Lipoprotein(a) and referrals to a specialist lipid clinic

Background Lp(a) is raised in approximately 1 in 5 of the population. Thresholds indicating a raised Lp(a) level vary; >70nmol/L for our assay, >125nmol/L in some studies; with a level >430nmol/L described in guidance as conferring a ASCVD risk equivalent to heterozygous familial hypercholesterolemia (hFH). Higher Lp(a) levels increase measured LDL level.[1] This may lead to increased referrals to a specialist lipid clinic and increased testing for hFH. Purpose To determine if raised Lp(a) levels are reflected in referrals as well as downstream investigations and treatment. Methods An ethically approved retrospective cohort study was performed including consecutive adult patients attending a specialist lipid clinic over a six-month period. Patient data analyzed included demographics, clinical characteristics, treatments and biochemical profiles. Those with a level >70nmol/L were considered to have raised Lp(a). Groups were compared using Chi-squared tests and t-tests. Results 330 patients had a Lp(a) result available. 39% had a Lp(a) level >70nmol/L, 33% with >125nmol/L and 5% with >430nmol/L [Figure 1]. 55% of those with a Lp(a) >70nmol/L were female and their mean age was 49 years (SD+/-13), both consistent with the cohort as a whole. The percentages referred due to ‘high cholesterol’ or ‘assessment for familial hypercholesterolemia’ was equivalent for the raised versus normal Lp(a) groups (50% v 47%; p=0.42). The groups were also similar in terms of; family history of early CVD (40% each), baseline cholesterol levels (8.2 v 7.8mmol/L; p=0.12), baseline LDL levels (5.7 v 5.5mmol/L; p=0.34), genetic testing for hFH (61% v 58%; p=0.59), positive hFH genotypes (17% v 21%; p=0.57) and treatment with a high-intensity statin (34% v 30%; p=0.26). Conclusions The high proportion of patients with raised Lp(a) in this cohort indicates raised Lp(a) increases the likelihood of referral to a lipid clinic. While limited by the moderate cohort size, increased levels were not reflected by differences in reasons for referral, baseline cholesterol levels, tests for hFH or treatment. Cohort stratified by Lp(a) level.