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PCSK9 inhibition

Aggressive lipid-lowering achieved similar LDL-C targets regardless of Lp(a) level in 263 peripheral artery disease patients, with no excess amputation or death at high Lp(a) (Lipids Health Dis 2025)

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

Lipids Health Dis · · 6

Gebauer K, Malyar NM, Varghese J, Reinecke H, Brix TJ, Engelbertz C

This retrospective study examined 263 patients with lower extremity artery disease treated at a tertiary hospital between 2017 and 2022, grouped by Lp(a) (below 30, 30-90, above 90 mg/dL), to assess aggressive lipid-lowering therapy's impact on amputation and survival. Elevated Lp(a) (30 mg/dL or above) was present in 32%, and 16% had levels above 90 mg/dL. Baseline LDL-C fell from 89 to 61 mg/dL at follow-up with no difference between Lp(a) groups, though those with elevated Lp(a) more often had statin intensification (16% vs. 35% vs. 33%, P = 0.005), added ezetimibe (50% vs. 58% vs. 73%, P = 0.028), and added PCSK9 inhibitors (2% vs. 3% vs. 8%, P = 0.043). No significant differences were seen in revascularisation, amputation, or death across Lp(a) groups. The authors conclude aggressive lipid-lowering achieved LDL-C targets in high-risk patients with elevated Lp(a) regardless of level, without an observed increase in amputation or death at high Lp(a).

Read the paper (DOI)PubMed

Original abstract

Background: 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.

Methods: 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.

Results: 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).

Conclusions: 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.

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Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.