Position Statement Provides Guidance on the Management of Adults Patients with Elevated Lipoprotein(a).
Summary provided by Dr Natalie C. Ward
Elevated lipoprotein (a) [Lp(a)] is now recognised as an independent and causative risk factor for atherosclerotic cardiovascular disease and calcific aortic valve disease, according to the recently released Australian Atherosclerosis Society Position Statement. Elevated Lp(a) is known to be strongly associated with an increased risk of myocardial infarction, stroke, peripheral artery disease, heart failure and cardiovascular mortality. Predominantly determined by genetics, approximately 1 in 5 people have elevated Lp(a) levels, making it the most common inherited monogenic cause of coronary artery disease. In Australia and New Zealand, translating to approximately 5.1 and 1 million people, respectively, which may be further influenced by the multicultural make up of both countries. There is currently limited data available on elevated Lp(a) in Aboriginal, Torres Strait Islander and Māori populations.
It is a continuous relationship between Lp(a) concentration and cardiovascular risk; and it is now recognised that Lp(a) levels >100 nmol/L (>50 mg/dL) are indicative of high-risk within Caucasian populations. While no treatments specifically targeting Lp(a) are currently clinically available, measurement of Lp(a) should be conducted via selective screening of high-risk individuals, to assess and stratify risk. Diet and lifestyle interventions do not have any direct effect on Lp(a) levels, however reduction of all modifiable risk factors, particularly low-density lipoprotein cholesterol (LDL-C) levels via the initiation or intensification of preventative treatments, is crucial for reducing overall cardiovascular risk in both primary and secondary prevention.
Although there are limitations regarding the measurement of Lp(a), methodological advances including the development of assays that are less sensitive to apo(a) isoforms, and standardised reference material have improved its assessment. Other conditions, including impaired renal function, hypothyroidism, menopause, and inflammatory conditions can also impact Lp(a) concentrations. While the focus of this Position Statement is on adults, it is important to note that in children, Lp(a) concentrations vary throughout childhood, only appearing to plateau at 15 years of age. This is particularly relevant when considering cascade testing of relatives of individuals with elevated Lp(a). To assist with implementing measurement of Lp(a) a Medicare Benefits Schedule item for testing and an ICD-10 code for elevated Lp(a) should be established and approved.
The implementation of Lp(a) assessment into routine clinical practice for the prevention of cardiovascular disease will require multiple approaches. Cardiovascular risk calculators incorporating Lp(a) should be developed and validated to improve risk assessment. Patients identified as having elevated Lp(a) should be appropriately referred and have access to consumer-friendly resources that support and communicate the implications of this risk factor. While treatment options are currently limited, personalised care plans are needed to stress the importance of adherence to management of behavioural risk factors and preventative medications targeting modifiable risk factors including hypercholesterolaemia, hypertension, obesity, and diabetes. Advocacy groups of patients and relevant stakeholders also have an important role to play.
By Natalie C. Ward, Gerald F. Watts and David R. Sullivan
Weblink: https://www.heartlungcirc.org/article/S1443-9506(22)01231-8/pdf