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Protective effects of combined eptifibatide and ticagrelor in patients with unstable angina undergoing percutaneous coronary intervention: a single-center experience

BMC Cardiovascular Disorders volume 25, Article number: 312 (2025) Cite this article

Abstract

Background

We evaluated the safety and effectiveness of combined eptifibatide and ticagrelor in patients with unstable angina pectoris undergoing percutaneous coronary intervention (PCI).

Methods

Patients with unstable angina pectoris who underwent PCI from January 2019 to December 2020 were included. All patients were treated with aspirin and ticagrelor as dual antiplatelet therapy and divided into two groups: the eptifibatide + ticagrelor group (180 µg/kg bolus plus 1 µg/kg/min continuous intravenous eptifibatide infusion after PCI for 24 h [n = 152]) and the ticagrelor group (without eptifibatide infusion [n = 152]). Thromboelastography and light transmission aggregometry were used to measure the adenosine diphosphate-induced platelet aggregation rate (PAR). High sensitivity troponin T (hs-TnT), N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (hs-CRP), and heart-type fatty acid-binding protein (h-FABP) were measured. In-hospital and 12-month major adverse cardiovascular events (MACEs) and bleeding events were evaluated.

Results

The PAR significantly declined at 1, 12, and 24 h after continuous intravenous eptifibatide and returned to the pretreatment level 24 h after discontinuation. All patients in the eptifibatide + ticagrelor group achieved a PAR < 10%. The percentage of patients with a PAR < 10% was significantly higher than in the ticagrelor group (P < 0.001). The increases in hs-TnT (P < 0.001), NT-proBNP (P < 0.05), and h-FABP (P < 0.05) were less pronounced. The eptifibatide + ticagrelor group exhibited lower rates of in-hospital and 12-month myocardial infarction (MI) and in-hospital MACEs (P < 0.05). The rate of bleeding events was not significantly different.

Conclusion

Eptifibatide rapidly reduced the PAR in patients with unstable angina pectoris and reduced the rates of MI, in-hospital MACEs, and 12-month MI, without increasing bleeding events. The combined use of eptifibatide and ticagrelor was safe and effective.

Trial registration

The registry was registered in the Chinese Clinical Trial Registry (ChiCTR2500096895). The date of registration was 2025-02-08, and it was “Retrospectively registered”.

Peer Review reports

Introduction

Coronary artery disease (CAD) is the leading cause of death worldwide. Revascularization is an optimal treatment option for CAD; however, revascularization procedures, such as percutaneous coronary intervention (PCI), can cause further damage to the coronary artery endothelium, activate platelets, and increase the risk of PCI-related myocardial injury [1]. Antiplatelet drugs are important treatments for patients with CAD, with ticagrelor being one of the preferred options for patients with acute coronary syndrome (ACS) owing to its strong antiplatelet effect [2]. The degree of platelet inhibition with antiplatelet drugs is related to major adverse cardiovascular events (MACEs) following PCI. Specifically, greater platelet inhibition is associated with a lower incidence of adverse cardiovascular events and confers great clinical benefit [3]. Recent antithrombotic therapeutic strategies in patients undergoing PCI focus on personalized antiplatelet therapy. Researchers have shown that P2Y12 inhibitor monotherapy is safe and effective in both complex and non-complex PCI, reducing the bleeding risk without compromising ischemic outcomes. The shift from rigid protocols to dynamic personalized antiplatelet therapy has improved the outcomes of patients with ACS. Balancing ischemic protection and bleeding avoidance requires continuous reassessment based on patient evolution and new evidence [4, 5].

