (MI), aortic valve stenosis and heart failure. Of the different therapies that can be used to reduce elevated Lp(a), only apheresis shows a reduction in CVD events. Currently, the most important management strategy is to optimise all other CVD risk factors, particularly low-density-lipoprotein cholesterol (LDL-C). In patients with progressive CVD, de
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