Acute profound thrombocytopenia associated with glycoprotein IIb/IIIa receptor inhibitor after percutaneous coronary intervention: therapy insights from a single center 6-year experience | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Acute profound thrombocytopenia associated with glycoprotein IIb/IIIa receptor inhibitor after percutaneous coronary intervention: therapy insights from a single center 6-year experience Yue Wu, Kaiyue Feng, Lei Liu, Xiaojuan Fan This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9038136/v1 This work is licensed under a CC BY 4.0 License Status: Under Revision Version 1 posted 14 You are reading this latest preprint version Abstract Background Acute profound thrombocytopenia is an infrequent, but potentially serious, even fatal complication associated with intravenous glycoprotein IIb/IIIa receptor inhibitors (GPI), which are widely used in acute coronary syndrome and percutaneous coronary intervention (PCI). Treatment with steroids and intravenous immunoglobulin (IVIg) is recommended for GPI-induced thrombocytopenia (GIT), but its efficacy is rarely reported. Methods In this retrospective study, we enrolled 21 patients who developed acute profound thrombocytopenia (defined as a platelet count < 20 ×10⁹/L) following PCI with GPI treatment. We analyzed their clinical characteristics, the timing of detected thrombocytopenia, the use of steroid and IVIg treatment, and the subsequent platelet count trends and outcomes. Results Among the 21 patients, 7 were female, and the median age was 63 years. Tirofiban and eptifibatide were administered to 12 and 9 patients, respectively. Thrombocytopenia was detected on the day of PCI in 9 patients. Among the remaining 12, one case was identified following the onset of intracerebral hemorrhage with coma, while the other 11 were discovered during routine blood tests on postoperative day 1. The median platelet count dropped sharply from 143 × 10⁹/L preoperatively to 4 × 10⁹/L after GPI treatment. Following the onset of profound thrombocytopenia, 11 patients underwent treatment with both steroids and IVIg, 6 received steroids alone, and 4 received neither intervention. Patients were categorized into three treatment groups (steroid plus IVIg, steroid alone, or no-intervention) with the aim of analyzing whether steroid/IVIg therapy promoted platelet recovery. No such beneficial effect was found. A separate analysis, grouping patients by whether thrombocytopenia was detected on the day of PCI (early-detection group and later-detection group), showed that those with an early diagnosis and consequent prompt withdrawal of the GPI exhibited a statistically significant faster platelet recovery. The median time to platelet recovery > 20×10⁹/L was significantly shorter in the early-detection group (24 hours) than in the later-detection group (72 hours) with p = 0.017. Conclusions GIT is characterized by rapid onset. Early detection of thrombocytopenia is essential for immediate GPI discontinuation, which is the cornerstone of platelet recovery. Steroids and IVIg did not improve platelet recovery in our cohort. glycoprotein IIb/IIIa receptor inhibitor percutaneous coronary intervention thrombocytopenia immunoglobulin steroids Figures Figure 1 Figure 2 Introduction Glycoprotein IIb/IIIa is the dominant integrin on platelet, which can bind to fibrinogen to crosslink platelets, and is essential for platelet activation and aggregation. Glycoprotein IIb/IIIa receptor inhibitors (GPI) are used globally in patients with acute coronary syndrome or undergoing percutaneous coronary intervention (PCI) 1 , 2 . Thrombocytopenia is an infrequent but potentially serious complication associated with intravenous GPI, abciximab, eptifibatide, and tirofiban 3 , 4 . The thrombocytopenia ranges from mild platelet decline (50 ~ 100 ×10⁹/L), to severe (20 ~ 50 ×10⁹/L), to profound (< 20 ×10⁹/L). The incidence of profound thrombocytopenia is low, with most cases reported in the form of case studies. The majority of patients who experienced profound thrombocytopenia following GPI therapy recovered uneventfully, but severe bleeding and fatalities had been reported, which were associated with longer in-hospital times, increased healthcare costs, morbidity, and even mortality 5 . There have been relatively few attempts to offer guidance to clinicians in the treatment of profound thrombocytopenia because there have been no randomized studies of different treatments. Treatment with steroids and intravenous immunoglobulin (IVIg) is recommended for these patients 6 , but its efficacy is rarely reported. Here, we conducted a retrospective study to investigate the efficacy of steroid and IVIg therapy, as well as other factors influencing platelet recovery, in patients who developed profound thrombocytopenia after undergoing PCI with GPI treatment. Research design and methods Study design and patients This is a single-center, retrospective study. Consecutive patients undergoing PCI at the cardiovascular department of the First Affiliated Hospital of Xi’an Jiaotong University from January 2019 to December 2025 were screened. Patients who received PCI and GPI treatment and then developed profound thrombocytopenia (platelet count < 20 ×10⁹/L) were enrolled. The study was approved by the ethics committee of our institution (XJTU1AF2025LSYY-945). Written informed consent was waived due to a retrospective design. Clinical data collection The following information from patients’ clinical records was collected for our study: age, sex, height and weight, diagnosis at presentation (acute myocardial infarction, AMI; unstable angina, UA), previous history of PCI, hypertension, diabetes mellitus (DM) and chronic kidney disease (CKD), co-existing heart failure (HF). Laboratory results including white blood cell count (WBC), platelet count before PCI, alanine aminotransferase (ALT) and estimated glomerular filtration rate (eGFR) was also recorded. Concomitant heparin therapy, oral dual antiplatelet drugs, the PCI time, the timing of detected thrombocytopenia, the use of steroid and IVIg treatment, the subsequent platelet count trends, associated symptoms, and outcomes were all documented in detail. Study Groups To assess the impact of IVIg/steroids treatment on platelet recovery, patients were categorized into three therapeutic cohorts: those receiving combined IVIg and steroid therapy (IVIg Plus steroid group), those receiving steroids alone (steroid group), and the no-intervention group. The day of PCI was designated as day 0. Patients were further stratified into two groups based on the timing of thrombocytopenia detection: early-detection group (identified on day 0) and later-detection group (identified on the day after PCI). Statistical analysis Analyses were performed by SPSS version 25.0. Continuous variables were presented as median values with interquartile ranges (IQRs), and categorical variables were presented as counts and frequencies. Differences between the two groups were compared by the use of the Mann-Whitney test for continuous variables and χ2 test or the Fisher exact test for categorical variables as appropriate. A two-tailed p < 0.05 was regarded as statistically significant in all calculations. Results Approximately 50,000 patients who underwent PCI were screened, from which 22 patients were ultimately identified as developing profound thrombocytopenia (the lowest platelet count < 20 ×10⁹/L ) postoperatively. We found that all 22 patients received GPI drugs during the PCI procedure or after PCI. Based on literature reports, GPI-induced thrombocytopenia (GIT) typically occurs within 24 hours after drug administration. One patient developed thrombocytopenia on the third postoperative day and was excluded due to the possibility of heparin-induced thrombocytopenia (HIT). The remaining 21 patients, whose lowest platelet count was detected on the day of PCI or the first postoperative day, were ultimately enrolled in our study. Their detailed clinical characteristics are presented in Table 1 . Among the 21 patients, 7 were female, and the mean age was 61 years, 4 were diagnosed with acute myocardial infarction, 17 were diagnosed with unstable angina, 15 had hypertension, 5 had diabetes mellitus, 3 had chronic kidney disease, 5 had heart failure, and 8 had a history of previous PCI. All patients received intraoperative heparin anticoagulation. Tirofiban and eptifibatide were administered to 12 and 9 patients, respectively. Thrombocytopenia was detected on the day of PCI in 9 patients, with the earliest case identified during PCI procedure based on a blood draw taken 30 minutes post-GPI initiation. The remaining patients were diagnosed approximately 2–4 hours after the PCI procedure and intravenous GPI administration. Among the remaining 12, one case was identified following the onset of intracerebral hemorrhage with coma, while the other 11 were discovered during routine blood tests on postoperative day 1. The median platelet count dropped sharply from 143 × 10⁹/L preoperatively to 4 × 10⁹/L after PCI. Table 1 The clinical characteristics, the timing of detected thrombocytopenia, the