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Platelet Aggregation Effect of Tirofiban Compared with Abciximab among Patients on Percutaneous Coronary Interventions: A Systematic Review
*Corresponding author: Dr. Paridhi Mathur, Department of Medical Affairs, Mankind Pharma Ltd., New Delhi, India. paridhimathur95@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Mathur A, Jaiswal B, Mathur P, Singal R, Mitra SK. Platelet Aggregation Effect of Tirofiban Compared with Abciximab among Patients on Percutaneous Coronary Interventions: A Systematic Review. J Card Crit Care TSS. 2026;10:7-15. doi: 10.25259/JCCC_57_2025
Abstract
Platelet aggregation plays a vital role in atherothrombosis and percutaneous coronary intervention (PCI) complications. In this systematic review, tirofiban and abciximab, glycoprotein IIb/IIIa inhibitors, were compared for efficacy and safety in PCI, based on five randomized trials and 539 participants, adhering to the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. Both drugs were effective and tolerable in most cases. Tirofiban had a reduced risk of thrombocytopenia and comparable rates of bleeding to abciximab. Intracoronary tirofiban has potential over intravenous administration, particularly in ST-elevation myocardial infarction, with better 30-day outcomes and thrombolysis in myocardial infarction grade 3 flow, without an increased risk of bleeding. The choice of treatment should be based on the individual patient. Future clinical benefits should be substantiated by larger trials to provide guidance for best practices.
Keywords
Abciximab
Glycoprotein IIB/IIIA antagonists
Percutaneous coronary intervention
Platelet aggregation
Tirofiban
INTRODUCTION
Glycoprotein IIb/IIIa receptor antagonists, such as abciximab and tirofiban, are important for preventing platelet aggregation during percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS).[1] They inhibit the binding of fibrinogen and von Willebrand factor to the activated platelets, thereby preventing thrombus formation. Tirofiban binds reversibly to the receptor and has a more rapid dissociation rate than abciximab, with greater dosage flexibility and lower bleeding risk.[2] Although tirofiban has a slower onset of maximal platelet inhibition (PI) than abciximab,[3,4] subsequent time points show similar inhibition,[5] and diabetic patients may gain more from tirofiban.[6] Tirofiban also has a reduced risk of thrombocytopenia[7] and similar rates of major bleeding.[8] These two drugs have similar effects on mortality and myocardial infarction (MI).[8,9] Intracoronary (IC) tirofiban administration, especially in the setting of ST-elevation MI (STEMI), resulted in better thrombolysis in MI grade 3 flow, improved left ventricular ejection fraction, and reduced 30-day major adverse cardiovascular events (MACE) without elevating bleeding risk.[10] This review was performed to assess the comparative efficacy, safety, and clinical outcomes of abciximab and tirofiban in patients undergoing PCI, emphasizing their respective pharmacological benefits as well as optimal strategies for application.
METHODS
Literature search
A systematic review adhering to the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines was conducted to evaluate the effects of tirofiban and abciximab on platelet aggregation in patients undergoing PCI during and after the procedure. The study selection process included solely randomized clinical trials (RCTs) while excluding case reports, non-RCTs, laboratory studies, observational studies, uncontrolled trials, and review articles. Researchers examined PubMed and Google Scholar records from their beginnings to current data using PCI, tirofiban, and abciximab terms while applying filters for human studies, the English language, and clinical trials. The search spanned from the inception of each database to the latest available information. This approach ensured a comprehensive and systematic evaluation of existing literature regarding the comparative efficacy of tirofiban and abciximab in the context of PCI. The search strategy utilized the following terms: (‘percutaneous coronary intervention’[MeSH Terms] OR ‘percutaneous coronary intervention’[Text Word]) AND (‘tirofiban’[MeSH Terms] OR ‘tirofiban’[Text Word] OR ‘abciximab’[MeSH Terms] OR ‘abciximab’[Text Word]). The results were limited by the following filters: Humans, English, and Clinical Trial.
Participants/Population
The population of interest included patients who had recently undergone PCI with tirofiban as the intervention and abciximab as the comparator, focusing on platelet aggregation and inhibition as the primary outcomes.
Data extraction (selection and coding)
Two independent reviewers utilized a pre-designed data extraction form to collect relevant information from the selected studies. Any disagreements that arose during this process were resolved through one-to-one discussions between the reviewers. The main contents of the data collection form included basic information of studies (title, authors, year, age, sex, and comorbidities), indication, dose, aim, method, and results.
