Aspirin Resistance Research Articles

Assessment of Aspirin and Clopidogrel Resistance in Patients Undergoing Cardiovascular Surgery: A Single-Center Cross-Sectional Study

We aimed to investigate antiplatelet drug resistance utilizing light transmission-lumiaggregometry (LT-LA) and the Platelet Function Analyzer-100 (PFA-100) in patients undergoing cardiovascular surgery. The study included 60 patients diagnosed with stable coronary artery disease and peripheral vascular diseases that required surgery. Participants were divided into three groups: patients receiving aspirin (ASA) (n=21), patients receiving clopidogrel (CLO) (n=19), and patients receiving dual therapy (ASA+CLO) (n=20). Aggregation and secretion tests by LT-LA and closure time by the PFA-100 were used to measure antiplatelet drug resistance. Based on the adenosine diphosphate (ADP)-induced aggregation test, 43% of patients were resistant to ASA, 22% to CLO, and 15% to dual therapy. Diabetes, hypertension, and hyperlipidemia were the most commonly identified comorbid disorders. In patients with comorbid risk factors, the median value of platelet aggregation response to ADP was significantly higher in the ASA group than in the CLO and dual therapy groups (p=0.0001). In patients receiving ASA monotherapy, the maximum amplitude of aggregation response to platelet agonists was ≥70% in 43% of patients for ADP and 28% for collagen by LT-LA. Elevated ADP (≥0.29 nmol) and collagen (≥0.41 nmol)-induced adenosine triphosphate release were found by LT-LA in 66% of patients utilizing an ADP agonist and 80% of patients using a collagen agonist undergoing ASA therapy. Closure times obtained with the PFA-100 were normal in 28% of patients using collagen-ADP cartridges and 62% of patients using collagen-epinephrine (CEPI) cartridges who received ASA. Recurrent thrombosis and bleeding were observed in 12 (20%) patients with cardiovascular disease. Three of these individuals (25%) showed ASA resistance with normal responses to ADP-induced aggregation (≥70%) and secretion (≥0.29 nmol), as well as normal CEPI closure times. Our findings suggest that antiplatelet drug monitoring by LT-LA and PFA-100 may be useful for high-risk and complicated cardiovascular patients.

Aspirin Responsiveness in a Cohort of Pediatric Patients with Right Ventricle to Pulmonary Artery Conduits and Transcatheter Valve Replacement Systems.

The aim of this study was to determine the rate of aspirin responsiveness in a cohort of pediatric patients with in situ xenograft valved right ventricle to pulmonary artery (RV-PA) conduits and/or transcatheter valve replacements (TVR). Aspirin is routinely prescribed to these patients. Optimizing anti-platelet therapy could promote valve longevity and reduce the risk of infective endocarditis in this at-risk group. This was a prospective, observational study. Patients were recruited from both ward and outpatient settings. Patients were eligible if under 18 years and taking aspirin. Non-response to aspirin was defined as >20% platelet aggregation using light transmission platelet aggregometry (LTA) and <50% platelet inhibition by thromboelastography with platelet mapping (TEGPM). Participants were invited to provide a confirmatory sample in cases of aspirin resistance and dose adjustments were made. Thirty patients participated. Median age was 9 years (2 months to 18 years). The majority (93%) had complex right ventricular outflow tract pathology. 13 (43%) had an RV-PA conduit and 24 (80%) had a TVR, with valve situated in conduit in 7 (23%) cases. Rate of aspirin non-response on initial testing was 23% (n=7/30) with median LTA 74.55% (60-76%) and TEG 13.25% (0-44%) in non-responders. Non-responders were more likely to be under 1 year. Two patients required dose increases and one patient non-adherence to dose was identified. Four patients on repeat testing were responsive to aspirin by laboratory tests. The rate of aspirin non-response on laboratory testing in this cohort of patients was 23% and resulted in therapeutic intervention in 10%.

Key Mutant Genes and Biological Pathways Involved in Aspirin Resistance in the Residents of the Chinese Plateau Area.