use of steroid and immunoglobulin treatment, and the subsequent platelet count trends and outcomes between the early-GIT detection and late-detection group Male, n (%) The Whole (n = 21) The early-detection group (n = 9) The late-detection group (n = 12) P value 14(66.7%) 6(66.7%) 8(66.7%) 1.000 Age, years 63(58–65) 64(58–66) 62(51–71) 0.702 BMI, kg/m² 23.7(22.3–24.5) 23.7(22.1–24.6) 23.9(22.2–26.7) 0.702 Presentation, n (%) UA 17(81.0%) 7(77.8%) 10(83.3%) 1.000 AMI 4(19.0%) 2(22.2%) 2(16.7%) NS History of disease, n (%) Previous PCI 8(38.1%) 2(22.2%) 6(50.0%) 0.367 CKD 3(14.3%) 1(11.1%) 2(16.7%) 1.000 HP 15(71.4%) 6(66.7%) 9(75.0%) 1.000 DM 5(23.8%) 3(33.3%) 2(16.7%) 0.611 Heart failure 5(23.8%) 1(11.1%) 4(33.3%) 0.338 Laboratory test ALT, U/L 21(18–29) 21(18–31) 22(15–29) 1.000 eGFR, mL/min/1.73 m² 92(86–103) 98(84–103) 92(87–103) 0.808 NT-proBNP, mmol/L 186.0(68.7-484.5) 259.0(69.7-358.4) 157.9(59.5-627.1) 1.000 WBC, 10^9/L 6.9(4.8–7.9) 7.8(4.5–8.2) 5.9(5.0-7.5) 0.382 Concomitant medication Heparin during PCI, n (%) Eptifibatide, n (%) Tirofiban, n (%) 21(100%) 9(42.9%) 12(57.1%) 9(100%) 3(33.3%) 6(66.7%) 12(100%) 6(50.0%) 6(50.0%) NS 0.625 0.691 Ticagrelor, n (%) 4(19.0%) 3(33.3%) 1(8.3%) 0.238 Clopidogrel, n (%) Therapy after GIT 17(81.0%) 6(66.7%) 11(91.7%) 0.635 Detection of GIT on the day of PCI, n (%) 9(42.9%) 9(100%) 0(0%) NS Steroids therapy after GIT, n (%) 17(81.0%) 9(100%) 8(66.7%) 0.104 Immunoglobulin therapy after GIT, n (%) 11(52.4%) 5(55.6%) 6(50.0%) 1.000 Combination of steroids and Immunoglobulin therapy, n (%) Non-interveion, n (%) 11(52.4%) 4(19.0%) 5(55.6%) 0(0%) 6(50.0%) 4(33.3%) 1.000 0.104 Outcomes, n (%) Suspend dual antiplatelet therapy after GIT, n (%) 9(42.9%) 5(55.6%) 4(36.4%) 0.653 Thrombotic event after GIT,, n (%) 0(0%) 0(0%) 0(0%) NS Bleeding event, n (%) Fatal intracranial hemorrhage Petechiae gingival bleeding procedural access site oozing 4(19.1%) 1(4.8%) 1(4.8%) 1(4.8%) 1(4.8%) 1(11.1%) 0(0%) 0(0%) 0(0%) 1(11.1%) 3(25.0%) 1(8.3%) 1(8.3%) 1(8.3%) 0(0%) 0.504 Platelet count trend Platelet count before PCI, 10^9/L 193(148–253) 219(164–348) 239(191–277) 0.754 Platelet count at the timing of detection of GIT, 10^9/L 6(4–23) 20(5–75) 4(3–35) 0.023 The lowest platelet count after GIT, 10^9/L 4(2–8) 2(2–19) 4(2–5) 0.422 Platelet count on the day of PCI (D0), 10^9/L 6(2–19) 6(2–19) NS NS Platelet count on the day after PCI (D1), 10^9/L 6(3–23) 23(13–45) 4(2–5) 0.001 Platelet count on the second day after PCI (D2), 10^9/L 26(10–45) 42(29–69) 11(7–20) 0.006 Time to platelet recovery > 20 (×10⁹/L) post-PCI, hours 48(24–72) 24(24–48) 72(48–72) 0.017 Time to platelet recovery > 50 (×10⁹/L) post-PCI, hours 72(48–96) 48(48–72) 96(72–102) 0.190 Time to platelet recovery > 100 (×10⁹/L) post-PCI, hours 120(96–126) 96(96–120) 120(120–126) 0.053 UA, unstable angina; AEMI, acute myocardial infarction; PCI, percutaneous coronary intervention; CKD, chronic kidney disease; HP, hypertension; DM, diabetes mellitus; ALT, alanine aminotransferase; eGFR: estimated Glomerular Filtration Rate; PLT, platelet; NT-proBNP: N-terminal pro-B-type Natriuretic Peptide; WBC, white blood cell; GIT, glycoprotein IIb/IIIa receptor inhibitors induced thrombocytopenia; Following the onset of profound thrombocytopenia, 11 patients underwent treatment with both steroids and IVIg, 6 received steroids alone, and 4 received neither intervention. Patients were categorized into three treatment groups (steroid plus IVIg, steroid alone, or no-intervention) to analyze whether steroid/IVIg therapy promoted platelet recovery. No such beneficial effect was found. Given that the no-intervention group comprised only 4 patients, which may compromise the statistical validity, we reclassified the patients into the IVIg treatment group (n = 11) and the no-IVIg treatment group (n = 10) (Table 2 ). The results indicated that there was still no significant difference in platelet recovery between the two groups, suggesting that IVIg therapy did not contribute to platelet recovery (Fig. 1 ). To study other factors affecting platelet recovery, we grouped patients by whether thrombocytopenia was detected on the day of PCI (early-detection group, n = 9; and later-detection group, n = 12), and showed that those with an early diagnosis and consequent prompt withdrawal of the GPI exhibited a statistically significant faster platelet recovery (Fig. 2 ). The median time to platelet recovery > 20×10⁹/L was significantly shorter in the early-detection group than in the later-detection group (24 hours vs 72 hours, p = 0.017). In all patients, the median time for platelet recovery to > 50×10⁹/L and > 100×10⁹/L was 72 and 120 hours, respectively. Table 2 The platelet count and its trend between the IVIg- treatment and non-IVIg treatment group Platelet count trend The whole (n = 21) IVIg treatment group (n = 11) Non-IVIg treatment group (n = 11) P value Platelet count before PCI, 10^9/L 193(148–253) 348(271–409) 192(144–242) 0.605 Platelet count at the timing of detection of GIT, 10^9/L 6(4–23) 5(5–13) 48(13–77) 0.233 The lowest platelet count after GIT, 10^9/L 4(2–8) 2(1–5) 11(2–19) 0.426 Platelet count on the day of PCI (D0), 10^9/L 6(2–19) 2(1–5) 11(2–19) 0.556 Platelet count on the day after PCI (D1), 10^9/L 6(3–23) 20(12–27) 37(13–73) 0.492 Platelet count on the second day after PCI (D2), 10^9/L 26(10–45) 42(25–51) 59(34–82) 0.492 Time to platelet recovery > 20 (×10⁹/L) post-PCI, hours 48(24–72) 24(24–60) 30(24–32) 0.904 Time to platelet recovery > 50 (×10⁹/L) post-PCI, hours 72(48–96) 48(48–84) 60(48–72) 0.515 Time to platelet recovery > 100 (×10⁹/L) post-PCI, hours 120(96–126) 96(84–132) 120(96–108) 0.414 IVIg, Immunoglobulin; PCI, percutaneous coronary intervention; GIT, glycoprotein IIb/IIIa receptor inhibitors induced thrombocytopenia; Outcomes among the 21 patients were as follows: delayed detection of thrombocytopenia was fatal in one case due to sudden intracerebral hemorrhage. The other 20 patients were discharged safely, with only three experiencing minor bleeding (e.g., petechiae, gingival bleeding, or procedural access site oozing). It was worth emphasizing that 7 patients experienced systemic shivering and chills resembling an allergic reaction postoperatively, with the incidence significantly higher than that observed in routine clinical practice. Discussion The main findings of the current study are as follows: GIT occurs shortly after exposure to GPI and is characterized by rapid onset. Early detection of thrombocytopenia is essential for immediate GPI discontinuation, which is the cornerstone of platelet recovery. Steroids and IVIg did not improve platelet recovery in our cohort. Since all enrolled patients received heparin for intraoperative anticoagulation, it is crucial to differentiate between GIT and HIT. The key differentiating features include the timing of onset, the severity of thrombocytopenia and clinical presentation. GIT typically develops rapidly within hours. HIT is classified into two types 7 : Type I and Type II. Type I HIT is a non-immune reaction that typically occurs within 1 to 2 days of heparin administration. It is characterized by a mild decrease in platelet count, generally fluctuating between 100 and 300 × 10⁹/L, and rarely falling below 100 × 10⁹/L. Type II HIT is immune-mediated and usually manifests between 4 and 14 days after initial heparin exposure. Furthermore, HIT primarily presents with thrombotic complications rather than bleeding, and the platelet count rarely falls below 20 × 10⁹/L. Although HIT antibodies were not tested in the enrolled patients to definitively exclude HIT, based on these three differentiating points, it is reasonable to conclude that the 21 patients included in the final analysis were diagnosed with GIT. The etiology of GIT remains unclear, but it is proposed that drug-dependent antibodies which bind platelets in the presence of GPI is the cause of the rapid fall of platelet level 8 . So, treatment with steroids and intravenous IVIg is recommended for these patients. In our retrospective study, 11 patients underwent treatment with both steroids and IVIg, 6 received steroids alone, and 4 received neither intervention following the onset of profound thrombocytopenia. To mitigate statistical errors arising from the small sample size, we employed two grouping strategies: one categorized enrolled patients into three groups (steroid plus IVIg, steroid alone, or no-intervention), while the other divided patients into two groups (disregarding steroid use: IVIg treatment group and no-IVIg treatment group). The final analysis indicated that there were no statistically significant differences in platelet recovery between groups, suggesting that IVIg/steroids therapy did not contribute to platelet recovery. The key factor for platelet recovery lies in the timely detection of platelet decline and the prompt cessation of the GPI agent. Our study revealed that the median time required for platelet recovery to above 20 ×10⁹/L was significantly shorter in the early detection group than in the later detection group (24 hours vs 72 hours, p = 0.017). Platelet counts on postoperative day 