Glycoprotein IIb/IIIa receptor inhibitors (GPIs), such as eptifibatide, block the final pathway of platelet aggregation. Therefore, conventional doses of GPIs combined with ticagrelor are associated with a high bleeding risk [6]. Previous studies have shown that the use of eptifibatide peri-PCI can reduce the incidence of 48-h and 30-day MACEs, with no significant increase in major bleeding. Moreover, eptifibatide administration significantly improves blood flow after PCI and is associated with improved myocardial perfusion [7, 8]. Chinese guidelines (2019) for acute ST-segment elevation myocardial infarction (STEMI) suggest that high-risk patients undergoing coronary artery angiography (CAG) with a heavy thrombosis load and patients who have not been administered an appropriate loading dose of P2Y12 inhibitor should be administered intravenous eptifibatide [9].

In the Platelet Inhibition and Patient Outcomes (PLATO) study, patients had a lower rate of definite stent thrombosis and higher rates of minor and major bleeding with ticagrelor than with clopidogrel, whereas there was no such difference between ticagrelor and clopidogrel after GPI treatment. Although GPIs effectively reduce ischemic events by inhibiting platelet aggregation, their use is significantly associated with an increased risk of bleeding, which remains a major clinical concern. In the ISAR-REACT 2 study, GPIs reduced ischemic events in troponin-positive patients with ACS but increased major bleeding [10]. The European Society of Cardiology 2023 ACS guidelines suggest that GPIs are not recommended for routine upstream use in patients with non-ST elevation-ACS. GPIs may be considered during PCI in cases where there is a high thrombus burden or no reflow [11]. At present, ticagrelor is the main antiplatelet drug for ACS. Owing to its strong effect in platelet inhibition, few studies have evaluated the effects of combined administration of GPIs with ticagrelor versus ticagrelor alone. In this study, we aim to evaluate the safety and effectiveness of combined ticagrelor and low-dose eptifibatide after revascularization by PCI in East Asian patients with unstable angina pectoris.

Methods

Study subjects

In this retrospective observational study, patients diagnosed with unstable angina pectoris who underwent elective PCI from January 2019 to December 2021 at The First Affiliated Hospital of Soochow University, Suzhou, China were enrolled. The selection criteria for unstable angina pectoris were initial angina, worsening exertional angina, and resting angina, with or without ischemia on electrocardiography. The exclusion criteria were (1) positive high-sensitivity troponin T (hs-TnT) at admission (> 5-times the upper limit of normal); (2) thrombocytopenia (platelet count < 50 × 109/L) or a decreased hemoglobin concentration (< 10 g/dL) and not receiving dual antiplatelet therapy (DAPT); and (3) CAG only or PCI failure in the present study.

A total of 304 patients were enrolled. All patients were treated with aspirin (100 mg once daily) and ticagrelor (90 mg twice daily) as DAPT, as well as daily statin therapy, immediately after admission. The patients were divided into two groups by the surgeon. Patients with multivessel lesions or high thrombus burden with a higher ischemic risk were chosen to use eptifibatide. The eptifibatide + ticagrelor group received a 180 µg/kg bolus + 1 µg/kg/min continuous intravenous eptifibatide infusion after PCI for 24 h (n = 152). The ticagrelor group did not undergo eptifibatide infusion (n = 152).

This study was approved by the Institutional Review Board of The First Affiliated Hospital of Soochow University (ethics approval no. 20190025001), and all patients provided written informed consent before participation.

Data collection

All patients underwent routine examinations after hospitalization. Routine blood measurements included hemoglobin, leukocyte, erythrocyte, and platelet measurements; liver and kidney function tests; and blood lipid concentration measurements. Medications were also recorded. After selective coronary revascularization, the number of diseased vessels and the number of implanted stents were recorded. According to the patient’s condition, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, angiotensin receptor/neprilysin inhibitors, β-blockers, and anticoagulation were administered. The study flowchart is presented in Fig. 1.

