When should Lipoprotein(a) be measured?

To the Editor

We read with interest the paper by Cegla et al. entitled “Lp(a): When and how to measure it”. ¹ We appreciate the information presented in this recent article, because the Lp(a) field is under extensive investigation with the arrival of specific Lp(a)-lowering therapies.

In the section “When should Lp(a) be measured?”, the authors refer to the Hyperlipidaemia Education and Atherosclerosis Research Trust United Kingdom (HEART UK) recommendations to perform Lp(a) measurement in five specific groups: (1) those with a personal or family history of premature atherosclerotic cardiovascular disease (CVD) (<60 years of age); (2) first degree relatives of those with high Lp(a) plasma concentrations (>200 nmol/L); (3) familial hypercholesterolaemia, or other genetic forms of dyslipidaemia; (4) calcific aortic valve stenosis; (5) those with a borderline increased (but <15%) 10-year risk of a cardiovascular event. ² In addition to these recommendations, we suggest that the recent European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) Guidelines for Management of Dyslipidaemias ³ should have been also mentioned in this manuscript.

The ESC/EAS guidelines are widely used in Europe and apply the Systematic Coronary Risk Estimation (SCORE) 10-year risk of fatal CVD. These have charts for low-risk regions including the UK. These guidelines recommend Lp(a) measurement at least once in each adult person’s lifetime to identify those with very high inherited Lp(a) levels >430 nmol/L, whose lifetime risk of atherosclerotic CVD is comparable to that of heterozygous familial hypercholesterolaemia. ³

We measured Lp(a) in 54 young adults (age range 18 years to 40 years) with type 1 diabetes (T1D) and without previous cardiovascular events who were being monitored in our unit. Our aim was to evaluate the Lp(a) levels in nmol/L and classify the CVD risk conferred by Lp(a) in this population. It is known that young adults with T1D still experience an increased cardiovascular morbidity and mortality rate despite an improved CVD risk factor management. ⁴ Results are presented as median values (25–75 percentiles). Of the total, 64.6% (34) patients were male, with median age of 29.5 (26.8-37.0) years, median T1D duration of 12.5 (5.8-20.0) years and median HbA1c of 7.4% (7.1–8.8%). Median Lp(a) levels was 17.0 (6.0-39.0) nmol/L, with a minimum of 6 and a maximum of 251 nmol/L.

According to CVD risk based on Lp(a) percentile distributions,^2,5 16.7% (nine) individuals were reclassified to minor CVD risk (Lp(a) 32–90 nmol/L), 7.4% (four) to moderate risk (90–200 nmol/L) and 5.6% (three) to high risk (200–400 nmol/L). However, no patient had Lp(a) >400 nmol/L associated with very high risk.

On the other hand, 11.1% (six) patients had high Lp(a) levels (>120 nmol/L), the cut-off considered as a clinical pertinent risk level by ESC/EAS Guidelines and in T1D.^6,7 The prevalence of high Lp(a) >120 nmol/L was similar to that reported in the largest study of Lp(a) in T1D (16.3%). ⁷ Among patients not treated with lipid-lowering drugs, Lp(a) was high in 6.3% (3/48) individuals.

In conclusion, either the HEART UK ² or the ESC/EAS ³ recommendations for Lp(a) measurement identified individuals with high risk in this young population. Adding Lp(a) measurement to routine clinical practice may improve their CVD risk assessment and prevention, justifying intensive treatment from an early age.