Aspirin is used to prevent and treat cardiovascular diseases; however, some patients develop aspirin resistance. We aimed to explore the potential molecular mechanisms underlying aspirin resistance in people living in the Chinese plateau area. In total, 91 participants receiving aspirin treatment from the Qinghai plateau area were divided into the aspirin resistance and aspirin sensitivity groups. Genotyping was performed using the Sequence MASSarray. Differentially mutated genes between the two groups were analyzed using MAfTools. The annotation of differentially mutated genes was conducted based on the Metascape database. In total, 48 differential SNP and 22 differential InDel mutant genes between the aspirin resistance and aspirin sensitivity groups were screened using Fisher's exact test (P < 0.05). After the χ2 test, a total of 21 SNP mutant genes, including ZFPL1 and TLR3, and 19 InDel mutant genes were found to be differentially expressed between the two groups (P < 0.05). Functional analysis revealed that these differential SNP mutations were mainly enriched in aspirin resistance pathways, such as the Wnt signaling pathway. Furthermore, these genes were related to many diseases, including various aspirin indications. This study identified several genes and pathways that could be involved in arachidonic acid metabolic processes and aspirin resistance progression, which will provide a theoretical understanding of the molecular mechanism of aspirin resistance.

Comparison of Thromboembolic Events Between Pipeline Embolization Device (PED) Shield and PED/PED Flex: A Propensity Score-Matched Analysis.

The pipeline embolization device (PED) Flex with Shield technology is a third-generation flow diverter used for intracranial aneurysm treatment designed to decrease thrombogenicity through a phosphorylcholine coating. Herein, we aim to compare the rate of thromboembolic events in PED with Shield technology and PED without it through propensity score matching. We conducted a retrospective analysis of aneurysms treated with PED first-generation/PED Flex and PED with Shield between 2013 and 2023 at a single academic institution. Patients were matched through propensity score by controlling for confounding factors including age, smoking history, diabetes, previous subarachnoid hemorrhage, modified Rankin Scale pretreatment, location, aneurysm size, previous treatment, and clopidogrel or aspirin resistance. After matching, we evaluated for periprocedural and postoperative thromboembolic events. Data analysis was performed using Stata 14. A total of 543 patients with 707 aneurysms treated in 605 procedures were included in the analysis. From these, 156 aneurysms were treated with PED with Shield (22.07%) and 551 (77.93%) without Shield technology. Propensity score matching resulted in 84 matched pairs. The rate of thromboembolic events was 3.57% for PED Shield and 10.71% for PED first-generation/PED Flex ( P = .07), while retreatment rates were 2.38% for PED Shield and 8.32% for PED Flex ( P = .09). Complete occlusion at first ( P = .41) and last imaging follow-up ( P = .71), in-stent stenosis ( P = .95), hemorrhagic complications ( P = .31), and functional outcomes ( P = .66) were comparable for both groups. This is the first study in the literature performing a propensity scored-matched analysis comparing PED with PED with Shield technology. Our study suggests a trend toward lower thromboembolic events for PED Shield, even after controlling for aspirin and clopidogrel resistance, and a trend toward lower aneurysm retreatment rates with PED Shield, without reaching statistical significance.

Impact of hemodialysis on efficacies of the antiplatelet agents in coronary artery disease patients complicated with end-stage renal disease

It is controversial whether hemodialysis affects the efficacy of the antiplatelet agents. We aimed to investigate the impact of hemodialysis on efficacies of the antiplatelet agents in coronary artery disease (CAD) patients complicated with end-stage renal disease (ESRD). 86 CAD patients complicated with ESRD requiring hemodialysis were consecutively enrolled. After 5-day treatment with aspirin and clopidogrel or ticagrelor, the platelet aggregations induced by arachidonic acid (PLAA) or adenosine diphosphate (PLADP), and the P2Y12 reaction unit (PRU) were measured before and after hemodialysis. The propensity matching score method was adopted to generate a control group with normal renal function from 2439 CAD patients. In patients taking aspirin, the PLAA remained unchanged after hemodialysis. In patients taking clopidogrel, the PLADP (37.26 ± 17.04 vs. 31.77 ± 16.09, p = 0.029) and corresponding clopidogrel resistance (CR) rate (23 [48.9%] vs. 14 [29.8%], p = 0.022) significantly decreased after hemodialysis, though PRU remained unchanged. Subgroup analysis indicated that PLADP significantly decreased while using polysulfone membrane (36.8 ± 17.9 vs. 31.1 ± 14.5, p = 0.024). In patients taking ticagrelor, PLADP, and PRU remained unchanged after hemodialysis. ESRD patients had higher incidences of aspirin resistance (AR) and CR compared to those with normal renal function (AR: 16.1% vs. 0%, p = 0.001; CR: 48.4% vs. 24.8%, p = 0.024). Hemodialysis does not have negative effect on the efficacies of aspirin, clopidogrel and ticagrelor in ESRD patients with CAD. ESRD patients have higher incidences of AR and CR compared with those with normal renal function.Trial registration ClinicalTrials.gov Identifier: NCT03330223, first registered January 4, 2018.