1 and day 2 also differed significantly between the two groups (Table 1 ). In summary, IVIg treatment provided no clinical benefit for GIT. For patients undergoing PCI and receiving GPI treatment, the most critical measure is early detection of thrombocytopenia and prompt withdrawal of the causative agent. Previous findings 8 indicated that GIT could be caused by drug-dependent antibodies, either naturally occurring or induced by prior drug exposure. Thus, GIT may occur upon first exposure to GPI or upon re-exposure. In our study, there were 8 patients with a history of PCI who may be exposed to GPI without developing GIT, but developed severe GIT upon re-exposure. This finding aligns with previous research conclusions 9 , 10 , indicating that the potential risk of GIT cannot be overlooked regardless of whether GPI is used for the first time or upon re-exposure. Regarding the timing of GIT occurrence, thrombocytopenia can occur shortly after GPI exposure. For instance, in our study, one patient experienced platelet decreases within half an hour of GPI exposure. Case reports have also indicated that a decrease in platelet count can be detected as early as 10 minutes after drug GPI administration 10 . As for the time to platelet recovery in patients with profound GIT, our study showed that the median time required for platelets to recover to over 100×10⁹/L is 120 hours which was consistent with previous case reports 10 – 12 . Previous literature 10 , 13 have reported GIT can be accompanied by systemic allergic reactions such as chills and shivering. This phenomenon was also observed in our retrospective study with a notably high incidence. However, based on clinical records, we found that physicians often misattributed allergic reactions to contrast media, failing to recognize them as possible GIT symptoms and leading to neglected prompt platelet testing. This highlights the need for clinician training on this issue, to ensure that when managing patients with allergic reactions after PCI, they consider the possibility of GIT and immediately order platelet testing for early identification. Because thrombocytopenia may occur rapidly and be asymptomatic, many cases were discovered during routine blood tests on postoperative day 1. Although GIT does not routinely lead to severe bleeding complications, one patient in our study died from cerebral hemorrhage as a complication of thrombocytopenia that was not detected and managed in time, with a subsequent platelet count as low as 1 ×10⁹/L. This tragic outcome again underscores the critical importance of early detection and prompt discontinuation of GPI. Since there are no commercially available assays that can be performed rapidly enough to detect GIT, the most critical measure is to perform platelet count testing within 2 hours after GPI administration. Early detection of GIT and timely drug discontinuation can prevent further platelet decline, thereby avoiding prolonged hospitalization and potential adverse events. Steroids and IVIg did not improve platelet recovery for profound GIT. Conclusions GIT occurs shortly after exposure to GPI and is characterized by rapid onset. Early detection of thrombocytopenia is essential for immediate GPI discontinuation, which is the cornerstone of platelet recovery. Steroids and IVIg did not improve platelet recovery in our cohort. Declarations Conflicts of interest The authors have no conflicts of interest to disclose. Ethics approval and consent to participate The study was approved by the ethics committee of our institution (No. XJTU1AF2025LSYY-945). Written informed consent was waived due to a retrospective design. Clinical trial number Not applicable. Funding This work was supported by the National Natural Science Foundation of China (82425004). Author Contribution XF and YW conceived and designed the study. XF, KF and LL collected and analyzed the data. YW wrote the first draft of the manuscript. All authors reviewed and edited the manuscript and approved the final version of the manuscript. Acknowledgement We thank for the assistance of Ling Bai from the First Affiliated Hospital of Xi’an Jiaotong University for her valuable contribution to the interpretation and analysis of the data. Data Availability Data supporting the conclusions of this article are included within the article and available from the corresponding authors on reasonable request. Data Availability Data supporting the conclusions of this article are included within the article and available from the corresponding authors on reasonable request. References Bosch X, Marrugat J, Sanchis J. Platelet glycoprotein IIb/IIIa blockers during percutaneous coronary intervention and as the initial medical treatment of non-ST segment elevation acute coronary syndromes. Cochrane Database Syst Rev. 2013;2013(11):Cd002130. Safley DM, Venkitachalam L, Kennedy KF, Cohen DJ. Impact of Glycoprotein IIb/IIIa Inhibition in Contemporary Percutaneous Coronary Intervention for Acute Coronary Syndromes: Insights From the National Cardiovascular Data Registry. JACC Cardiovasc interventions. 2015;8(12):1574–82. Rikken S, van 't Hof AWJ, Ten Berg JM, Kereiakes DJ, Coller BS. Critical Analysis of Thrombocytopenia Associated With Glycoprotein IIb/IIIa Inhibitors and Potential Role of Zalunfiban, a Novel Small Molecule Glycoprotein Inhibitor, in Understanding the Mechanism(s). J Am Heart Association. 2023;12(24):e031855. Wang J, Zou D. Tirofiban-induced thrombocytopenia. Ann Med. 2023;55(1):2233425. Masood F, Hashmi S, Chaus A, Hertsberg A, Ehrenpreis ED. Complications and Management of Eptifibatide-Induced Thrombocytopenia. Annals pharmacotherapy. 2021;55(12):1467–73. Huxtable LM, Tafreshi MJ, Rakkar AN. Frequency and management of thrombocytopenia with the glycoprotein IIb/IIIa receptor antagonists. Am J Cardiol. 2006;97(3):426–9. Han G, Song S, Wan S, et al. Heparin-Induced Thrombocytopenia and Thrombosis in Patients With or Without a Thrombophilia Background: A Systematic Review Involved 602 Cases. Int J vascular Med. 2025;2025:9338124. Bougie DW, Wilker PR, Wuitschick ED, et al. Acute thrombocytopenia after treatment with tirofiban or eptifibatide is associated with antibodies specific for ligand-occupied GPIIb/IIIa. Blood. 2002;100(6):2071–6. Attaya S, Kanthi Y, Aster R, McCrae K. Acute profound thrombocytopenia with second exposure to eptifibatide associated with a strong antibody reaction. Platelets. 2009;20(1):64–7. Li Y, Qiu J, Gao Y, Li G. Case report: reuse of tirofiban leads to very severe thrombocytopenia. Front Cardiovasc Med. 2023;10:1130552. Liu J, Oorloff MD, Nadella A, Yan Y, Zhou N. Tirofiban-induced acute profound thrombocytopenia in endovascular therapy for acute ischemic stroke: a rare case report. BMC Neurol. 2025;25(1):355. Gheith Z, Kilani A, Nguyen T. 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Cite Share Download PDF Status: Under Revision Version 1 posted Editorial decision: Revision requested 17 Apr, 2026 Reviews received at journal 13 Apr, 2026 Reviews received at journal 08 Apr, 2026 Reviews received at journal 08 Apr, 2026 Reviewers agreed at journal 05 Apr, 2026 Reviewers agreed at journal 30 Mar, 2026 Reviews received at journal 20 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers invited by journal 18 Mar, 2026 Editor invited by journal 10 Mar, 2026 Editor assigned by journal 09 Mar, 2026 Submission checks completed at journal 09 Mar, 2026 First submitted to journal 05 Mar, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-9038136","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":609665802,"identity":"df76cfb8-c805-49c8-9407-30b850585c1b","order_by":0,"name":"Yue Wu","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Yue","middleName":"","lastName":"Wu","suffix":""},{"id":609665803,"identity":"94b72a1e-a4ae-464c-8d1e-b12ae7bc4318","order_by":1,"name":"Kaiyue Feng","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Kaiyue","middleName":"","lastName":"Feng","suffix":""},{"id":609665806,"identity":"04c20db8-2618-4ece-8549-95e2cfb40b96","order_by":2,"name":"Lei Liu","email":"","orcid":"","institution":"","correspondingAuthor":false,"prefix":"","firstName":"Lei","middleName":"","lastName":"Liu","suffix":""},{"id":609665808,"identity":"8a634ded-a037-4d4e-b517-d3f8781866bc","order_by":3,"name":"Xiaojuan Fan","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA2UlEQVRIie3PMQrCMBSA4VcKcYnNmqDoFSIugniXgFCXzOIgIgiZeoCKl4kE4lI6dxD0CB3rIBjF2cZNMD8kEHgfjwCEQj8YGZpTUwMCiAv3RB6E5UiwHBAFJD0JrzDvYYAvCDsoMZ6pZMNtV0O9NEAO28+E9I2eywJRbhMR5aUBetYtW7apMHLlyCXjcVcZ4FS0/EXL0W7Cn1swj+9epJLjGFZvEvkQltk0ygrE9o4cs3KBadVCSGdn4aYsSSweXZvldEDyFvLOvm7tDvaad619B0OhUOgfewBANEACu/8bNQAAAABJRU5ErkJggg==","orcid":"","institution":"","correspondingAuthor":true,"prefix":"","firstName":"Xiaojuan","middleName":"","lastName":"Fan","suffix":""}],"badges":[],"createdAt":"2026-03-05 08:54:18","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9038136/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9038136/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":105282517,"identity":"5a911d21-3e9e-487a-b511-6eee56bcbf5e","added_by":"auto","created_at":"2026-03-24 10:28:25","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":18621,"visible":true,"origin":"","legend":"\u003cp\u003eNo significant difference was observed in platelet recovery between the IVIg treatment group and the no-IVIg treatment group on postoperative day 1 and day 2.