Platelet function was assessed using various methods across the included studies. The primary method was light transmission aggregometry, which measures the change in light transmission through a suspension of platelet-rich plasma as platelets aggregate. While this method is considered the gold standard, it is laboratory-intensive. Other studies utilized point-of-care assays, which provide faster results but may have less precision. The choice of assay can influence the reported efficacy of antiplatelet agents, and this was considered during data synthesis.
Quality assessment
Two independent evaluators meticulously assessed all selected studies in this systematic review, employing the RoB 2 tool for thorough analysis, resulting in the synthesis and interpretation of study findings. The appraisal questions were answered with “Yes,” “No,” or “Unclear,” where “Yes” indicated low risk of bias (ROB) and “No” indicated poor quality or unfulfilled criteria and high ROB.
RESULTS
Literature search strategy
A PRISMA flowchart depicting the search strategy based on the inclusion and exclusion criteria is shown in Figure 1. A total of 226 research articles were initially retrieved based on MeSH and keywords. After 45 duplicate documents were removed, the remaining 181 articles were subjected to title and abstract screening. Only 21 articles were selected for the full-text analysis based on the inclusion and exclusion criteria. Upon full-text analysis of these 21 research articles, five relevant articles were selected for the study.
- Preferred Reporting Items for Systematic Reviews and Meta-analyses flow diagram for database searches in the systematic review.
Clinical study characteristics
Studies on 539 patients have been conducted in several countries, three from the USA,[3,5,6,11] and one each from Germany[5] and Italy.[3,5,6,11,12] Saltzman et al. included 95 patients, Neumann et al. included 60, Valgimigli et al. included 175, Kini et al. included 183, and Kereiakes et al. included 29.[3,5,6,11,12] Previous studies have compared glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban, and eptifibatide) in patients undergoing PCI among diverse populations and settings. Kereiakes et al. detected variations in PI onset and degree among inhibitors in 29 patients with unstable angina.[3] Neumann et al. reported equivalent antiplatelet activities of abciximab, tirofiban, and eptifibatide in 60 patients with coronary artery disease.[5] The TEAM pilot study Kini et al. also detected similar 30-day MACE and enzyme release rates in 180 high-risk PCI patients with 90% PI.[11] Valgimigli et al. compared high-dose tirofiban and sirolimus-eluting stents with abciximab and bare-metal stents in 175 acute MI patients and achieved better outcomes with the tirofiban-sirolimus combination.[12] Saltzman et al. demonstrated that both tirofiban and abciximab significantly inhibited platelets and C-reactive protein (CRP) levels in 95 elective or unstable angina PCI patients with normal creatine kinase-MB levels.[6] Collectively, these investigations indicated similar safety and efficacy profiles for these inhibitors, warranting their application in various clinical contexts with judicious patient choice [Supplementary Material].
ROB analysis
The ROB analysis of the included studies revealed varying levels of potential bias. The studies by Kereiakes et al., Kini et al., Neumann et al., and Valgimigli et al. had varying levels of risk for bias, while Saltzman et al. showed a low ROB across all domains.[3,5,6,11,12] These assessments indicated that, while some studies had methodological strengths, others had areas of potential bias that could impact the reliability of their findings.
PI and aggregation
Tirofiban showed a diminished PI magnitude and slower maximal effect than abciximab and eptifibatide, with 10-min residual aggregation of 26.5% for tirofiban compared to 6.4% for abciximab.[3] At 2 h, Residual Platelet Function Aggregation decreased equivalent platelet aggregation for all three agents.[5] The TEAM pilot study showed >90% inhibition of platelets in high-risk PCI patients without excessive bleeding.[11] Tirofiban with sirolimus-eluting stents enhanced clinical outcomes compared to abciximab with bare-metal stents.[12] Tirofiban showed more initial inhibition than abciximab in diabetes, with hs-CRP correlating negatively with PI in those given abciximab[6] [Table 1].
