Lipid experts say there is a strong case for a Medicare item to reimburse testing for lipoprotein (a) because of its unique role as an independent risk factor for cardiovascular disease.
Associate Professor David Sullivan, a clinical biochemist at the Royal Prince Alfred Hospital, Sydney, told the national conference of the Royal College of Pathologists of Australasia (RCPA) that there would be great benefit from making Lp (a) level testing available to clinicians because it was pro-atherogenic, pro-inflammatory and pro-thrombotic and testing would provide diagnostic and prognostic information to clinicians beyond that of traditional lipid measures such as LDL-cholesterol.
Speaking at the Pathology Update 2022 meeting in Sydney, Dr Sullivan said he was part of a group working on an application to the Medicare Services Advisory Committee aiming to make Lp (a) testing available for some target groups.
He explained that Lp (a) was an LDL particle attached to an apolipoprotein whose primary role in the body was as a transporter of oxidised phospholipids. It was predominantly under genetic control, highly prone to deposition in the arterial wall and its levels were not influenced by current lipid treatments such as statins. Its other properties also made it an independent risk factor for aortic stenosis and venous thrombosis, he noted.
Dr Sullivan said that while Lp (a) was seen as a superior measure of cardiovascular risk compared to LDL-cholesterol levels, it was not likely to replace it in assessment of cardiovascular risk in the near future.
“We would lose a lit bit if we moved away from traditional lipid measurement because they have almost become the standard currency, like the US dollar. I think we’re doing reasonably well in most scenarios with non-HDL cholesterol,” he said.
And while some researchers were already suggesting it could be used as a universal screening tool in the population or for assessing people who were resistant to current therapies, Dr Sullivan said the Medicare application would focus on use as an initial cardiovascular risk assessment in select groups.
“I think you could make a good case for testing patients who have the need for cardiovascular assessment, either on the basis of a family history of premature coronary disease or personal history — or those who are estimated to be at intermediate risk of cardiovascular disease,” he said.
The results could be used to guide decisions on intensified risk factor management, and in the near future there are expected to be agents available that will lower Lp (a) levels he added.
While Lp (a) levels may be modified by agents such as niacin and PSCK9 inhibitors such as evolocumab, a phase 3 trial — the HORIZON study — is currently underway to assess the effect of an antisense therapy pelacarsen that inhibits the production of apolipoprotein (a) in the liver to target elevated Lp (a) levels.
“[But] it can still make a useful contribution even if we don’t have Lp (a) lowering therapies because we will do a better job of recognising the at-risk population and targeting them for treatment,” he said.
Dr Sullivan said an Australian Atherosclerosis Society working group was already looking at the thresholds of Lp (a) that would be used to define low, medium and high risk. Because it was an LDL-based particle with variable mass, the measures would likely be in millimoles, he said, and the working group was also looking at data on how Lp (a) levels could be combined with other measures such as coronary calcium scores to further clarify cardiovascular risk in a precision medicine approach.
“The diagnostic, prognostic and therapeutic implications do warrant a Medicare schedule reimbursement,” he told the meeting.
“Targeting the whole population I think is going to be unacceptable for a variety of reasons. There’s a tradition of starting small and I think the challenge for us is to identify those patients who would derive the most benefit from Lp (a) testing, those most at need,” he concluded.