Fig. 1
figure 1

Study flowchart. CAG: coronary artery angiography; Hb: hemoglobin; hs-TnT: high-sensitivity troponin T; PCI: percutaneous coronary intervention

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Platelet aggregation rate (PAR) assessment

The PAR was assessed to evaluate platelet function. Blood samples were collected from the median cubital vein in sodium citrate anticoagulation tubes. The timepoints for the PAR assessment were prior to eptifibatide infusion; at 1, 12, and 24 h after eptifibatide infusion; and at 24 h after eptifibatide discontinuation. The blood sampling timepoints were the same in the ticagrelor group. The adenosine diphosphate (ADP)-induced PAR was measured by thromboelastography (Haemoscope Corp., US) and light transmission aggregometry (LTA) (Nanjing Xierjian Medical Instrument Co. Ltd., China) according to the respective manufacturer’s instructions. Specifically, thromboelastography and LTA were used to report the platelet inhibition rate, and the platelet inhibition rate was subtracted from 100 to obtain the PAR.

PCI-related myocardial injury

Blood was collected from all patients prior to and at 24 h after PCI to determine the concentrations of hs-TnT, N-terminal pro-brain natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (hs-CRP), and heart-type fatty acid-binding protein (h-FABP). Chemiluminescence and enzyme-linked immunosorbent assays were used, and the detection kits were provided by Nanjing FCMCS Biotechnology Co. Ltd. (China).

Cardiovascular prognosis and bleeding follow-up

The patients were followed up in hospital and at 12 months after discharge to assess adverse cardiovascular events and bleeding. The cardiovascular endpoints included all-cause mortality (primary endpoint), occurrence of myocardial infarction (MI), target vessel revascularization, stent thrombosis, stroke, transient ischemic attack, and overall MACEs. MI included types 1 and 4. Type 1 refers to classic spontaneous MI, and type 4 refers to PCI-related MI. The type of MI was defined according to whether the patient had postoperative chest pain together with hs-TnT > 5-times the upper limit of normal. The Bleeding Academic Research Consortium criteria were used to define the degree of bleeding (8). Minor bleeding was defined as skin bruising, subcutaneous ecchymosis, nosebleed, and bleeding gums, while major bleeding was defined as fatal bleeding, significant bleeding requiring blood transfusion, gastrointestinal bleeding, or intracranial hemorrhage with a hemoglobin decrease of ≥ 3 g/dL. Kaplan–Meier curves were produced for in-hospital and 12-month MACEs, as well as for bleeding events.

Statistical analysis

SPSS 27.0 software was used for the statistical analysis. Measurement data are presented as the mean ± standard deviation (x ± s). The mean values were compared between the groups using the independent-samples t-test after testing the distribution normality of the data using the Kolmogorov–Smirnov test, which revealed that the data were normally distributed. Count data are presented as rates and were compared using the chi-square test. The Kaplan–Meier method was used to produce curves of MACEs and bleeding events. P < 0.05 was considered statistically significant. The data used to support the findings of this study are available from the corresponding author upon reasonable request.

Results

Patients’ clinical characteristics

There were no significant differences in the baseline clinical data between the two groups (Table 1), with the exception of the number of diseased coronary arteries, which was significantly higher in the eptifibatide + ticagrelor group than in the ticagrelor group (P < 0.05).

Table 1 Patients’ baseline characteristics
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Comparison of the PAR

The baseline ADP-induced PAR assessed by thromboelastography was similar between the two groups after DAPT with aspirin + ticagrelor. The PAR declined significantly in the eptifibatide + ticagrelor group at 1, 12, and 24 h (P < 0.001 vs. baseline) after intravenous eptifibatide infusion. Conversely, the PAR in the ticagrelor group remained constant (P > 0.05 vs. baseline). At 24 h after eptifibatide discontinuation, the PAR returned to pretreatment levels (P < 0.001 vs. 12 h) (Fig. 2a). The PAR assessed by LTA showed a similar trend (Fig. 2b). Eptifibatide quickly decreased the PAR and continued to exert inhibitory effects during use. The detailed data on the PAR are shown in Table 2.