\u003c/p\u003e","description":"","filename":"Picture1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-9038136/v1/fdfbb482a4630fc8678862a9.jpg"},{"id":105282581,"identity":"6d4a996e-73b5-4cbf-8d17-d222739d1678","added_by":"auto","created_at":"2026-03-24 10:28:27","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":31532,"visible":true,"origin":"","legend":"\u003cp\u003ePatients in the early-detection group achieved significantly better platelet recovery than those in the later-detection group by discontinuing GPI immediately when thrombocytopenia was observed on the day of surgery.\u003c/p\u003e","description":"","filename":"Picture2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-9038136/v1/117f11a540761e3d0b7d034e.jpg"},{"id":105282595,"identity":"1b529ff7-ddb6-41a8-aefe-136879e7f205","added_by":"auto","created_at":"2026-03-24 10:28:32","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":919168,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9038136/v1/82735bba-e88a-4992-90c8-1e08872db546.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Acute profound thrombocytopenia associated with glycoprotein IIb/IIIa receptor inhibitor after percutaneous coronary intervention: therapy insights from a single center 6-year experience","fulltext":[{"header":"Introduction","content":"\u003cp\u003eGlycoprotein IIb/IIIa is the dominant integrin on platelet, which can bind to fibrinogen to crosslink platelets, and is essential for platelet activation and aggregation. Glycoprotein IIb/IIIa receptor inhibitors (GPI) are used globally in patients with acute coronary syndrome or undergoing percutaneous coronary intervention (PCI)\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e,\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e. Thrombocytopenia is an infrequent but potentially serious complication associated with intravenous GPI, abciximab, eptifibatide, and tirofiban\u003csup\u003e\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e,\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u003c/sup\u003e. The thrombocytopenia ranges from mild platelet decline (50\u0026thinsp;~\u0026thinsp;100 \u0026times;10⁹/L), to severe (20\u0026thinsp;~\u0026thinsp;50 \u0026times;10⁹/L), to profound (\u0026lt;\u0026thinsp;20 \u0026times;10⁹/L). The incidence of profound thrombocytopenia is low, with most cases reported in the form of case studies. The majority of patients who experienced profound thrombocytopenia following GPI therapy recovered uneventfully, but severe bleeding and fatalities had been reported, which were associated with longer in-hospital times, increased healthcare costs, morbidity, and even mortality\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e. There have been relatively few attempts to offer guidance to clinicians in the treatment of profound thrombocytopenia because there have been no randomized studies of different treatments. Treatment with steroids and intravenous immunoglobulin (IVIg) is recommended for these patients\u003csup\u003e\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u003c/sup\u003e, but its efficacy is rarely reported. Here, we conducted a retrospective study to investigate the efficacy of steroid and IVIg therapy, as well as other factors influencing platelet recovery, in patients who developed profound thrombocytopenia after undergoing PCI with GPI treatment.\u003c/p\u003e"},{"header":"Research design and methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy design and patients\u003c/h2\u003e \u003cp\u003eThis is a single-center, retrospective study. Consecutive patients undergoing PCI at the cardiovascular department of the First Affiliated Hospital of Xi\u0026rsquo;an Jiaotong University from January 2019 to December 2025 were screened. Patients who received PCI and GPI treatment and then developed profound thrombocytopenia (platelet count\u0026thinsp;\u0026lt;\u0026thinsp;20 \u0026times;10⁹/L) were enrolled. The study was approved by the ethics committee of our institution (XJTU1AF2025LSYY-945). Written informed consent was waived due to a retrospective design.\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eClinical data collection\u003c/h3\u003e\n\u003cp\u003eThe following information from patients\u0026rsquo; clinical records was collected for our study: age, sex, height and weight, diagnosis at presentation (acute myocardial infarction, AMI; unstable angina, UA), previous history of PCI, hypertension, diabetes mellitus (DM) and chronic kidney disease (CKD), co-existing heart failure (HF). Laboratory results including white blood cell count (WBC), platelet count before PCI, alanine aminotransferase (ALT) and estimated glomerular filtration rate (eGFR) was also recorded. Concomitant heparin therapy, oral dual antiplatelet drugs, the PCI time, the timing of detected thrombocytopenia, the use of steroid and IVIg treatment, the subsequent platelet count trends, associated symptoms, and outcomes were all documented in detail.\u003c/p\u003e\n\u003ch3\u003eStudy Groups\u003c/h3\u003e\n\u003cp\u003eTo assess the impact of IVIg/steroids treatment on platelet recovery, patients were categorized into three therapeutic cohorts: those receiving combined IVIg and steroid therapy (IVIg Plus steroid group), those receiving steroids alone (steroid group), and the no-intervention group.\u003c/p\u003e \u003cp\u003eThe day of PCI was designated as day 0. Patients were further stratified into two groups based on the timing of thrombocytopenia detection: early-detection group (identified on day 0) and later-detection group (identified on the day after PCI).\u003c/p\u003e \u003cdiv id=\"Sec6\" class=\"Section2\"\u003e \u003ch2\u003eStatistical analysis\u003c/h2\u003e \u003cp\u003eAnalyses were performed by SPSS version 25.0. Continuous variables were presented as median values with interquartile ranges (IQRs), and categorical variables were presented as counts and frequencies. Differences between the two groups were compared by the use of the Mann-Whitney test for continuous variables and χ2 test or the Fisher exact test for categorical variables as appropriate. A two-tailed p\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was regarded as statistically significant in all calculations.\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cp\u003eApproximately 50,000 patients who underwent PCI were screened, from which 22 patients were ultimately identified as developing profound thrombocytopenia (the lowest platelet count\u0026thinsp;\u0026lt;\u0026thinsp;20 \u0026times;10⁹/L ) postoperatively. We found that all 22 patients received GPI drugs during the PCI procedure or after PCI. Based on literature reports, GPI-induced thrombocytopenia (GIT) typically occurs within 24 hours after drug administration. One patient developed thrombocytopenia on the third postoperative day and was excluded due to the possibility of heparin-induced thrombocytopenia (HIT). The remaining 21 patients, whose lowest platelet count was detected on the day of PCI or the first postoperative day, were ultimately enrolled in our study. Their detailed clinical characteristics are presented in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e. Among the 21 patients, 7 were female, and the mean age was 61 years, 4 were diagnosed with acute myocardial infarction, 17 were diagnosed with unstable angina, 15 had hypertension, 5 had diabetes mellitus, 3 had chronic kidney disease, 5 had heart failure, and 8 had a history of previous PCI. All patients received intraoperative heparin anticoagulation. Tirofiban and eptifibatide were administered to 12 and 9 patients, respectively. Thrombocytopenia was detected on the day of PCI in 9 patients, with the earliest case identified during PCI procedure based on a blood draw taken 30 minutes post-GPI initiation. The remaining patients were diagnosed approximately 2\u0026ndash;4 hours after the PCI procedure and intravenous GPI administration. Among the remaining 12, one case was identified following the onset of intracerebral hemorrhage with coma, while the other 11 were discovered during routine blood tests on postoperative day 1. The median platelet count dropped sharply from 143 \u0026times; 10⁹/L preoperatively to 4 \u0026times; 10⁹/L after PCI.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eThe clinical characteristics, the timing of detected thrombocytopenia, the use of steroid and immunoglobulin treatment, and the subsequent platelet count trends and outcomes between the early-GIT detection and late-detection group\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e \u003cp\u003eMale, n (%)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eThe Whole\u003c/p\u003e \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;21)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eThe early-detection group\u003c/p\u003e \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;9)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eThe late-detection group\u003c/p\u003e \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;12)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eP\u003c/p\u003e \u003cp\u003evalue\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003ctr\u003e 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colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eUA\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e17(81.