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Platelet adhesion and aggregation at the site of coronary stenting can have catastrophic clinical and economic consequences. Therefore, effective platelet inhibition is vital during and after percutaneous coronary intervention. Eptifibatide is an intravenous antiplatelet agent that blocks the final common pathway of platelet aggregation and thrombu...
Context in source publication
Context 1
... (Integrilin ® ; Schering- Plough, Kenilworth, NJ, USA), is one of three intravenous GP IIb/IIIa inhibitors approved for use in the US market, the others being abciximab (ReoPro ® ; Eli Lilly and Company, Indianapolis, IN, USA) and tirofiban (Aggrastat ® ; Medicure Inc., Winnipeg, MB, Canada). Basic pharmacologic differ- ences between eptifibatide and other intravenous GP IIb/IIIa inhibitors are summarized in Table 1. 10,11 The current review evaluates in detail the clinical and economic impact of using eptifibatide as an antiplatelet agent in coronary stenting. ...
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Background:
Despite its limitations, unfractionated heparin (UFH) has been the standard anticoagulant used during percutaneous coronary intervention (PCI). This study compared the safety of low-dose UFH with sequential enoxaparin with that of UFH in patients with diabetes mellitus (DM) and complex coronary artery disease receiving elective PCI.
M...
ABSTRACT
Intracoronary thrombosis triggered by ruptured or eroded atherosclerotic plaques constitutes the predom- inant underlying cause of acute coronary syndromes (ACS). Thrombin is considered a central enzyme in hemostasis and thrombosis, and a well-established target for anticoagulant therapies. Bivalirudin was introduced in the clinical practi...
Citations
... Epifibatide is cleared by the kidneys, and its plasma half-life is about 1.5-2 h. Because of its short half-life, in patients without renal insufficiency, a cessation of epifibatide infusion restores normal hemostatic platelet function within 15-30 min [20]. It should be noted that eptifibatide is contraindicated in patients undergoing hemodialysis. ...
Objectives: The optimal treatment strategy for ischemic stroke in patients presenting with tandem occlusions of the internal carotid artery remains controversial. Several studies have demonstrated better clinical outcomes after eptifibatide, which is a short half-life antiplatelet agent. This retrospective analysis focused on the safety and efficacy of low-dose eptifibatide administration in stroke patients with tandem lesions. Methods: We evaluated the results of endovascular treatment in 148 stroke patients with tandem lesions. Patients in whom balloon angioplasty alone resulted in satisfactory cerebral flow did not receive eptifibatide (33 patients); others received this drug together with stent implantation (115 patients). Eptifibatide was given as an intravenous bolus of 180 μg/kg and then in a modified low dose of 1 μg/kg/min for 24 hours. Results: There were no statistically significant differences between both groups regarding 30-day mortality, frequency of thrombotic events, or hemorrhagic complications. An analysis of clinical status at 30-day follow-up revealed that the administration of eptifibatide was associated with a statistically significant better outcome: a higher rate of either no neurological symptoms or only mild symptoms (4 NIHSS points maximally). Conclusions: The administration of eptifibatide in stroke patients presenting with tandem lesions is relatively safe. Moreover, treatment with this drug can improve clinical outcomes in these challenging patients.
... Previous studies have demonstrated relative cost-savings for percutaneous coronary intervention with eptifibatide compared to abciximab. 23 Post-acute benefits of eptifibatide in terms of reduced complications and re-intervention have also been shown with respect to quality-adjusted-life-years 24 and overall costs to third-party payers, all prior to the introduction of a generic formulation of the drug in 2016. 25 Cangrelor (Kengreal), a newer, intravenous P2Y12 inhibitor with a half-life of 3-5 min is another candidate synergistic dual antiplatelet bridging agent which merits discussion. ...
Background
Prophylactic carotid artery stenting (CAS) is an effective strategy to reduce perioperative stroke in patients with severe carotid stenosis who require cardiothoracic surgery (CTS). Staging both procedures (CAS-CTS) during a single hospitalization presents conflicting demands for antiplatelet therapy and the optimal pharmacologic strategy between procedures is not established. The purpose of this study is to present our initial experience with a “bridging” protocol for staged CAS-CTS.