| Author | Intervention | Comparison | Background | Method | Age |
|---|---|---|---|---|---|
| Kereiakes et al. 1999[3] | Tirofiban was administered as a 0.4 mg/kg/min bolus for 30 min intravenously, followed by a 0.1 mg/kg/min infusion over 20–24 h. | Abciximab was administered as a 0.25 mg/kg bolus intravenously, followed by a 0.125 mg/kg/min (to a maximum of 10 mg/min) intravenous infusion, which was administered continuously over 12 h. |
All patients received concurrent therapy with aspirin 325 mg orally daily. Patients who underwent intracoronary stent deployment also received a single dose of ticlopidine 250 mg orally immediately after PCI (no loading dose) and twice daily thereafter. Heparin administration at the time of PCI was standardized: for abciximab, a 70 U/kg heparin bolus (not to exceed 7,000 U) was given to achieve an activated clotting time of≥200 s; for tirofiban and eptifibatide, a 100 U/kg heparin bolus (not to exceed 10,000 U) was administered to achieve an activated clotting time of ≥300 s. Intravenous heparin was not administered after PCI, and vascular access sheaths were removed early when the activated clotting time was <180 s. All patients followed a critical care pathway for vascular hemostasis, which included femostop for 4 h, pressure dressing for 6 h, and bed rest until the following morning. Vascular closure devices were not used in this study. |
Ex vivo platelet function was compared using both standard light transmission aggregometry and RPFA during and after the administration of abciximab, eptifibatide, or tirofiban in approved dose regimens on a randomized basis at the time of PCI in patients with unstable angina pectoris. | - |
| Neumann et al. 2001[5] | A 10 μg/ kg bolus of tirofiban was given, followed by a continuous infusion at a rate of 0.15 μg/kg/min for a duration of 72 h. | A bolus of abciximab at a dose of 0.25 mg/kg of body weight was given, followed by a continuous infusion at a rate of 10 μg/min for a duration of 12 h. | In the abciximab group, the peri-interventional heparin dose was set at 70 U/kg, while in the other groups, it was 100 U/kg. All patients were administered ticlopidine and aspirin (100 mg twice a day), beginning 1–8 h before the procedure. Ticlopidine was given at a dosage of 500 mg twice a day for the initial three doses, followed by 250 mg for a duration of 4 weeks. | Sixty patients undergoing coronary stenting were randomly allocated to receive one of three treatments: abciximab (administered as a 0.25 mg/kg bolus followed by a 10 μg/min infusion for 12 h), tirofiban (given as a 10 μg/kg bolus with a 0.15 μg/kg/min infusion over 72 h), or eptifibatide (provided as a 180 μg/kg bolus and a 2 μg/kg/min infusion for 72 h). Blood samples were collected at various intervals to evaluate platelet function through flow cytometry, turbidimetric aggregometry, and the RPFA. |
Abciximab (Mean±SD): 67±10 tirofiban (Mean±SD): 64±12 |
| Kini et al. 2002[11] | A 10 μg/ kg bolus of tirofiban was administered, followed by a 12-h infusion at a rate of 0.15 μg/kg/min. | Abciximab was administered as a bolus of 0.25 mg/kg, followed by a continuous infusion at a rate of 0.125 μg/kg/min, with a cap of 10 micrograms/min, for a duration of 12 h. | CK-MB and troponin I levels were assessed for all patients at the start, between 6 and 8 h, and again 12–24 h following the procedure. Patients continued taking aspirin (81–325 mg) and clopidogrel (75 mg, if a stent was placed) for a duration of 30 days. | At the 10-min mark, if PI reached 90%, a second half-dose of the study medication was given, and the PCI procedure commenced. Ten min following the second half-bolus, the PI was recalculated, but no further bolus doses of GP inhibitors were administered due to safety concerns. Abciximab was given as a bolus of 0.25 mg/kg, followed by a continuous infusion at a rate of 0.125 μg/kg/min, with a maximum limit of 10 μg/min, for a duration of 12 h. A 10 μg/kg bolus of tirofiban was administered, followed by a continuous infusion at a rate of 0.15 μg/kg/min for a duration of 12 h. A 180 μg/kg bolus of eptifibatide was administered, followed by a continuous infusion at a rate of 2 μg/kg/min for a duration of 12 h. CK-MB and troponin I levels were assessed for all patients at the start, between 6 and 8 h, and again 12–24 h following the procedure. Aspirin, in doses ranging from 81 to 325 mg, and clopidogrel at 75 mg (if a stent was placed) were administered for a duration of 30 days. | A total of 180 patients (mean age 65±11 years) |