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e7(77.8%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e10(83.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1.000\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAMI\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4(19.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e2(22.2%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e2(16.7%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" 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colname=\"c5\"\u003e \u003cp\u003e1.000\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDM\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5(23.8%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e3(33.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e2(16.7%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.611\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHeart failure\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e5(23.8%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1(11.1%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4(33.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.338\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eLaboratory test\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eALT, U/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21(18\u0026ndash;29)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e21(18\u0026ndash;31)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e22(15\u0026ndash;29)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1.000\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eeGFR, mL/min/1.73 m\u0026sup2;\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e92(86\u0026ndash;103)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e98(84\u0026ndash;103)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e92(87\u0026ndash;103)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.808\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNT-proBNP, mmol/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e186.0(68.7-484.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e259.0(69.7-358.4)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e157.9(59.5-627.1)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1.000\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWBC, 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6.9(4.8\u0026ndash;7.9)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e7.8(4.5\u0026ndash;8.2)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e5.9(5.0-7.5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.382\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eConcomitant medication\u003c/b\u003e\u003c/p\u003e \u003cp\u003eHeparin during PCI, n (%)\u003c/p\u003e \u003cp\u003eEptifibatide, n (%)\u003c/p\u003e \u003cp\u003eTirofiban, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21(100%)\u003c/p\u003e \u003cp\u003e9(42.9%)\u003c/p\u003e \u003cp\u003e12(57.1%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e9(100%)\u003c/p\u003e \u003cp\u003e3(33.3%)\u003c/p\u003e \u003cp\u003e6(66.7%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e12(100%)\u003c/p\u003e \u003cp\u003e6(50.0%)\u003c/p\u003e \u003cp\u003e6(50.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNS\u003c/p\u003e \u003cp\u003e0.625\u003c/p\u003e \u003cp\u003e0.691\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTicagrelor, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4(19.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e3(33.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e1(8.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.238\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eClopidogrel, n (%)\u003c/p\u003e \u003cp\u003e\u003cb\u003eTherapy after GIT\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e17(81.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e6(66.7%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e11(91.7%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.635\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDetection of GIT on the day of PCI, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e9(42.9%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e9(100%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNS\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSteroids therapy after GIT, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e17(81.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e9(100%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e8(66.7%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.104\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eImmunoglobulin therapy after GIT, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e11(52.4%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e5(55.6%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e6(50.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1.000\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCombination of steroids and Immunoglobulin therapy, n (%)\u003c/p\u003e \u003cp\u003eNon-interveion, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e11(52.4%)\u003c/p\u003e \u003cp\u003e4(19.0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e5(55.6%)\u003c/p\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e6(50.0%)\u003c/p\u003e \u003cp\u003e4(33.3%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e1.000\u003c/p\u003e \u003cp\u003e0.104\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eOutcomes, n (%)\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSuspend dual antiplatelet therapy after GIT, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e9(42.9%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e5(55.6%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4(36.4%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.653\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eThrombotic event after GIT,, n (%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNS\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eBleeding event, n (%)\u003c/p\u003e \u003cp\u003eFatal intracranial hemorrhage\u003c/p\u003e \u003cp\u003ePetechiae\u003c/p\u003e \u003cp\u003egingival bleeding\u003c/p\u003e \u003cp\u003eprocedural access site oozing\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4(19.1%)\u003c/p\u003e \u003cp\u003e1(4.8%)\u003c/p\u003e \u003cp\u003e1(4.8%)\u003c/p\u003e \u003cp\u003e1(4.8%)\u003c/p\u003e \u003cp\u003e1(4.8%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e1(11.1%)\u003c/p\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003cp\u003e1(11.1%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e3(25.0%)\u003c/p\u003e \u003cp\u003e1(8.3%)\u003c/p\u003e \u003cp\u003e1(8.3%)\u003c/p\u003e \u003cp\u003e1(8.3%)\u003c/p\u003e \u003cp\u003e0(0%)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.504\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003ePlatelet count trend\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count before PCI, 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e193(148\u0026ndash;253)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e219(164\u0026ndash;348)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e239(191\u0026ndash;277)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.754\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count at the timing of detection of GIT, 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6(4\u0026ndash;23)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e20(5\u0026ndash;75)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4(3\u0026ndash;35)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.023\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eThe lowest platelet count after GIT, 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4(2\u0026ndash;8)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e2(2\u0026ndash;19)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4(2\u0026ndash;5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.422\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count on the day of PCI (D0), 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6(2\u0026ndash;19)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e6(2\u0026ndash;19)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eNS\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNS\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count on the day after PCI (D1), 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6(3\u0026ndash;23)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e23(13\u0026ndash;45)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e4(2\u0026ndash;5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.001\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count