The Model for Clinical, Laboratory, and Genetic Prediction of Recurrent Ischemic Stroke against the Background of Laboratory Aspirin Resistance using Machine Learning

The aim of the study was to determine the incidence of laboratory aspirin resistance; and to study the associations of genetic markers and clinical and laboratory parameters (including parameters of the platelet hemostasis) in patients with non-cardioembolic ischemic stroke using machine learning methods to assess the prognosis of recurrent ischemic strokes. Clinical and laboratory data (including induced platelet aggregation) were analyzed from 296 patients with ischemic stroke who were treated in the stroke center of City Clinical Hospital No. 1 named after. N.I. Pirogov. The frequencies of polymorphic variants of the ITGB3, GPIba, TBXA2R, ITGA2, PLA2G7, HMOX1, PTGS1, PTGS2, ADRA2A, ABCB1, PEAR1 genes and intergenic region 9p21.3) in patients with non-cardioembolic ischemic stroke, which were identified using hydrogel biochip technology, were determined. Using the developed machine learning model, additional clinical and genetic factors influencing the development of laboratory aspirin resistance and recurrent ischemic stroke were studied. In the future, the identified factors can be used for differentiated prevention of recurrent ischemic strokes.

Antiplatelet Resistance in Coronary Artery Bypass Grafting: A Systematic Review.

This systematic review examines the occurrence and implications of resistance to primary antiplatelet agents, aspirin and clopidogrel, often utilised in patients undergoing coronary artery bypass grafting (CABG), alongside the methodologies for assessment of such resistance. An extensive literature search across various databases such as PubMed, MEDLINE via Ovid, Embase, and Cochrane CENTRAL until May 2024 was conducted to identify studies evaluating antiplatelet resistance in on-pump and off-pump CABG patients. Following quality assessment, only high-quality studies were incorporated into this review. This review included 19 studies with 3,915 patients, four of which were randomised controlled trials and 15 were observational studies. Aspirin resistance incidence ranged from 11.0% to 51.5%, while clopidogrel resistance was 22%. Antiplatelet resistance, assessed through a wide variety of methods, was associated with a 13 times increase in the risk of vein graft occlusion and increased rates of mortality, myocardial infarction, and target vessel revascularisation in the case of clopidogrel resistance. The effect of cardiopulmonary bypass on antiplatelet resistance remains ambiguous. The academic literature lacks a standardised definition for antiplatelet resistance. Assessment methodologies greatly vary, leading to noninterchangeable outcomes. While aspirin resistance has a conflicting overall significant impact on adverse outcomes, clopidogrel resistance correlates with poorer clinical outcomes.

Comparison of the Efficacy between 81 Mg Bid of Aspirin and 162 Mg Od of Aspirin in Splenectomized Thalassemic Patients with Aspirin Resistance

Backgroud: Currently, aspirin is widely used in splenectomized thalassemic patients. Despite taking 81 mg of aspirin daily, some patients develop venous thromboembolic complications, and these patients are referred to as “aspirin-resistance”. Then, increasing dose of aspirin to 162 mg/day is one of treatment options. It is not known if which regimen of aspirin at dose of 162 mg/day (1 tab po bid VS 2 tabs po once daily) is more effective in these patients. Methods: This is a prospective randomized cross-over study in splenectomized thalassemic patients between 2022 and 2023 at Siriraj Hospital. All splenectomized thalassemic patients aged from 18 to 60 years who have been taking aspirin of 81 mg/day were enrolled and evaluated for aspirin resistance (ASA-resist) by platelet aggregation test using arachidonic acid as agonist (PAT-AA). Patients with 81-mg aspirin resistance were randomly assigned to the following 7-day regimens in a crossover design: aspirin 81 mg twice daily (ASA1x2) or aspirin 162 mg once daily (ASA2x1), and their PAT-AA was assessed after each regimen. Results: A total of 64 patients (41 women) with a median age of 32.5 years were mostly Hb E/beta-thalassemia (86%) whereas 53% were transfusion-dependent thalassemia (TDT). ASA-resist was found in 24 patients (37.5%). The 'ASA1x2' showed a higher prevalence of ASA-resist than 'ASA2x1' but no statistical significance (52.4% vs.35%; OR 2.0; 95%CI, 0.58-7.17; p=0.265). For 'ASA1x2' regimen, serum ferritin level of ≥1200 ng/mL was significantly associated with ASA-resist (OR 10.7; 95%CI, 1.4-82.0; p=0.030). For 'ASA2x1' regimen, ASA-resist was significantly associated with TDT (p=0.015) and serum ferritin level of ≥1200 ng/mL (OR 20.0; 95%CI, 1.7-238.6; p=0.017). Conclusions: The “aspirin 81 mg twice daily” regimen showed a higher prevalence of aspirin resistance than “aspirin 162 mg once daily” regimen in splenectomized thalassemic patients with aspirin resistance, and an elevated serum ferritin level was significantly associated with aspirin resistance in both regimens.