| Valgimigli et al. 2005[12] | Tirofiban was administered as a 25 μg/kg bolus over a period of 3 min, followed by a continuous infusion at a rate of 0.15 μg/kg/min for a duration of 18–24 h. | Abciximab was given as a 0.25 mg/kg bolus over a period of 3 min, followed by a continuous infusion at a rate of 0.125 μg/kg/min for 12 h. | Each patient was administered aspirin, starting with an oral loading dose of 160–325 mg, followed by a daily oral dose of 80–125 mg indefinitely. In addition, they received clopidogrel, beginning with a 300 mg oral loading dose, then continuing with 75 mg/day for a minimum of 3 months. Before the procedure, heparin was administered at a dose of 50 U/kg, with additional doses given as needed to ensure and sustain an ACT of no <200 s. | In the STRATEGY study, a prospective, single-blind, randomized controlled trial was carried out at a single referral center in Italy from March 6, 2003, to April 23, 2004. A total of 175 patients, with a median age of 63 years and an interquartile range of 55–72, who had STEMI or a suspected new left bundle-branch block, were randomized. Participants were divided into two groups: one received a single high-dose bolus of tirofiban along with sirolimus-eluting stents (n=87), while the other was given a standard dose of abciximab with bare-metal stents (n=88). The primary endpoint was a composite of death, non-fatal MI, stroke, or binary restenosis at 8 months. Among the secondary outcomes were the absence of significant cardiac or cerebrovascular adverse events, which include composite of death, reinfarction, stroke, and repeat TVR, assessed at 30 days and 8 months. | Abciximab (Median; IQR): 63; 55–72 Tirofiban (Median; IQR): 62; 54–72 |
| Saltzman et al. 2010[6] | Tirofiban was given as a bolus initially, followed by an infusion at a rate of 0.15 µg/kg/min for a duration of 12 h. | Abciximab was administered as a 0.25 mg/kg bolus just before the PCI, followed by a 12-h infusion at a rate of 0.125 µg/kg/min, with a cap of 10 mg. | At the start of the PCI procedure, heparin was given to reach an ACT target of 200–250 s. | A total of 95 patients, who met the eligibility criteria consecutively, were assigned at random to receive either tirofiban or abciximab prior to undergoing stent placement for native coronary artery revascularization. The clinical outcomes assessed were mortality, nonfatal MI, and TVR through coronary artery bypass grafting or PCI within 30 days following the procedure. The medications were evaluated for variations in platelet aggregation using a RPFA, along with assessments of the inflammatory marker CRP at regular intervals after drug administration during PCI. | - |
| Author | Gender | Co-morbidities | Results | Conclusion | |
| Kereiakes et al. 1999[3] | Abciximab, male n=/60%); tirofiban, male n=7/78% |
Diabetes • Tirofiban (n=4/40%) • Abciximab (n=3/30%) Cigarette smoker • Tirofiban (n=1/10%); • Abciximab (n=7/70%) |
Light transmission aggregometry revealed that tirofiban resulted in less intense PI compared to eptifibatide or abciximab. Furthermore, the 30-min bolus approach for tirofiban led to a slower achievement of peak PI following the start of the bolus infusion. | The trends in platelet function observed suggested potential differences, but whether these would translate into clinical outcome differences awaited definition by larger-scale randomized clinical trials comparing these platelet GP IIb/IIIa inhibitors. | |
| Neumann et al. 2001[5] | Abciximab, Male n=16; tirofiban n=Male: 17 |
Active smoker • Abciximab (n=8) • Tirofiban (n=8) Hypercholesterolemia • Abciximab (n=15) • Tirofiban (n=16) Hypertension • Abciximab (n=15) • Tirofiban (n=16) Diabetes • Abciximab (n=6) • Tirofiban (n=4) Unstable angina • Abciximab (n=7) • Tirofiban (n=6) |
Based on the RPFA, 2 h following infusion, abciximab reduced platelet aggregation to 5.9±7.8% of the baseline level, tirofiban to 5.0±5.4%, and eptifibatide to 7.8±7.1% (P=0.42). The results from turbidimetric aggregometry using adenosine diphosphate as a stimulant were comparable. The inhibition percentage of platelet aggregation following thrombin receptor activation was 45.8±16.8% with abciximab, 51.3±17.6% with tirofiban, and 52.9±14.8% with eptifibatide (P=0.37). During the infusion, tirofiban and eptifibatide sustained their level of PI. Flow cytometry results indicated that the decrease in monocyte-platelet interaction was similar across the groups: 20.0±21.9% for abciximab, 23.8±18.2% for tirofiban, and 21.0±19.8% for eptifibatide, with a P=0.87. | At the doses currently recommended, abciximab, tirofiban, and eptifibatide resulted in comparable levels of platelet aggregation inhibition and similarly reduced the interaction between platelets and monocytes. | |
