# PCSK9 inhibitors in real life—Cardiometabolic risk management in dyslipidemic patients in Vienna

**Authors:** M Ferch, C Sert, P Fellinger, A Kautzky-Willer, Y Winhofer-Stöckl

PMC · DOI: 10.1007/s00508-024-02402-9 · Wiener Klinische Wochenschrift · 2024-08-13

## TL;DR

This study shows that PCSK9 inhibitors effectively lower LDL cholesterol in patients in Vienna, especially when used with statins.

## Contribution

The study provides real-world evidence of PCSK9 inhibitors' effectiveness and sustainability in routine clinical practice.

## Key findings

- 44.9% of patients reached their LDL-C target after about 14 months of PCSK9 inhibitor treatment.
- Patients on statins had a higher success rate (51.0%) compared to non-users (22.7%).
- LDL-C levels decreased significantly and remained stable over 14 months.

## Abstract

Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors have emerged as important therapeutic options for patients unable to achieve the low-density lipoprotein cholesterol (LDL‑C) target or to tolerate alternative lipid-lowering agents. The aim of this study was to investigate the efficacy of PCSK9 inhibitor treatment in tertiary routine care, by determining the percentage of patients reaching individual LDL‑C target levels 1 year after treatment initiation.

Patients routinely started on PCSK9 inhibitors at our lipid clinic between 2017 and 2020 were retrospectively analyzed. Attainment of the LDL‑C target, utilization of follow-ups, cardiovascular events and effects on laboratory parameters were investigated.

In this study 347 patients were included, with the majority managed in secondary prevention (94.5%). The LDL‑C target was achieved by 44.9% after ca. 14 months, with differences between statin users and non-users (51.0% vs. 22.7%; p < 0.001). The median LDL‑C decreased from 126.00 mg/dL at baseline to 48 mg/dL (−61.6%; −77.00 mg/dL; p < 0.001) after ~2 months and to 60 mg/dL (−52.9%; −59.00 mg/dL; p < 0.001) after ~14 months. Median lipoprotein(a) levels decreased significantly from 184.0 nmol/L to 165.5 nmol/L (−25.9%; −25.5 nmol/L; p = 0.001) after ~2 months, whereas no effects on creatine kinase, amylase and lipase were detectable. Of the patients 15% utilized 4 follow-ups. The PCSK9 inhibitor intolerance occurred in 3.5% of patients.

With the effect of LDL-lowering remaining constant over 14 months, PCSK9 inhibitor treatment showed effective and sustainable LDL‑C lowering in a majority of patients in secondary prevention, bringing them closer to the recommended LDL‑C goal, particularly those under concomitant statin medication. Treatment with PCSK9 inhibitors appears to be well-tolerated, confirming data from clinical trials in real life.

The online version of this article (10.1007/s00508-024-02402-9) contains supplementary material, which is available to authorized users.

## Linked entities

- **Proteins:** PCSK9 (proprotein convertase subtilisin/kexin type 9)
- **Diseases:** dyslipidemia (MONDO:0002525)

## Full-text entities

- **Genes:** PCSK9 (proprotein convertase subtilisin/kexin type 9) [NCBI Gene 255738] {aka FH3, FHCL3, HCHOLA3, LDLCQ1, NARC-1, NARC1}
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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Source: https://tomesphere.com/paper/PMC12081568