Appeal type: Experimental
Decision: Insurer Denial Overturned

Summary Reviewer 3 
A 48-year-old male enrollee has requested reimbursement for laboratory testing on 12/2/22. The Health 
Insurer has denied this request and reported that services at issue were investigational for the 
evaluation of the enrollees premature coronary artery disease and hyperlipidemia. The physician 
reviewer found that the elevated lipoprotein(a) is causally implicated in ASCVD, and testing in specific 
patients may help to tailor the appropriate intensity of preventive measures. Khera and colleagues 
found that lipoprotein(a) is a strong predictor of risk when it remains high in patients who are already on 
statin. Select patients that may benefit from lipoprotein(a) testing after a shared decision-making 
discussion include individuals with premature CAD with the absence of traditional risk factors. The 
results of testing in these patients may trigger an escalation of therapy. Lipoprotein(a) testing may be 
reasonable in patients with recurrent or progressive ASCVD despite adequate control of other risk 
factors. Lipoprotein(a) testing may be generally recommended for patients with a personal history of 
premature cardiovascular disease, recurrent cardiovascular disease while on statin therapy, and a 
greater or equal to 10% ten-year risk of cardiovascular disease. The primary reason for screening 
patients for lipoprotein(a) is to help further identify those at high risk for heart disease, especially in the 
absence of other major risk factors and to help identify those patients who may require more intensive 
lipid therapy. Patients with significantly elevated lipoprotein(a) should generally be treated to a target of 
less than 50mg/dl. There is a lack of randomized controlled trials on if targeted lowering of 
lipoprotein(a) improves clinical outcomes. Studies on the lipoprotein(a) lowering effect of currently 
available therapies are ongoing, and there is currently no targeted treatment to lower lipoprotein(a) as 
neither lifestyle therapy nor statin therapy impacts lipoprotein(a) levels. One treatment option is daily 
niacin, which may lower lipoprotein(a) by 20% to 30%. However, niacin has not been associated with 
improved cardiac outcomes despite its known beneficial effect on all lipid markers as well as 
lipoprotein(a). Statins have shown mixed results and, in some cases, have actually been shown to 
increase lipoprotein(a). PCSK9 inhibitors lower lipoprotein(a), but the contribution of lipoprotein(a) 
reduction to reduced ASCVD risk is undetermined. Lipoprotein apheresis lowers lipoprotein(a) and is  selectively used for patients with elevated lipoprotein(a) and recurrent ASCVD events regardless of LDL 
levels. Antisense oligonucleotides are undergoing investigation as a novel lipoprotein(a) targeting 
treatment. Sabatine and colleagues report that the addition of a PCSK9 inhibitor reduced lipoprotein(a) 
levels by 27% and resulted in a reduction in major adverse cardiovascular events (MACE). Schwartz and 
colleagues report that a PCSK9 inhibitor had increased MACE reduction in individuals with higher 
baseline lipoprotein(a) levels. In this case, given that the lipoprotein(a) testing would have aided in 
determining if the patient requires more advanced therapy, such as with PCSK9 inhibitor, the service at 
issue was likely to have been more beneficial for the evaluation of the patient than standard laboratory 
testing. Therefore, laboratory testing on 12/2/22 was likely to have been more beneficial for the 
evaluation of the patients condition than any available standard therapy.