Fig. 2
figure 2

Platelet aggregation rate assessment. (a) Platelet aggregation rate measured by TEG. (b) Platelet aggregation rate measured by LTA. Eptifibatide quickly inhibited platelet aggregation. *P < 0.001 vs. baseline; #P < 0.001 vs. ticagrelor group; &P < 0.001 vs. 24 h after eptifibatide discontinuation. LTA: light transmission aggregometry; TEG: thromboelastography

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Table 2 Platelet aggregation rate
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After eptifibatide infusion, all patients (100%) achieved a PAR < 10%. The percentage of patients with a PAR < 10% at baseline (15.7%) and in the ticagrelor group (11.2–17.1%) was significantly lower than after eptifibatide infusion (P < 0.001) (Fig. 3). Thromboelastography showed that the reaction time (R value, Fig. 4A) and kinetics (K value, Fig. 4B) were prolonged, and the α angle (Fig. 4C) and maximum amplitude (MA, Fig. 4D) were decreased in the eptifibatide + ticagrelor group compared with the ticagrelor group (Fig. 4). These results show that eptifibatide + ticagrelor had a stronger effect on reducing platelet aggregation than ticagrelor alone.

Fig. 3
figure 3

Percentage of patients with platelet aggregation of < 10% at different timepoints. *P < 0.001 vs. baseline; #P < 0.001 vs. ticagrelor group; &P < 0.001 vs. 24 h after eptifibatide discontinuation

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Fig. 4
figure 4

The R value and K value were prolonged and the α angle and MA value were decreased in the eptifibatide + ticagrelor group compared with the ticagrelor group. *P < 0.001 vs. ticagrelor group. R value: reaction time; K value: kinetics; MA: maximum amplitude

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PCI-related myocardial injury

The serum concentrations of hs-TnT, NT-proBNP, hs-CRP, and h-FABP in patients prior to and at 24 h after PCI are shown in Fig. 5A and D. There was no significant difference in preoperative serum hs-TnT (51.40 ± 27.51 vs. 53.23 ± 26.12 pg/mL, respectively, P > 0.05), NT-proBNP (395.81 ± 202.09 vs. 391.58 ± 224.62 pg/mL, respectively, P > 0.05), hs-CRP (44.98 ± 21.44 vs. 43.83 ± 18.59 pg/mL, respectively, P > 0.05), or h-FABP (2799.79 ± 1223.05 vs. 2571.65 ± 1133.39 pg/mL, respectively, P > 0.05) between the eptifibatide + ticagrelor group and the ticagrelor group. After PCI, the serum biomarker concentrations increased significantly in both groups. However, the concentrations of hs-TnT (123.04 ± 67.85 vs. 194.82 ± 99.94 pg/mL, P < 0.001), NT-proBNP (1166.07 ± 646.51 vs. 1330.97 ± 695.15 pg/mL, P < 0.05), and h-FABP (4226.13 ± 1824.56 vs. 4755.89 ± 1694.19 pg/mL, P < 0.05) were significantly lower in the eptifibatide + ticagrelor group than in the ticagrelor group (Table 3). These results suggest that eptifibatide infusion reduced PCI-related myocardial injury (Fig. 5).

Table 3 Biochemical markers in the two groups before and after PCI
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Fig. 5
figure 5

Serum hs-TnT, NT-proBNP, hs-CRP, and h-FABP concentrations before and after PCI. Hs-TnT (*P < 0.001) (a), NT-proBNP (*P < 0.05) (b), and h-FABP (*P < 0.05) (d) were significantly lower in the eptifibatide + ticagrelor group than in the ticagrelor group after PCI, while hs-CRP (c) was not significantly different. h-FABP: heart-type fatty acid-binding protein; hs-CRP: high-sensitivity C-reactive protein; hs-TnT: high-sensitivity troponin T; NT-proBNP: N-terminal pro-brain natriuretic peptide; PCI: percutaneous coronary intervention