| Kini et al. 2002[11] | - | - | The TEAM pilot study emphasized the significance of achieving more than 90% PI in patients undergoing high-risk PCI. It showed that this level of inhibition could be reached in the majority of patients by administering a half-bolus of any GP IIb/IIIa inhibitor. This approach did not lead to an increase in major or minor bleeding, periprocedural myocardial necrosis, or 30-day MACE across all three GP IIb/IIIa inhibitors. | PCI in patients with 90% PI resulted in lower CK-MB release and 30-day MACE compared to PCI performed in the group without achieving 90% PI, although the difference was not statistically significant. | |
| Valgimigli et al. 2005[12] | Abciximab, Male n=61/69% Tirofiban, Male n=67/77% |
Diabetes • Tirofiban (n=15/17%) • Abciximab (n=11/12%) Hypertension • Tirofiban (n=48/55%) • Abciximab (n=44/50%) Smoker • Tirofiban (n=34/39%) • Abciximab (n=36/41%) |
In the group receiving tirofiban along with a sirolimus-eluting stent, 14 out of 74 patients (19%; 95% CI, 10–28%) achieved the primary endpoint. In contrast, in the group treated with abciximab and a bare-metal stent, 37 out of 74 patients (50%; 95% CI, 44–56%) reached the same endpoint (hazard ratio, 0.33; 95% CI, 0.18–0.60;P<0 0.001). The group receiving tirofiban along with a sirolimus-eluting stent experienced a significantly lower cumulative incidence of death, reinfarction, stroke, or TVR at 18%, compared to 32% in the group treated with abciximab and a bare-metal stent (hazard ratio, 0.53; 95% CI, 0.28–0.92;P=0.04), primarily due to a decrease in TVR. In the group receiving tirofiban along with sirolimus-eluting stents, 6 out of 67 patients (9%; 95% CI, 2–16%) experienced binary restenosis. In contrast, 24 out of 66 patients (36%; 95% CI, 26–46%) in the group treated with abciximab and bare-metal stents encountered the same condition (P=0.002). | The use of tirofiban in conjunction with sirolimus-eluting stents for treating infarcted arteries has shown potential in enhancing patient outcomes and reducing healthcare costs for those experiencing a MI and undergoing primary intervention. | |
| Saltzman et al. 2010[6] | - | - | Platelet aggregation did not show any notable differences at the 10-, 20-, 30-, and 45-min intervals during the procedure. In patients with diabetes, abciximab demonstrated significantly less PI than tirofiban at the 10-min mark, with values of 84.17±8.28% compared to 90.40±5.79% (P=0.0097). In patients receiving abciximab, a Spearman correlation coefficient model revealed that high-sensitivity C-reactive protein was inversely correlated with PI over time, with a coefficient of−0.7307 and a P=0.0002. | During PCI, there is no significant difference in the level of PI between tirofiban and abciximab. The study found that tirofiban exhibited a stronger inhibitory effect in diabetic groups at the initial time point. During PCI, there may be an inverse relationship between PI and CRP levels. | |
PCI: Percutaneous coronary intervention, TVR: Target vessel revascularization, CRP: C-reactive protein, MI: Myocardial infarction, ACT: Activated clotting time, RPFA: Rapid platelet function assay, MACE: Major adverse cardiac events, PI: Platelet inhibition, CK-MB: Creatine kinase-myocardial band, IOR: Interquartile range, CI: Confidence interval, IQR: Interquartile range, GP: Glycoprotein
DISCUSSION
Tirofiban, a glycoprotein IIb/IIIa antagonist, inhibits platelet aggregation and significant cardiac events during PCI when combined with aspirin and heparin. It acts by binding to the Glycoprotein (GP) IIb/IIIa receptors and inducing rapid inhibition. However, it was less protective than abciximab against 30-day ischemic complications in patients with stents. Tirofiban bolus administration for over 30 min results in prolonged peak inhibition and lower intensity than abciximab and eptifibatide.[3] Abciximab shows more potent inhibition and can maintain endothelial function after stenting. IC administration of tirofiban is beneficial for patients with STEMI. This review compares abciximab with tirofiban, emphasizing the drug choice based on clinical and pharmacological profiles.
