# Predictive value of HPSE for major adverse cardiovascular events in patients with ST-segment elevation myocardial infarction

**Authors:** Wenyan Liu, Zonghu Jia, Bin Li, Yuhong Hu, Xuechao Tang, Zhen Li, Ruimin Chen, Zheng Wang, Shuo Yang, Zhenyu Niu, Shufang Han, Qun Jin

PMC · DOI: 10.3389/fcvm.2026.1743115 · Frontiers in Cardiovascular Medicine · 2026-02-12

## TL;DR

High levels of HPSE in coronary blood predict major cardiovascular events in patients with heart attacks, improving risk assessment.

## Contribution

HPSE is shown as an independent predictor of MACE in STEMI patients, enhancing the GRACE score's predictive power.

## Key findings

- STEMI patients with MACE had significantly higher coronary HPSE levels (5.08 ng/mL vs. 3.68 ng/mL).
- HPSE remained an independent predictor of MACE after adjusting for risk factors (HR = 1.693).
- Combining HPSE with the GRACE score improved MACE prediction (AUC = 0.849).

## Abstract

Although early mortality rates have decreased following reperfusion therapies such as percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI), they remain at risk for major adverse cardiovascular events (MACE). Heparanase (HPSE) is an endogenous β-D-glucuronosidase and plays a key role in inflammation and vascular remodeling. This study investigated the predictive value of HPSE for MACE after STEMI.

This prospective observational study included 207 consecutive STEMI patients who received primary PCI. Coronary blood was collected 10 min after balloon dilation. Coronary HPSE levels were measured by enzyme-linked immunosorbent assay (ELISA). Patients were followed for 6 months to record the occurrence of MACE.

During the 6-month follow-up period, 53 patients (25.6%) experienced MACE. Patients who experienced MACE had significantly higher coronary HPSE levels than those without (5.08 ± 1.27 ng/mL vs. 3.68 ± 1.20 ng/mL, P < 0.001). In multivariate Cox regression analysis, after adjusting for established risk factors, elevated HPSE levels remained an independent predictor of MACE (HR = 1.693, 95% CI: 1.323–2.165, P < 0.001). ROC analysis showed that a combined HPSE and GRACE model predicted MACE with an AUC of 0.849 (95% CI: 0.787-0.911, P < 0.001). Kaplan–Meier analysis revealed significantly lower MACE-free survival in the high HPSE group (log-rank P < 0.001).

Coronary HPSE is an independent predictor of 6-month MACE in STEMI patients. It also enhances the predictive capability of the GRACE score. Because of this, HPSE serves as a promising biomarker that can help doctors assess risk more accurately and guide clinical decisions.

## Linked entities

- **Proteins:** HPSE (heparanase)
- **Diseases:** ST-segment elevation myocardial infarction (MONDO:0041656)

## Full-text entities

- **Genes:** Hpse (heparanase) [NCBI Gene 15442] {aka HSE1, Hpa, Hpr1}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, HPSE (heparanase) [NCBI Gene 10855] {aka HPA, HPA1, HPR1, HPSE1, HSE1}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, TNNI3 (troponin I3, cardiac type) [NCBI Gene 7137] {aka CMD1FF, CMD2A, CMH7, RCM1, TNNC1, cTnI}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}
- **Diseases:** acute myocardial injury (MESH:D056486), ventricular remodeling (MESH:D020257), heart disease (MESH:D006331), HS (MESH:D009084), infarct (MESH:D007238), heart failure (MESH:D006333), ventricular fibrillation (MESH:D014693), ventricular tachycardia (MESH:D017180), myocardial necrosis (MESH:D009336), atherosclerosis (MESH:D050197), microvascular damage (MESH:D017566), MIRI (MESH:D015427), thrombosis (MESH:D013927), Acute or chronic infectious disease (MESH:D013969), atrioventricular block (MESH:D054537), coronary artery occlusion (MESH:D054059), AMI (MESH:D009203), Cardiovascular Diseases (MESH:D002318), cardiomyopathy (MESH:D009202), Chest Pain (MESH:D002637), ST-segment elevation myocardial infarction (MESH:D000072657), autoimmune (MESH:D001327), arrhythmias (MESH:D001145), bleeding (MESH:D006470), neurological disorders (MESH:D009461), ischemia (MESH:D007511), acute coronary syndromes (MESH:D054058), inflammation (MESH:D007249), hepatic insufficiency (MESH:D048550), angina (MESH:D000787), edema (MESH:D004487), psychiatric (MESH:D001523), renal insufficiency (MESH:D051437), valvular heart disease (MESH:D006349), cancer (MESH:D009369)
- **Chemicals:** LDL-C (-), HS (MESH:D006497)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

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## References

30 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935887/full.md

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Source: https://tomesphere.com/paper/PMC12935887