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Cardiovascular prognosis and bleeding

Cardiovascular prognosis and bleeding were assessed in hospital and at 12 months after discharge. The eptifibatide + ticagrelor group exhibited lower rates of in-hospital MI and MACEs than the ticagrelor group (P < 0.05). The rate of 12-month MI was also lower (P < 0.05). Overall, 12-month MACEs and in-hospital and 12-month bleeding events were not significantly different between the two groups. Patient prognosis and Kaplan–Meier curves for MACEs and bleeding are shown in Fig. 6, and the detailed data are shown in Table 4.

Fig. 6
figure 6

Prognosis evaluation (A) and Kaplan–Meier curves for in-hospital and 12-month MACEs and bleeding events (B-E). The eptifibatide + ticagrelor group had lower rates of in-hospital MACEs (*P < 0.05)

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Table 4 Cardiovascular maces and bleeding
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Discussion

This study revealed several key findings. First, eptifibatide significantly reduced the PAR at 1, 12, and 24 h, which returned to baseline 24 h after eptifibatide discontinuation. Moreover, after eptifibatide infusion, 100% of patients achieved a PAR < 10%. Second, after PCI, the increases in hs-TnT, NT-proBNP, and h-FABP were significantly less pronounced in the eptifibatide group, suggesting that eptifibatide reduced PCI-related myocardial injury. Finally, the group treated with eptifibatide exhibited lower rates of in-hospital and 12-month MI. Moreover, the rate of in-hospital MACEs was lower, while the rate of bleeding events was not significantly different.

Antiplatelet therapy is essential for the treatment of CAD. Ticagrelor rapidly inhibits platelet aggregation in patients with CAD, thus reducing the incidence of cardiovascular events. Moreover, GPIs significantly decrease the incidence of cardiovascular events by occupying GP IIb/IIIa receptor binding sites on the surface of platelets and inhibiting platelet aggregation [12, 13].

Previous studies have demonstrated the benefits of GPIs in patients with ACS. In the PURSUIT trial, eptifibatide significantly reduced the 30-day incidence of mortality or MI and demonstrated the greatest benefit in high-risk patients. Eptifibatide increased major bleeding, but there was no significant difference in life-threatening bleeding, and this bleeding risk was dose-dependent [14]. In the ESPRIT trial, eptifibatide reduced the 48-hour composite of mortality, MI, urgent revascularization, and thrombotic bailout, with sustained benefit at 30 days. It also increased major bleeding, but there was no increase in fatal bleeding. Minor bleeding was also more common [15]. A lower percentage platelet aggregation correlated with a lower MACE rate 30 days after PCI. Moreover, eptifibatide reduced composite endpoints at 48 h, 96 h, 7 days, and 30 days after PCI in patients with ACS (10). Similar results have been observed in patients with STEMI and non-ST segment elevation ACS. The Thrombolysis in Myocardial Infarction flow (TIMI) grade also improved after eptifibatide infusion in patients with STEMI. Moreover, GPIs are recommended for emergency cases of spontaneous coronary artery dissection [16,17,18].