on the second day after PCI (D2), 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e26(10\u0026ndash;45)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e42(29\u0026ndash;69)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e11(7\u0026ndash;20)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.006\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTime to platelet recovery\u0026thinsp;\u0026gt;\u0026thinsp;20 (\u0026times;10⁹/L) post-PCI, hours\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e48(24\u0026ndash;72)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e24(24\u0026ndash;48)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e72(48\u0026ndash;72)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.017\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTime to platelet recovery\u0026thinsp;\u0026gt;\u0026thinsp;50 (\u0026times;10⁹/L) post-PCI, hours\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e72(48\u0026ndash;96)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e48(48\u0026ndash;72)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e96(72\u0026ndash;102)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.190\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTime to platelet recovery\u0026thinsp;\u0026gt;\u0026thinsp;100 (\u0026times;10⁹/L) post-PCI, hours\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e120(96\u0026ndash;126)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e96(96\u0026ndash;120)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e120(120\u0026ndash;126)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e0.053\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003ctfoot\u003e \u003ctr\u003e\u003ctd colspan=\"5\"\u003eUA, unstable angina; AEMI, acute myocardial infarction; PCI, percutaneous coronary intervention; CKD, chronic kidney disease; HP, hypertension; DM, diabetes mellitus; ALT, alanine aminotransferase; eGFR: estimated Glomerular Filtration Rate; PLT, platelet; NT-proBNP: N-terminal pro-B-type Natriuretic Peptide; WBC, white blood cell; GIT, glycoprotein IIb/IIIa receptor inhibitors induced thrombocytopenia;\u003c/td\u003e\u003c/tr\u003e \u003c/tfoot\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eFollowing the onset of profound thrombocytopenia, 11 patients underwent treatment with both steroids and IVIg, 6 received steroids alone, and 4 received neither intervention. Patients were categorized into three treatment groups (steroid plus IVIg, steroid alone, or no-intervention) to analyze whether steroid/IVIg therapy promoted platelet recovery. No such beneficial effect was found. Given that the no-intervention group comprised only 4 patients, which may compromise the statistical validity, we reclassified the patients into the IVIg treatment group (n\u0026thinsp;=\u0026thinsp;11) and the no-IVIg treatment group (n\u0026thinsp;=\u0026thinsp;10) (Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The results indicated that there was still no significant difference in platelet recovery between the two groups, suggesting that IVIg therapy did not contribute to platelet recovery (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). To study other factors affecting platelet recovery, we grouped patients by whether thrombocytopenia was detected on the day of PCI (early-detection group, n\u0026thinsp;=\u0026thinsp;9; and later-detection group, n\u0026thinsp;=\u0026thinsp;12), and showed that those with an early diagnosis and consequent prompt withdrawal of the GPI exhibited a statistically significant faster platelet recovery (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The median time to platelet recovery\u0026thinsp;\u0026gt;\u0026thinsp;20\u0026times;10⁹/L was significantly shorter in the early-detection group than in the later-detection group (24 hours vs 72 hours, p\u0026thinsp;=\u0026thinsp;0.017). In all patients, the median time for platelet recovery to \u0026gt;\u0026thinsp;50\u0026times;10⁹/L and \u0026gt;\u0026thinsp;100\u0026times;10⁹/L was 72 and 120 hours, respectively.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eThe platelet count and its trend between the IVIg- treatment and non-IVIg treatment group\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\" morerows=\"1\" rowspan=\"2\"\u003e \u003cp\u003ePlatelet count trend\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eThe whole\u003c/p\u003e \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;21)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eIVIg treatment group\u003c/p\u003e \u003cp\u003e(n\u0026thinsp;=\u0026thinsp;11)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eNon-IVIg treatment group (n\u0026thinsp;=\u0026thinsp;11)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eP value\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c2\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e\u0026nbsp;\u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count before PCI, 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e193(148\u0026ndash;253)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e348(271\u0026ndash;409)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e192(144\u0026ndash;242)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.605\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count at the timing of detection of GIT, 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6(4\u0026ndash;23)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e5(5\u0026ndash;13)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e48(13\u0026ndash;77)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.233\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eThe lowest platelet count after GIT, 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e4(2\u0026ndash;8)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e2(1\u0026ndash;5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e11(2\u0026ndash;19)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.426\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count on the day of PCI (D0), 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6(2\u0026ndash;19)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e2(1\u0026ndash;5)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e11(2\u0026ndash;19)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.556\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count on the day after PCI (D1), 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e6(3\u0026ndash;23)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e20(12\u0026ndash;27)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e37(13\u0026ndash;73)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.492\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelet count on the second day after PCI (D2), 10^9/L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e26(10\u0026ndash;45)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e42(25\u0026ndash;51)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e59(34\u0026ndash;82)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.492\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTime to platelet recovery\u0026thinsp;\u0026gt;\u0026thinsp;20 (\u0026times;10⁹/L) post-PCI, hours\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e48(24\u0026ndash;72)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e24(24\u0026ndash;60)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e30(24\u0026ndash;32)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.904\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTime to platelet recovery\u0026thinsp;\u0026gt;\u0026thinsp;50 (\u0026times;10⁹/L) post-PCI, hours\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e72(48\u0026ndash;96)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e48(48\u0026ndash;84)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e60(48\u0026ndash;72)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.515\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTime to platelet recovery\u0026thinsp;\u0026gt;\u0026thinsp;100 (\u0026times;10⁹/L) post-PCI, hours\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e120(96\u0026ndash;126)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e96(84\u0026ndash;132)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e120(96\u0026ndash;108)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c5\"\u003e \u003cp\u003e0.414\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003ctfoot\u003e \u003ctr\u003e\u003ctd colspan=\"5\"\u003eIVIg, Immunoglobulin; PCI, percutaneous coronary intervention; GIT, glycoprotein IIb/IIIa receptor inhibitors induced thrombocytopenia;\u003c/td\u003e\u003c/tr\u003e \u003c/tfoot\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eOutcomes among the 21 patients were as follows: delayed detection of thrombocytopenia was fatal in one case due to sudden intracerebral hemorrhage. The other 20 patients were discharged safely, with only three experiencing minor bleeding (e.g., petechiae, gingival bleeding, or procedural access site oozing).