# Distribution of lipoprotein (a) levels in patients with lower extremity artery disease and their impact on amputation and survival: a retrospective study

**Authors:** Katrin Gebauer, Nasser M. Malyar, Julian Varghese, Holger Reinecke, Tobias J. Brix, Christiane Engelbertz

PMC · DOI: 10.1186/s12944-025-02542-5 · Lipids in Health and Disease · 2025-04-02

## TL;DR

This study examines how elevated lipoprotein (a) levels affect outcomes in patients with lower extremity artery disease and finds that aggressive lipid-lowering therapy does not increase amputation or mortality risks.

## Contribution

The study provides new insights into the impact of elevated Lp(a) levels and aggressive lipid-lowering therapy on outcomes in lower extremity artery disease patients.

## Key findings

- Elevated Lp(a) levels were found in 32% of patients, with 16% having values above 90 mg/dL.
- Aggressive lipid-lowering therapy achieved LDL-C targets in most patients without increasing amputation or mortality risks.
- Patients with higher Lp(a) levels received more intensive lipid-lowering treatments like statins and ezetimibe.

## Abstract

Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival.

Baseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30–90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed.

Of 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values ≥ 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL, p = 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%, p = 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%, p = 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%, p = 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%, p = 0.729), amputations (4% vs. 7% vs. 0%, p = 0.245) and death (8% vs. 5% vs. 3%, p = 0.436).

Aggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels.

The online version contains supplementary material available at 10.1186/s12944-025-02542-5.

## Linked entities

- **Proteins:** LPA (lipoprotein(a)), COG2 (component of oligomeric golgi complex 2)

## Full-text entities

- **Diseases:** LEAD (MESH:D002539), death (MESH:D003643)
- **Chemicals:** agents (-), Lipid (MESH:D008055), ezetimibe (MESH:D000069438)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

3 references — full list in the complete paper: https://tomesphere.com/paper/PMC11963429/full.md

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Source: https://tomesphere.com/paper/PMC11963429