Theoretically, GPIs combined with ticagrelor could enhance the antiplatelet effect and effectively inhibit platelet aggregation. However, few clinical studies have evaluated the effects of GPI treatment combined with ticagrelor owing to the high bleeding risk. Nevertheless, the PLATO study showed that in patients with ACS undergoing early PCI, ticagrelor reduced cardiovascular events compared with clopidogrel. Without GPI treatment, the rate of definite stent thrombosis was lower and the rate of minor/major bleeding was higher with ticagrelor than with clopidogrel. When GPIs were used, no such difference was observed between ticagrelor and clopidogrel. Those treated with a GPI were more likely to be younger, be male, and have undergo multivessel PCI. Overall, bleeding rates were higher among those treated with a GPI. GPIs inhibit platelet aggregation; thus, GPIs themselves lead to high rates of bleeding, thereby diminishing the differential impact of ticagrelor compared with clopidogrel on hemostasis. It follows that GPIs should be used with caution in patients taking ticagrelor due to the high bleeding risk. The dose of eptifibatide recommended in the 2018 European Society of Cardiology guidelines is 180 µg/kg bolus with continuous intravenous infusion at 2.0 µg/kg/min for 18 h [19, 20]. In the present study, we chose a lower dose of eptifibatide (1.0 µg/kg/min) because in our previous clinical work we have observed more bleeding events with the standard dose of 2.0 µg/kg/min when used in combination with ticagrelor. Therefore, we chose a lower dose infusion for platelet inhibition in patients with high ischemic risk, and this work was designed to evaluate if this low dose combination may be effective, with less bleeding events.

To our best knowledge, this is the first study to show that the combined use of low-dose eptifibatide and ticagrelor for 24 h after PCI is effective for inhibiting platelet aggregation. The PAR in the eptifibatide + ticagrelor group was significantly lower immediately after intravenous infusion and remained low at 1, 12, and 24 h. After eptifibatide discontinuation, the PAR rapidly returned to baseline. All of the patients (100%) achieved a PAR < 10% in the eptifibatide + ticagrelor group, suggesting quick, sustained, and strong inhibition of platelet aggregation with eptifibatide. In-hospital and 12-month bleeding events were not significantly different between the group treated with ticagrelor alone and the group treated with ticagrelor + eptifibatide, suggesting that the combined use of low-dose eptifibatide and ticagrelor for 24 h after PCI was safe.

The current treatment strategy for ACS is revascularization plus drug therapy. During PCI, the balloon and stent squeeze the damaged plaque. After the endothelium is damaged, platelets are further activated, which increases the risk of thrombosis during and after revascularization. PCI-related myocardial injury is very common and is often associated with elevated hs-TnT, as well as angina symptoms, after PCI. A previous study showed that PCI-related myocardial injury manifested as hs-TnT elevation in 28.7% of patients who underwent elective PCI. Moreover, PCI-related myocardial injury was associated with increased events at 30 days and 1 year, which highlights the importance of reducing PCI-related myocardial injury [21]. In the present study, the elevations in serum hs-TnT, NT-proBNP, and h-FABP were significantly less pronounced in the eptifibatide + ticagrelor group, suggesting that eptifibatide infusion reduced PCI-related myocardial injury. Patients in the eptifibatide + ticagrelor group exhibited lower rates of in-hospital MI and MACEs. In the present study, types 1 and 4 MI were included. We defined MI according to whether the patient had postoperative chest pain and whether hs-TnT was > 5-times the upper limit of normal. Troponin elevation is common after PCI, especially complex PCI, which explains why the incidence of MI was high in this study. Moreover, 12-month MI was lower in the eptifibatide + ticagrelor group than in the ticagrelor group.

Patients with atrial fibrillation or other conditions requiring long-term oral anticoagulation often undergo PCI for CAD. Balancing the bleeding risk and thrombotic risk is complex. Triple therapy combining an oral anticoagulant (OAC) with dual antiplatelet therapy is effective in this population, but it increases the risk of major bleeding, including intracranial hemorrhage. Dual therapy refers to the use of an OAC plus single antiplatelet therapy, which is supported by trials showing lower bleeding with comparable thrombotic protection compared with triple therapy. The duration of therapy also varies. The optimal strategy balances ischemic protection and bleeding minimization, with a shift toward direct OAC-based dual therapy for most patients. However, individualized decisions based on risk scores are critical [22].

Patients with STEMI often require rapid and potent platelet inhibition during PCI. Ticagrelor has a delayed onset (2–4 h for full effect), while cangrelor provides immediate platelet inhibition. Cangrelor provides rapid additive platelet inhibition in ticagrelor-pretreated patients with STEMI without increasing bleeding, making it a viable option for optimizing PCI outcomes. However, further trials are needed to confirm the clinical benefits of this approach [23].