\u003c/p\u003e \u003cp\u003eIt was worth emphasizing that 7 patients experienced systemic shivering and chills resembling an allergic reaction postoperatively, with the incidence significantly higher than that observed in routine clinical practice.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThe main findings of the current study are as follows: GIT occurs shortly after exposure to GPI and is characterized by rapid onset. Early detection of thrombocytopenia is essential for immediate GPI discontinuation, which is the cornerstone of platelet recovery. Steroids and IVIg did not improve platelet recovery in our cohort.\u003c/p\u003e \u003cp\u003eSince all enrolled patients received heparin for intraoperative anticoagulation, it is crucial to differentiate between GIT and HIT. The key differentiating features include the timing of onset, the severity of thrombocytopenia and clinical presentation. GIT typically develops rapidly within hours. HIT is classified into two types\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e: Type I and Type II. Type I HIT is a non-immune reaction that typically occurs within 1 to 2 days of heparin administration. It is characterized by a mild decrease in platelet count, generally fluctuating between 100 and 300 \u0026times; 10⁹/L, and rarely falling below 100 \u0026times; 10⁹/L. Type II HIT is immune-mediated and usually manifests between 4 and 14 days after initial heparin exposure. Furthermore, HIT primarily presents with thrombotic complications rather than bleeding, and the platelet count rarely falls below 20 \u0026times; 10⁹/L. Although HIT antibodies were not tested in the enrolled patients to definitively exclude HIT, based on these three differentiating points, it is reasonable to conclude that the 21 patients included in the final analysis were diagnosed with GIT.\u003c/p\u003e \u003cp\u003eThe etiology of GIT remains unclear, but it is proposed that drug-dependent antibodies which bind platelets in the presence of GPI is the cause of the rapid fall of platelet level\u003csup\u003e\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e. So, treatment with steroids and intravenous IVIg is recommended for these patients. In our retrospective study, 11 patients underwent treatment with both steroids and IVIg, 6 received steroids alone, and 4 received neither intervention following the onset of profound thrombocytopenia. To mitigate statistical errors arising from the small sample size, we employed two grouping strategies: one categorized enrolled patients into three groups (steroid plus IVIg, steroid alone, or no-intervention), while the other divided patients into two groups (disregarding steroid use: IVIg treatment group and no-IVIg treatment group). The final analysis indicated that there were no statistically significant differences in platelet recovery between groups, suggesting that IVIg/steroids therapy did not contribute to platelet recovery. The key factor for platelet recovery lies in the timely detection of platelet decline and the prompt cessation of the GPI agent. Our study revealed that the median time required for platelet recovery to above 20 \u0026times;10⁹/L was significantly shorter in the early detection group than in the later detection group (24 hours vs 72 hours, p\u0026thinsp;=\u0026thinsp;0.017). Platelet counts on postoperative day 1 and day 2 also differed significantly between the two groups (Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). In summary, IVIg treatment provided no clinical benefit for GIT. For patients undergoing PCI and receiving GPI treatment, the most critical measure is early detection of thrombocytopenia and prompt withdrawal of the causative agent.\u003c/p\u003e \u003cp\u003ePrevious findings\u003csup\u003e\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u003c/sup\u003e indicated that GIT could be caused by drug-dependent antibodies, either naturally occurring or induced by prior drug exposure. Thus, GIT may occur upon first exposure to GPI or upon re-exposure. In our study, there were 8 patients with a history of PCI who may be exposed to GPI without developing GIT, but developed severe GIT upon re-exposure. This finding aligns with previous research conclusions\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e,\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u003c/sup\u003e, indicating that the potential risk of GIT cannot be overlooked regardless of whether GPI is used for the first time or upon re-exposure.\u003c/p\u003e \u003cp\u003eRegarding the timing of GIT occurrence, thrombocytopenia can occur shortly after GPI exposure. For instance, in our study, one patient experienced platelet decreases within half an hour of GPI exposure. Case reports have also indicated that a decrease in platelet count can be detected as early as 10 minutes after drug GPI administration\u003csup\u003e\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u003c/sup\u003e. As for the time to platelet recovery in patients with profound GIT, our study showed that the median time required for platelets to recover to over 100\u0026times;10⁹/L is 120 hours which was consistent with previous case reports\u003csup\u003e\u003cspan additionalcitationids=\"CR11\" citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003ePrevious literature\u003csup\u003e\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e,\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e\u003c/sup\u003e have reported GIT can be accompanied by systemic allergic reactions such as chills and shivering. This phenomenon was also observed in our retrospective study with a notably high incidence. However, based on clinical records, we found that physicians often misattributed allergic reactions to contrast media, failing to recognize them as possible GIT symptoms and leading to neglected prompt platelet testing. This highlights the need for clinician training on this issue, to ensure that when managing patients with allergic reactions after PCI, they consider the possibility of GIT and immediately order platelet testing for early identification.\u003c/p\u003e \u003cp\u003eBecause thrombocytopenia may occur rapidly and be asymptomatic, many cases were discovered during routine blood tests on postoperative day 1. Although GIT does not routinely lead to severe bleeding complications, one patient in our study died from cerebral hemorrhage as a complication of thrombocytopenia that was not detected and managed in time, with a subsequent platelet count as low as 1 \u0026times;10⁹/L. This tragic outcome again underscores the critical importance of early detection and prompt discontinuation of GPI.\u003c/p\u003e \u003cp\u003eSince there are no commercially available assays that can be performed rapidly enough to detect GIT, the most critical measure is to perform platelet count testing within 2 hours after GPI administration. Early detection of GIT and timely drug discontinuation can prevent further platelet decline, thereby avoiding prolonged hospitalization and potential adverse events. Steroids and IVIg did not improve platelet recovery for profound GIT.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eGIT occurs shortly after exposure to GPI and is characterized by rapid onset. Early detection of thrombocytopenia is essential for immediate GPI discontinuation, which is the cornerstone of platelet recovery. Steroids and IVIg did not improve platelet recovery in our cohort.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e \u003ch2\u003eConflicts of interest\u003c/h2\u003e \u003cp\u003eThe authors have no conflicts of interest to disclose.\u003c/p\u003e \u003c/p\u003e\u003cp\u003e \u003ch2\u003eEthics approval and consent to participate\u003c/h2\u003e \u003cp\u003eThe study was approved by the ethics committee of our institution (No. XJTU1AF2025LSYY-945). Written informed consent was waived due to a retrospective design.\u003c/p\u003e \u003c/p\u003e\u003cp\u003e \u003ch2\u003eClinical trial number\u003c/h2\u003e \u003cp\u003eNot applicable.\u003c/p\u003e \u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e \u003cp\u003eThis work was supported by the National Natural Science Foundation of China (82425004).\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eXF and YW conceived and designed the study. XF, KF and LL collected and analyzed the data. YW wrote the first draft of the manuscript. All authors reviewed and edited the manuscript and approved the final version of the manuscript.\u003c/p\u003e\u003ch2\u003eAcknowledgement\u003c/h2\u003e\u003cp\u003eWe thank for the assistance of Ling Bai from the First Affiliated Hospital of Xi\u0026rsquo;an Jiaotong University for her valuable contribution to the interpretation and analysis of the data.\u003c/p\u003e\u003ch2\u003eData Availability\u003c/h2\u003e\u003cp\u003eData supporting the conclusions of this article are included within the article and available from the corresponding authors on reasonable request.\u003c/p\u003e\n\u003ch3\u003eData Availability\u003c/h3\u003e\n\u003cp\u003eData supporting the conclusions of this article are included within the article and available from the corresponding authors on reasonable request.