Methods
A retrospective review of staged CAS-CTS procedures at a single referral center was performed. All patients had multivessel coronary and/or valvular disease and severe carotid stenosis (>70%). Patients not previously on aspirin were also started on aspirin prior to surgery, followed by eptifibatide during CAS (intraprocedural bolus followed by post-procedural infusion which was continued until the morning of surgery). Pre- and perioperative (30 days) neurologic morbidity and mortality was the primary endpoint.
Results
11 CAS procedures were performed in 10 patients using the protocol. The median duration of eptifibatide bridge therapy was 36 h (range 24–288 h). There was one minor bleeding complication (1/11, 9.1%) and no major bleeding complications during the bridging and post-operative period. There was one post-operative, non-neurologic death and zero perioperative ischemic strokes.
Conclusions
For patients undergoing staged CAS-CTS, Eptifibatide bridging therapy is a viable temporary antiplatelet strategy with a favorable safety profile. This strategy enables a flexible range of time-intervals between procedures.
... Eptifibatide acts as a blood platelet (thrombocyte) glycoprotein IIb/IIIa receptor antagonist, preventing its natural substrate, fibrinogen, from binding. This inhibits platelet aggregation and ultimately stops blood clot (thrombi) formation (Hashemzadeh et al. 2008;Pasala et al. 2014). Eptifibatide is administered intravenously to patients undergoing percutaneous coronary intervention (angioplasty) and patients with acute coronary syndrome (unstable angina) who experienced cardiac ischemia at rest within the previous 24 h (Shah et al. 2009; Integrilin package insert 2011). ...
Although peptide drugs make up only about 2% of all drugs approved by the United States Food and Drug Administration (FDA), they play important roles in the treatment of certain diseases where no small molecule drugs or therapeutic antibodies can fulfil. A primary reason for the strong preference of small molecules over peptides is the latter’s susceptibility to degradation by human proteases, resulting in very short systemic half-lives. To circumvent this, peptide chemists have resorted to introducing unnatural amino acids and chemical modifications to enhance their metabolic stabilities. Hence, understanding how peptide drugs are metabolized by the human body will help in the design of more stable peptide drugs. This review covers 25 FDA-approved peptide drugs up to 20 residues in length and details their metabolic and degradation pathways in the human body after administration.
... However, stenting causes platelet activation and aggregation that can lead to catastrophic thrombotic complications. Various antiplatelet agents that block different pathways in platelet activation and aggregation, have been introduced and used for preventing cardiovascular events after coronary stenting [4]. Eptifibatide is a platelet glycoprotein IIb/IIIa (GP IIb/ IIIa) receptor antagonist that inhibits fibrinogen binding to the activated GP IIb/IIIa site which prevents platelet-platelet interaction and clot formation [5]. ...
... Previously, eptifibatide was mainly used with bolus dose following infusion which showed significantly less complication 30 days after intervention [4,[6][7][8], but it accompanies with the increased risk of bleeding [4]. Other studies have shown that single bolus dose only can be as effective as infusion by improving long-term survival [9][10][11]. ...
... Previously, eptifibatide was mainly used with bolus dose following infusion which showed significantly less complication 30 days after intervention [4,[6][7][8], but it accompanies with the increased risk of bleeding [4]. Other studies have shown that single bolus dose only can be as effective as infusion by improving long-term survival [9][10][11]. ...
Background
Eptifibatide is a platelet glycoprotein IIb/IIIa receptor antagonist used for the prevention of cardiac ischemic complications of percutaneous coronary intervention (PCI). Eptifibatide has been used with bolus dose only or bolus plus infusion in patients undergoing PCI which have shown less complications, but the risk of bleeding has been increased. We aimed to compare the outcome and bleeding rate of bolus dose alone or plus infusion in elective PCI.
Methods
In this quasi-experimental study, we compared the outcome of elective PCI following single bolus dose intracoronary (41 patients) or bolus plus intravenous infusion (19 patients) of eptifibatide. In-hospital and follow-up major adverse cardiac events (MACEs) and bleeding rate were recorded and evaluated between groups.