This study has some limitations that should be considered. First, the follow-up period was short. Therefore, longer patient observation should be carried out to identify any longer term complications associated with the combined use of low-dose eptifibatide with ticagrelor after PCI. Second, this study only included East Asian patients, which may limit the generalizability of the findings. Moreover, the sample size was small, and the study adopted a retrospective design, which may limit the generalizability and reproducibility of the findings to other centers or populations. Third, as this was a retrospective clinical study, we tested platelet function using the method employed at our hospital. We acknowledge that it would have been useful to use a more well-validated method, such as the VerifyNow assessment. We will apply this method in our future research. Fourth, we did not perform propensity score matching to balance the baseline characteristics between the two groups. Finally, this study was limited to the population with unstable angina. Therefore, further research should focus on a broader population. In consideration of these limitations, prospective, randomized, blinded studies in a larger population of patients should be conducted in the future to validate the preliminary findings of this single-center retrospective study.

Conclusion

In conclusion, this study provides a preliminary indication that low-dose eptifibatide may be safe in patients with unstable angina pectoris treated with ticagrelor after PCI. Eptifibatide immediately reduced the postoperative PAR and reduced PCI-related myocardial injury in a safe and effective manner. The combined use of low-dose eptifibatide and ticagrelor in patients with unstable angina pectoris after PCI may be worthy of further exploration in large-sample, multicenter, prospective studies in the future.

Data availability

The data presented in this study are available on request from the corresponding author.

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Acknowledgements

Not applicable.

Funding

The present study was supported by Soochow University (H230885, H220142). The Multi-center Clinical Research Project for Major Diseases in Suzhou, (Grant Number: DZXYJ202302).

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Author notes

  1. Shangsong Shi, Zicheng Ling and Shaohua Gu contributed equally to this work.

Authors and Affiliations

  1. Department of Cardiovascular Medicine, First Affiliated Hospital of Soochow University, No.188 Shizi Road, Suzhou, 215006, Jiangsu, China

    Shangsong Shi, Tingbo Jiang & Lin Ling

  2. Department of Interal Medicine, Weiting Community Health Center of Suzhou Industrial Park, Suzhou, China

    Zicheng Ling

  3. Department of Nephrology, Kunshan Third Hospital, Suzhou, China

    Shaohua Gu

Authors
  1. Shangsong Shi
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  2. Zicheng Ling
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  3. Shaohua Gu
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  4. Tingbo Jiang
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  5. Lin Ling
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Contributions

Conceptualization, Shangsong Shi and Zicheng Ling; Data curation, Tingbo Jiang and Shaohua Gu; Formal analysis, Tingbo Jiang and Lin Ling; Methodology, Shangsong Shi, Tingbo Jiang and Lin Ling; Validation, Lin Ling; Writing– original draft, Shangsong Shi and Lin Ling; Writing– review & editing, Shangsong Shi, Tingbo Jiang and Lin Ling. All authors have read and approved the manuscript.

Corresponding author

Correspondence to Lin Ling.

Ethics declarations

Ethics approval and consent to participate

The study procedure conformed to the ethical guidelines of the Declaration of Helsinki, and approval for the study was obtained from the Institutional Review Board of The First Affiliated Hospital of Soochow University (ethics approval no. 20190025001). Informed consent was obtained from all patients involved in the study.

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Not applicable.

Competing interests

The authors declare no competing interests.

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Shi, S., Ling, Z., Gu, S. et al. Protective effects of combined eptifibatide and ticagrelor in patients with unstable angina undergoing percutaneous coronary intervention: a single-center experience. BMC Cardiovasc Disord 25, 312 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12872-025-04767-9

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  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12872-025-04767-9

Keywords

BMC Cardiovascular Disorders

ISSN: 1471-2261

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