Lipoprotein(a) levels can guide CV risk assessment and treatment
Lipoprotein(a) is an independent risk factor for atherosclerotic cardiovascular disease–related events, and plasma levels of Lp(a) could help refine risk assessment and influence treatment decisions, say the authors of a scientific statement from the National Lipid Association.
Don P. Wilson, MD, of Cook Children’s Medical Center, Fort Worth, Tex., and coauthors reviewed the evidence around testing of Lp(a) in clinical practice and its use in guiding treatment for both primary and secondary prevention. Their report is in the Journal of Clinical Lipidology.
Prospective, population-based studies point to a clear link between high Lp(a) levels and high risk of myocardial infarction, coronary heart disease, coronary artery stenosis, carotid stenosis, valvular aortic stenosis, ischemic stroke, cardiovascular mortality, and all-cause mortality, the authors wrote. This association was independent of the effect of other risk factors, including LDL cholesterol.
However, existing Lp(a) assays have not been globally standardized, and there is only incomplete evidence for age, sex, or ethnicity-specific cutoff points for high risk.
The authors suggested Lp(a) levels greater than 50 mg/dL (100 nmol/L) could be considered a risk factor that justifies the initiation of statin therapy. However ,they pointed out this level corresponded to the 80th population percentile in predominantly white populations, while in African American populations the equivalent cutoff was around 150 nmol/L.
On the issue of whom to test for Lp(a) serum levels, the authors said testing could reasonably be used to refine risk assessment for atherosclerotic cardiovascular disease in adults with first-degree relatives who experienced premature atherosclerotic cardiovascular disease, those with a personal history of the disease, or in those with severe hypercholesterolemia or suspected familial hypercholesterolemia.
However, statin therapy does not decrease Lp(a) levels, and there is also evidence that patients with high Lp(a) levels may not show as much LDL-C lowering in response to statin therapy.
“There is a lack of current evidence demonstrating that lowering Lp(a), independently of LDL-C, reduces ASCVD events in individuals with established ASCVD,” the authors wrote. “It appears that large absolute reductions in Lp(a) may be needed to demonstrate a significant clinical benefit.”
Despite this, the authors argued that in primary prevention, it was reasonable to use a Lp(a) level greater than 50 mg/dL (100 nmol/L) as a “risk-enhancing factor,” and in high-risk or very-high-risk patients with elevated LDL-C, it could prompt use of more intensive therapies.
Five authors disclosed honorarium or advisory board positions with the pharmaceutical sector. No other conflicts of interest were declared.
SOURCE: Wilson D et al. J Clin Lipidol. 2019 May 17. doi: 10.1016/j.jacl.2019.04.010.