Results
Both groups were comparable regarding baseline findings. Bolus only compared to bolus plus infusion group had lower in-hospital (19.5% vs. 31.6%) and follow-up MACE (15.4% vs. 17.6%), lower bleeding in-hospital (14.6% vs. 21.1%) and follow-up (2.4% vs. 5.3%) as well as lower mortality rate in hospital (4.9% vs. 15.8%), but higher follow-up mortality (10.3% vs. 0), but the difference was not significant.
Conclusions
We observed no significant difference regarding bleeding or MACE between intracoronary bolus infusion and bolus plus intravenous infusion of eptifibatide. It seems intracoronary bolus infusion of eptifibatide due to use of lower doses is a better choice in elective PCI to prevent post-PCI MACE.
... Eptifibatide offsets its additional treatment costs by avoiding costly repeat procedures and leads to positive quality-adjusted life years gained by preventing cardiovascular events lending themselves to transient or permanent lower quality of life [16]. However, the direct translation of these results into clinical practice of STEMI management is impossible, because of completely different populations in our and ESPRIT studies, the advent of drug eluting stent era, new oral antiplatelet drugs and recommendation for transradial access with reduced bleeding risk [19]. ...
Aim:
Study was aimed to assess the real-world costs of manual thrombectomy (MT) in selected ST segment-elevation myocardial infarction patients with intracoronary thrombus (IT).
Methods:
Study group (IT+) comprised 51 patients with MT applied and control group (IT-) comprised 56 patients without IT who underwent angioplasty alone. Costs comprised hospital care and cost of disposable materials used during primary angioplasty.
Results:
Complex management of patients with IT is more expensive, though allows to achieve clinical outcomes comparable to low-risk ST segment-elevation myocardial infarction patients without IT.
Conclusion:
A complex pharmaco-interventional strategy, with glycoprotein IIb/IIIa inhibitor and MT, though more expensive, may prove cost-effective.
... 12 The differences in cardiovascular outcomes were noticed among the GPI. 13 Previously, several foreign systematic reviews and meta-analysis had compared the efficacy and safety between abciximab and the small-molecule. [14][15][16] However, the main application of tirofiban in China, and it has not yet clear which would be of great benefit to the ACS comparing eptifibatide with tirofiban. ...
1 Background
Glycoprotein IIb/IIIa inhibitors were the strongest available antiplatelet therapy and have been shown to reduce cardiac ischemic complications in patients undergoing percutaneous coronary intervention. However, evidences are still lacking on the superiority of eptifibatide over tirofiban or vice versa in patients with acute coronary syndrome.
2 Objective
To compare the efficacy and safety of eptifibatide and tirofiban used among patients with acute coronary syndrome by performing a systematic review and meta‐analysis of randomized controlled trials.
3 Methods
A systematic search was conducted in Pubmed, Ovid/Medline, Ovid/Embase, Clinicaltrials.gov, CBM and CNKI to identify randomized controlled trials comparing eptifibatide with tirofiban for acute coronary syndrome until November 2015. The methodological quality was assessed with the Cochrane bias risk assessment tool.
4 Results
1256 patients from 9 randomized controlled trials were finally included. Compared with tirofiban, eptifibatide could reduce more risk of thrombolysis in myocardial infarction minor bleeding (RR 0.61, 95%CI 0.38, 0.98). However, no significant differences were observed for major adverse cardiac events (RR 0.41, 95%CI 0.15 to 1.12), major bleeding, thrombocytopenia in the two treatment groups. The relative treatment benefits were similar in subgroups of patients according to types of acute coronary syndrome, or undergoing percutaneous coronary intervention.
5 Conclusion
Available evidence suggests that the safety of eptifibatide is slightly superior to tirofiban in patients with acute coronary syndrome, but no significant difference was observed on efficacy. Future studies should focus on the randomized controlled trials with larger sample, multi‐center, long‐term follow‐up, high quality to compare the two drugs.
... But there is little known about the association of rs5787, rs3842788, and AR in Chinese stable pectoris patients. Another possible mechanism that may be involved in AR is the final pathway of platelet activation at the platelet glycoprotein (GP) IIb/IIIa receptor [5,6]. Kranzhofer and Ruef reported that GP IIIa (PlA) polymorphism is related to AR in Turkish patients with intracoronary stent restenosis, while another research that enrolled Germany patients with coronary artery disease (CAD) showed AR is unrelated to differences in the PlA1/A2 single nucleotide polymorphism [7]. ...