Comparison between tirofiban and abciximab
In comparing tirofiban with abciximab, the present review showed both common and differing results. The patients were predominantly males aged 63–67 years, often with diabetes, hypertension, and smoking history. Dosage regimens differed: Kereiakes et al. employed tirofiban (bolus 0.4 mg/kg/min and infusion 0.1 mg/kg/min) and abciximab (bolus 0.25 mg/kg, infusion 0.125 mg/kg/min for 12 h), both with aspirin, ticlopidine, and heparin.[3] Neumann et al. and Valgimigli et al. used similar dosages with clopidogrel.[5,12] Tirofiban has a slower and more reversible binding, whereas abciximab offers stronger immediate inhibition.[3,5] Neumann et al. reported similar PI: 5.9% in the abciximab group versus 5.0% in the tirofiban group (P = 0.42).[5] The TEAM pilot study highlighted the significance of >90% PI without increasing the risk of bleeding.[11] STRATEGY reported improved results with tirofiban and sirolimus-eluting stents compared with abciximab and bare-metal stents.[12] Saltzman et al. observed no significant differences, although tirofiban showed better initial inhibition in patients with diabetes.[6] Both medications share similar bleeding profiles, and abciximab causes more thrombocytopenia and vascular complications.[3,13] Choice must factor in comorbidities, stent type, and pharmacology.[3,5,11] Tirofiban, a non-peptide GP IIb/IIIa antagonist, provides reversible, dose-dependent inhibition, which is appropriate for patients with ACS who undergo PCI.[14] Abciximab, a monoclonal antibody, irreversibly binds with anti-inflammatory properties.
Kang et al. reported that tirofiban enhanced left ventricular ejection fraction and decreased CRP, interleukin (IL)-6, and tumor necrosis factor-alpha levels in patients with acute myocardial infarction.[15] Li et al. established that tirofiban combined with ticagrelor enhanced coagulation, myocardial injury markers (creatine kinase-myocardial band, troponin I), and control of inflammation.[16] Zhang et al. established decreased hs-CRP, IL-6, and soluble intercellular adhesion molecule-1 levels and improved function with tirofiban with PCI in STEMI.[17] Tirofiban also reduces stent thrombosis and inflammation.[18] Fabris et al. demonstrated reduced 30-day and 1-year mortality with prehospital tirofiban administration, without excess bleeding.[19] The reversible binding, short half-life, and pharmacokinetic predictability of tirofiban favor its use in surgical or high-risk patients. Abciximab, although potent, is less favored owing to its prolonged effects and excess thrombocytopenia.[3] Both are equipotent in inhibiting platelet aggregation; however, tirofiban permits flexible dosing and rapid recovery, which is advantageous for elderly or renally compromised patients. Ex vivo platelet testing provides pharmacodynamic information but does not always correlate with clinical outcomes. Decisions for treatment should be based on patient-specific variables, comorbidities, stent type, risk of bleeding, and real-world events such as MACE and bleeding and not solely on laboratory results.[20-22]
CONCLUSION
This systematic review highlighted that both tirofiban and abciximab are effective and safe glycoprotein IIb/IIIa inhibitors that can prevent platelet aggregation during PCI. Although there are nuances in their efficacy and safety profiles, careful consideration of these differences can help clinicians make informed decisions to optimize patient outcomes. Further research will further refine our understanding of these drugs and their optimal use in clinical practice. However, large-scale randomized clinical trials are necessary to fully elucidate the clinical implications of these differences. Future studies are crucial in providing definitive evidence to guide clinical practice and optimize treatment strategies for patients undergoing PCIs.
Acknowledgments:
The authors would like to thank Ascentia Innovations Pvt. Ltd. for providing write-up support.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
Patient’s consent is not required as there are no patients in this study.
Conflicts of interest:
Dr. Paridhi Mathur, Dr. Rajat Singal and Dr. Sandip Kumar Mitra are the employee of the Mankind Pharma Ltd.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that they have utilised the Paperpal tool during the writing process to enhance readability and eliminate grammatical errors. However, took full responsibility for the content.
Financial support and sponsorship: This study was funded by Mankind Pharma Ltd. Grant Number- 4106039158 dated 12.08.2024.
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