Prevalence of lipoprotein(a)
- Approximately 1 in 5 people worldwide have elevated Lp(a) levels1
- Lp(a) levels are approximately 70% to ≥90% genetically determined and elevated levels and can be passed down in families2
- Lifestyle modifications do not have a significant influence on Lp(a) levels3-5
- Lp(a) levels remain relatively consistent over a lifetime3-5
Epidemiological, Mendelian randomisation, and genetic studies involving hundreds of thousands of individuals strongly support a causal and continuous association between Lp(a) concentration and cardiovascular (CV) outcomes (particularly acute myocardial infarction (MI)) in different ethnicities; even when LDL-C levels are within the recommended range, which is referred to as residual cardiovascular risk.7-12
A multicentre cross-sectional epidemiological study sought to characterise patterns of Lp(a) levels in a global atherosclerotic cardiovascular disease (ASCVD) population and identify racial, ethnic, regional and gender differences (n=48,135). It was found that globally, Lp(a) is measured in a small minority of patients with ASCVD (13.9%) and is highest in Black, younger, and female patients. More than 25% of patients had levels exceeding the established threshold for increased CV risk, approximately 50 mg/dL or 125 nmol/L.6 In a 2022 UK Biobank study of 22,401 patients with incident ASCVD, median Lp(a) levels were moderately lower in patients with ASCVD, 29 nmol/L.6
In patients with cardiovascular disease (CVD), elevated Lp(a) independently increases recurrent MACE (Major Adverse Cardiovascular Events)17
Testing for Lp(a)
Building nationwide awareness of the consequences of elevated Lp(a) levels could help to improve the understanding of individual CVD risk. Improved awareness can enhance understanding of population ASCVD risk factors and associated interventions, as well as the CVD risk of family members due to the genetic link. It can also help to inform primary prevention interventions and patient management.
What are the recommendations for Lp(a)?
HEART UK – The UK’s only cholesterol charity
The importance of reducing Lp(a) associated CV risk requires a reappraisal for four main reasons:
- Genetic studies have demonstrated an unequivocal strong link between genes associated with increased Lp(a) and CV risk and as well as the protective effect of LPA null alleles or other strongly Lp(a)-decreasing alleles and CVD risk;
- New insights into Lp(a) assay methodology suggest that inaccurate quantitation of Lp(a) has led historically to its underestimation as a cardiovascular risk factor;
- Lp(a) contributes to aortic valve calcification and;
- The emergence of pipeline therapies for reducing Lp(a) levels.5
Positioning in wider cardiovascular disease policy
Improving ASCVD outcomes is one of the key ambitions within the NHS Long Term Plan.13
The prevention and treatment of CVD and its major risk factors, including obesity, is listed as one of the seven great healthcare challenges in the Life Sciences Vision (LSV).14
ICSs have been instructed to develop joint delivery plans with NHS England to tackle the biggest preventable diseases, starting with CVD.15
Lp(a) Taskforce16
The Lp(a) Taskforce is a diverse multi-stakeholder group that has been constituted to recognise Lp(a) as a key risk factor for ASCVD and to raise awareness of the value of screening for Lp(a) in routine clinical practice to improve ASCVD management.
Chaired by HEART UK, the Lp(a) Taskforce comprises members from across the lipid and cardiovascular disease community in the UK. This includes representation from the Association of Clinical Biochemistry and Laboratory Medicine, British Cardiovascular Society, British Atherosclerosis Society, Royal College of Pathologists, Royal Society of Medicine, UK NEQAS, WEQAS, Novartis Pharmaceuticals, Amgen, Roche Diagnostics and Randox Biosciences.
The Taskforce is calling for the inclusion of Lp(a) in the next update to the National Institute for Health and Care Excellence (NICE) clinical guideline, ‘Cardiovascular disease: risk assessment and reduction, including lipid modification’ (CG181)*.
* This is now called NG238
References:
- Enas EA, et al. Indian Heart J. 2019 Mar-Apr;71(2):99-112.
- Reyes-Soffer et al. Arteriosclerosis, Thrombosis, and Vascular Biology. 2022;42:e48–e60.
- Kenet G, et al. Circulation. 2010 Apr 27;121(16):1838-47.
- Kronenberg F, et al. Eur Heart J. 2022 Oct 14;43(39):3925-3946.
- Cegla J, et al. Atherosclerosis. 2019. 291:62-70
- Nissen SE, et al. Open Heart. 2022 Oct;9(2):e002060.
- Tsimikas S. J Am Coll Cardiol. 2017;69:692-711;
- Erqou S et al. JAMA. 2009;302(4):412-23;
- Kamstrup PR et al. JAMA. 2009;301(22):2331-9;
- Clarke R et al. N Engl J Med. 2009 ;361(26):2518-28;
- Kronenberg F, et al. Eur Heart J. 2022;43(39):3925–3946
- Vinci P, et al. Int J Environ Res Public Health. 2023 Sep 6;20(18):6721.
- NHS England. NHSLong-TermPlan.January2019. Available at https://www.longtermplan.nhs.uk/wp-content/uploads/2019/08/nhs-long-term-plan-version-1.2.pdf [Accessed July 2024]
- Department for Business, Energy and Industrial Strategy. Life Sciences Vision. July 2021. Available at: https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1013597/life-sciences-vision-2021.pdf [Accessed July 2024]
- Department of Health and Social Care. Health and Social Care Secretary speech on Health Reform. March 2022. Available at https://www.gov.uk/government/speeches/health-and-social-care-secretary-speech-on-health-reform [Accessed July 2024]
- Lp(a) Taskforce. A call to action from the Lipoprotein(a) Taskforce. Available from: https://www.heartuk.org.uk/downloads/health-professionals/a-call-to-action-from-the-lipoprotein(a)-taskforce---august-2023.pdf [Accessed July 2024]
- Madsen CM, et al. Arterioscler Thromb Vasc Biol. 2020;40(1):255–266
UK | July 2024 | 443356