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eBosch X, Marrugat J, Sanchis J. Platelet glycoprotein IIb/IIIa blockers during percutaneous coronary intervention and as the initial medical treatment of non-ST segment elevation acute coronary syndromes. Cochrane Database Syst Rev. 2013;2013(11):Cd002130.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSafley DM, Venkitachalam L, Kennedy KF, Cohen DJ. Impact of Glycoprotein IIb/IIIa Inhibition in Contemporary Percutaneous Coronary Intervention for Acute Coronary Syndromes: Insights From the National Cardiovascular Data Registry. JACC Cardiovasc interventions. 2015;8(12):1574\u0026ndash;82.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRikken S, van 't Hof AWJ, Ten Berg JM, Kereiakes DJ, Coller BS. Critical Analysis of Thrombocytopenia Associated With Glycoprotein IIb/IIIa Inhibitors and Potential Role of Zalunfiban, a Novel Small Molecule Glycoprotein Inhibitor, in Understanding the Mechanism(s). J Am Heart Association. 2023;12(24):e031855.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang J, Zou D. Tirofiban-induced thrombocytopenia. Ann Med. 2023;55(1):2233425.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMasood F, Hashmi S, Chaus A, Hertsberg A, Ehrenpreis ED. Complications and Management of Eptifibatide-Induced Thrombocytopenia. Annals pharmacotherapy. 2021;55(12):1467\u0026ndash;73.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHuxtable LM, Tafreshi MJ, Rakkar AN. Frequency and management of thrombocytopenia with the glycoprotein IIb/IIIa receptor antagonists. Am J Cardiol. 2006;97(3):426\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHan G, Song S, Wan S, et al. Heparin-Induced Thrombocytopenia and Thrombosis in Patients With or Without a Thrombophilia Background: A Systematic Review Involved 602 Cases. Int J vascular Med. 2025;2025:9338124.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBougie DW, Wilker PR, Wuitschick ED, et al. Acute thrombocytopenia after treatment with tirofiban or eptifibatide is associated with antibodies specific for ligand-occupied GPIIb/IIIa. Blood. 2002;100(6):2071\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAttaya S, Kanthi Y, Aster R, McCrae K. Acute profound thrombocytopenia with second exposure to eptifibatide associated with a strong antibody reaction. Platelets. 2009;20(1):64\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLi Y, Qiu J, Gao Y, Li G. Case report: reuse of tirofiban leads to very severe thrombocytopenia. Front Cardiovasc Med. 2023;10:1130552.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu J, Oorloff MD, Nadella A, Yan Y, Zhou N. Tirofiban-induced acute profound thrombocytopenia in endovascular therapy for acute ischemic stroke: a rare case report. BMC Neurol. 2025;25(1):355.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGheith Z, Kilani A, Nguyen T. Eptifibatide-Induced Severe Thrombocytopenia After ST-Elevation Myocardial Infarction (STEMI): A Case Report. Cureus. 2022;14(9):e29549.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eVayne C, Gu\u0026eacute;ry EA, Rollin J, Baglo T, Petermann R, Gruel Y. Pathophysiology and Diagnosis of Drug-Induced Immune Thrombocytopenia. J Clin Med 2020;9(7).\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"
[email protected]","identity":"bmc-cardiovascular-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bcar","sideBox":"Learn more about [BMC Cardiovascular Disorders](http://bmccardiovascdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bcar/default.aspx","title":"BMC Cardiovascular Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"glycoprotein IIb/IIIa receptor inhibitor, percutaneous coronary intervention, thrombocytopenia, immunoglobulin, steroids","lastPublishedDoi":"10.21203/rs.3.rs-9038136/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9038136/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e \u003cb\u003eBackground\u003c/b\u003e Acute profound thrombocytopenia is an infrequent, but potentially serious, even fatal complication associated with intravenous glycoprotein IIb/IIIa receptor inhibitors (GPI), which are widely used in acute coronary syndrome and percutaneous coronary intervention (PCI). Treatment with steroids and intravenous immunoglobulin (IVIg) is recommended for GPI-induced thrombocytopenia (GIT), but its efficacy is rarely reported.\u003c/p\u003e \u003cp\u003e \u003cb\u003eMethods\u003c/b\u003e In this retrospective study, we enrolled 21 patients who developed acute profound thrombocytopenia (defined as a platelet count\u0026thinsp;\u0026lt;\u0026thinsp;20 \u0026times;10⁹/L) following PCI with GPI treatment. We analyzed their clinical characteristics, the timing of detected thrombocytopenia, the use of steroid and IVIg treatment, and the subsequent platelet count trends and outcomes.\u003c/p\u003e \u003cp\u003e \u003cb\u003eResults\u003c/b\u003e Among the 21 patients, 7 were female, and the median age was 63 years. Tirofiban and eptifibatide were administered to 12 and 9 patients, respectively. Thrombocytopenia was detected on the day of PCI in 9 patients. Among the remaining 12, one case was identified following the onset of intracerebral hemorrhage with coma, while the other 11 were discovered during routine blood tests on postoperative day 1. The median platelet count dropped sharply from 143 \u0026times; 10⁹/L preoperatively to 4 \u0026times; 10⁹/L after GPI treatment. Following the onset of profound thrombocytopenia, 11 patients underwent treatment with both steroids and IVIg, 6 received steroids alone, and 4 received neither intervention. Patients were categorized into three treatment groups (steroid plus IVIg, steroid alone, or no-intervention) with the aim of analyzing whether steroid/IVIg therapy promoted platelet recovery. No such beneficial effect was found. A separate analysis, grouping patients by whether thrombocytopenia was detected on the day of PCI (early-detection group and later-detection group), showed that those with an early diagnosis and consequent prompt withdrawal of the GPI exhibited a statistically significant faster platelet recovery. The median time to platelet recovery\u0026thinsp;\u0026gt;\u0026thinsp;20\u0026times;10⁹/L was significantly shorter in the early-detection group (24 hours) than in the later-detection group (72 hours) with p\u0026thinsp;=\u0026thinsp;0.017.\u003c/p\u003e \u003cp\u003e \u003cb\u003eConclusions\u003c/b\u003e GIT is characterized by rapid onset. Early detection of thrombocytopenia is essential for immediate GPI discontinuation, which is the cornerstone of platelet recovery. Steroids and IVIg did not improve platelet recovery in our cohort.\u003c/p\u003e","manuscriptTitle":"Acute profound thrombocytopenia associated with glycoprotein IIb/IIIa receptor inhibitor after percutaneous coronary intervention: therapy insights from a single center 6-year experience","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-03-24 10:28:08","doi":"10.21203/rs.3.rs-9038136/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-04-17T09:30:50+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-13T09:10:06+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-08T23:43:16+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-08T15:24:35+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"47078900832691084966946023917737405106","date":"2026-04-05T23:16:52+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"108216151568331274239590505761963217744","date":"2026-03-30T10:48:15+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-20T08:11:27+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"156754823109525749363611065903704367516","date":"2026-03-19T12:26:45+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"54734632299207931169476267111376768092","date":"2026-03-19T10:49:32+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-03-18T21:09:36+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-03-10T10:44:16+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-03-10T02:33:24+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-03-10T02:32:45+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Cardiovascular Disorders","date":"2026-03-05T08:40:23+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"
[email protected]","identity":"bmc-cardiovascular-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bcar","sideBox":"Learn more about [BMC Cardiovascular Disorders](http://bmccardiovascdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bcar/default.aspx","title":"BMC Cardiovascular Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"9f7c0f33-abd0-4e39-bee1-2395fa353b00","owner":[],"postedDate":"March 24th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"in-revision","subjectAreas":[],"tags":[],"updatedAt":"2026-05-18T07:26:07+00:00","versionOfRecord":[],"versionCreatedAt":"2026-03-24 10:28:08","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9038136","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9038136","identity":"rs-9038136","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}
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