The identification of single nucleotide polymorphisms (SNPs) related to aspirin resistance (AR) is of great significance for the explanation why some individuals demonstrate an incomplete response to aspirin and for optimizing the antiplatelet therapy strategy. The study was designed to investigate the possible associated genetic markers and clinical factors of AR for Chinese patients with chronic stable angina after PCI and to analyze the association between TXA2, PGI2, hs-CRP level, AR, and gene polymorphisms. Totally 207 chronic stable angina patients who received 100 mg maintenance dose daily of aspirin for more than 7 days were enrolled. The inhibition of platelets was assessed using light transmittance aggregometry. TXB2, 6-keto-PGF1 α , and hs-CRP were measured by radioimmunoassay. Genotyping was performed using Taqman probe technique (rs5787 and rs5911) and gene sequencing technology (rs3842788). By using binary logistic regression analysis, the impact of clinical and genetic determinants on AR was evaluated. The prevalence of AR and aspirin semiresistance (ASR) was 3.86% and 20.76%, respectively, in Chinese chronic stable angina patients. rs5911 A/C and C/C versus A/A genotype (OR = 5.546, 95% CI = 1.812–11.404), rs3842788 A/G versus G/G genotype (OR = 8.358, 95% CI = 2.470–28.286), and blood stasis syndrome (BSS, OR = 10.220, 95% CI = 4.242–24.621) were associated with AR, but rs5787 variants were all homozygous of G/G genotype. Plasma TXB2 and hs-CRP increased significantly in AR and ASR group, while 6-keto-PGF1 α showed no difference, and TXB2 level was significantly higher in carriers of the rs3842788 A/G genotype. According to our results, rs5911 and rs3842788 are proved to be specific genetic markers of AR in Chinese chronic stable angina patients for the first time, and BSS was also proved to be a remarkable determinant for AR. The AR and ASR patients were with increased plasma TXB2 and hs-CRP levels, and the TXB2 level was influenced by the variation of rs3842788 genotype.
... [7] Many studies have reported an association between the PEAR1 gene and the coagulation system. [8][9][10]For example, variants of PEAR1 have been reported to be associated with increased platelet aggregation, playing important roles in agonistinduced platelet aggregation. [11,12] The strong associations between platelet aggregation and a common intronic variant of the PEAR1 gene have been identified in both African Americans and European Americans using sequencing approaches. ...
... [22,23] The contributions of the PEAR1 gene to the activation of platelets, inhibition of platelet progenitor cell proliferation, and interruption of platelet aggregation have been revealed. [9,11,12,22] The vital roles of the PEAR1 SNP have been revealed in many diseases: Sokol et al [24] found that patients with hyperlipidemia abortion had a higher incidence of the PEAR1 rs12041331 and rs12566888 SNPs than healthy people, and the T allele in the PEAR1 c. -9-4663G>T gene polymorphism had a protective effect on fetus abortion. Olivi et al [25] reported that there were no correlations between the selected 9 SNP loci of PEAR1 and the changes in diastolic and systolic blood pressure (P > 0.059), or in the incidence in patients with hypertension (P > 0.09). ...
To explore the correlation between platelet endothelial aggregation receptor-1 (PEAR1) genetic polymorphism and pulmonary thromboembolism (PTE).
Variant loci of the PEAR1 gene were screened in a PTE pedigree, followed by verification using Sanger sequencing. These polymorphic loci were validated in 101 PTE patients and 132 matched normal patients using MassARRAY single nucleotide polymorphism (SNP) genotyping methods. The frequency differences between the allele and genotypes were compared using the Hardy–Weinberg equilibrium test and Chi-square test. The correlation between the PEAR1 gene SNP and PTE was analyzed by comparing the between-group variance differences using the χ² test.
