Does routine measurement of lipoprotein(a) in a UK lipid clinic alter management in the absence of Lp(a)-specific therapy?

BACKGROUND: Elevated lipoprotein(a) [Lp(a)] is an inherited, causal risk factor for atherosclerotic cardiovascular disease (ASCVD). Despite guideline endorsement, its measurement is inconsistently adopted within the UK healthcare setting. Understanding whether identifying raised Lp(a) alters real-world management and lipid outcomes is key to guiding policy. OBJECTIVE: To evaluate the distribution of Lp(a) levels in a UK lipid clinic, quantify management changes across clinically relevant thresholds and explore the relationship between Lp(a) and final non-HDL-cholesterol (non-HDL-C) attainment. METHODS: This retrospective observational study included 337 patients attending a specialist lipid clinic. Demographics, atherosclerotic cardiovascular (ASCVD) disease status, HEART UK Lp(a) testing criteria, management actions, and final non-HDL-C values were analyzed. Lp(a) concentrations were initially grouped into five descriptive categories (<30, 30-49, 50-89, 90-179, and ≥180 mg/dL) for baseline characterization. For management-change analyses, categories <50 mg/dL were combined to reflect the ESC/EAS-defined threshold for elevated Lp(a), which served as the clinical reference point for assessing management impact. RESULTS: Management changes were observed in 3.5% of patients with Lp(a) < 50 mg/dL, 56% with 50-89 mg/dL, and 79% and 83% of those with 90-179 mg/dL and ≥180 mg/dL, respectively. Interventions involved medication up-titration, reinforcement of lifestyle measures, or strengthened clinical emphasis on the importance of lifelong lipid-lowering therapy. Family cascade screening was initiated exclusively among patients with Lp(a) ≥ 90 mg/dL, representing around one-third of this subgroup. Mean final non-HDL-C increased with Lp(a) category, while target attainment (<2.5 mmol/L) declined, likely reflecting the biochemical contribution of Lp(a)-cholesterol to the non-HDL-C fraction rather than suboptimal management. CONCLUSIONS: Routine Lp(a) testing meaningfully alters management and reveals a form of residual dyslipidaemia resistant to standard therapy. These findings, combined with recent cost-effectiveness modelling showing NHS and societal savings from one-time testing, support incorporation of Lp(a) measurement into universal cardiovascular risk assessment.