Three SNPs were identified in the PTE pedigree. There was a heterozygous transition of T>C in rs1952294, and a transition of C>T in rs778026543 in 2 members in the pedigree; however, the rs778026543 was not identified in the 101 PTE patients and 132 healthy controls. The genotype and allele frequencies of rs822442 did not differ significantly between PTE patients and healthy controls (P > 0.05). The variance difference at rs778026543 between pedigree members and healthy controls was significant (P < 0.001), supporting its potential heredity.
The PEAR1 polymorphism, rs778026543, but not rs1952294 and rs822442, may be a susceptibility SNP for PTE.
... Tissue damage occurs in many diseases, including diabetes, acute graft-versus-host disease, and cardiovascular disease. 1 Of these diseases, myocardial infarction, one of the leading causes of mortality, is the most common and difficult to treat in the clinic, because cardiomyocytes are not able to regenerate. 2 Tissue regeneration through stem/ progenitor cells has been studied extensively in a wide range of tissue repair applications, especially for regeneration of cardiomyocytes, owing to the unique pluripotency and regenerative properties of these cells. 3,4 However, tissue regeneration involves a series of biological processes, including mobilization of stem cells, angiogenesis, and synthesis of extracellular matrix. ...
Background
Cell therapy is a promising strategy for tissue regeneration. Key to this strategy is mobilization and recruitment of exogenous or autologous stem/progenitor cells by cytokines. However, there is no effective cytokine delivery system available for clinic application, in particular for myocardial regeneration. The aim of this study was to develop a novel cytokine delivery system that is stable in solution at physiological pH.
Methods
Four groups of self-assembled chitosan oligosaccharide/heparin (CSO/H) nanoparticles were prepared with various volume ratios of chitosan oligosaccharide to heparin (5:2, 5:4, 4:15, 1:5) and characterized by laser diffraction, particle size analysis, and transmission electron microscopy. The encapsulation efficiency and loading content of two cytokines, ie, stromal cell-derived factor (SDF)-1α and vascular endothelial growth factor (VEGF) were quantified using an enzyme-linked immunosorbent assay. The biological activity of the loaded SDF-1α and VEGF was evaluated using the transwell migration assay and MTT assay. The dispersion profiles for the cytokine-loaded nanoparticles were quantified using fluorescence molecular tomography.
Results
CSO/H nanoparticles were prepared successfully in solution with physiological pH. The particle sizes in the four treatment groups were in the range of 96.2–210.5 nm and the zeta potential ranged from −29.4 mV to 24.2 mV. The loading efficiency in the CSO/H nanoparticle groups with the first three ratios was more than 90%. SDF-1α loaded into CSO/H nanoparticles retained its migration activity and VEGF loaded into CSO/H nanoparticles continued to show proliferation activity. The in vivo dispersion test showed that the CSO/H nanoparticles enabled to VEGF to accumulate locally for a longer period of time.
Conclusion
CSO/H nanoparticles have a high cytokine loading capacity and allow cytokines to maintain their bioactivity for longer, are stable in an environment with physiological pH, and may be a promising cytokine delivery system for tissue regeneration.
Мета. Визначити ступінь впливу незалежних один від одного передопераційних чинників на єдиний залежний чинник - тривалість госпіталізації пацієнтів із гострим коронарним синдромом після екстреної ендоваскулярної реваскуляризації міокарда.
Матеріали і методи. Зібрано та статистично опрацьовано дані історій хвороб 40 пацієнтів віком до 60 років (1-ша група) та 40 пацієнтів віком 60 років і старше (2-га група). Методом статистичного опрацювання даних обрано кореляційно-регресійний аналіз.
Результати. У пацієнтів 1-ї групи на тривалість госпіталізації впливали (в порядку зменшення значущості): передопераційні показники гемоглобіну та гематокриту, рівні тропоніну І та загального холестерину, ступінь оклюзії коронарних артерій, індекс маси тіла, фракція викиду лівого шлуночка та об’єм післяопераційної крововтрати. У пацієнтів 2-ї групи єдиним фактором, що істотно вплинув на тривалість госпіталізації, був вік.
Висновки. Предикторами тривалості госпіталізації у віковій групі до 60 років слугують майже всі включені до дослідження незалежні фактори, тоді як у віковій групі 60 років і старше стійка кореляція характерна лише для фактора віку.