APROBATION OF PLATELET AGGREGATION INHIBITOR FROM ECHIS MULTISQUAMATIS SNAKE VENOM IN VITRO, IN VIVO AND EX VIVO

Snake venom-derived platelet aggregation inhibitors can be promising antiplatelet medications that can allow to avoid the risk of bleeding and treatment resistance, particularly in aspirin-resistant patients. Our study aimed to assess the effectiveness of a platelet aggregation inhibitor derived from Echis multisquamatis snake venom in various settings, including in vitro, in vivo, and ex vivo. Methods. We examined a polypeptide from Echis multisquamatis venom, purified using a recently developed chromatography protocol, across multiple models. This polypeptide was introduced into platelet-rich blood plasma and administered intravenously to rats. The effects on platelet aggregation were assessed using aggregometry, focusing on ADP-induced aggregation. Results &amp; Discussion. Our findings revealed that a concentration of 0.040 mg/ml significantly reduced platelet aggregation in vitro. Remarkably, this dosage also proved effective when administered intravenously in laboratory animals, reaffirming its potential as a robust antiplatelet agent. In the final phase of our study, the polypeptide demonstrated its ability to inhibit platelet aggregation in blood plasma of pregnant woman with aspirin resistance, presenting a promising avenue for innovative treatment approaches in such cases. Conclusion. This study underscores the potential of the Echis multisquamatis venom-derived polypeptide as a promising antiplatelet agent, effective in diverse scenarios, including aspirin resistance. Further research and clinical trials are imperative to fully harness its therapeutic potential.

Patients with metabolic dysfunction–associated steatotic liver disease have preserved in vitro responses to antiplatelet drugs

BackgroundPatients with metabolic dysfunction–associated steatotic liver disease (MASLD) are at a risk of developing cardiovascular disease. Antiplatelet therapy not only prevents cardiovascular disease in these patients, but may also lower the risk of progression into advanced stages of fibrosis. However, patients with MASLD-associated cirrhosis often have complex changes in the hemostatic system and have been excluded from randomized trials. ObjectivesThe aim of this study was to assess the potency of antiplatelet drugs in these patients with MASLD-associated cirrhosis. MethodsWe included patients with MASLD-associated cirrhosis (n = 19), patients with type 2 diabetes (DM2) and steatosis (n = 22), patients with steatosis only (n = 15), and healthy controls (n = 20). We measured basal platelet aggregation and activation using light transmission aggregometry and flow cytometry. We subsequently measured platelet aggregation and activation after in vitro addition of aspirin, cangrelor, and ticagrelor and compared the antiplatelet response in patients and healthy controls. ResultsRates of aspirin resistance as measured by light transmission aggregometry were similar between patients with MASLD-associated cirrhosis and healthy controls (21% vs 16%), but were significantly higher in patients with DM2 and steatosis (50% [P = .02] vs controls) and patients with steatosis only (53% [P = .05] vs controls). In patients with DM2 and steatosis, but not with MASLD-associated cirrhosis, the potency of cangrelor was significantly lower than that in healthy controls (P = .028). ConclusionThe in vitro potency of aspirin, cangrelor, and ticagrelor in samples of patients with MASLD-associated cirrhosis is similar to that of healthy controls. In contrast, the potency of commonly used antiplatelet drugs may be altered in patients with DM2 and steatosis and in patients with steatosis only.

11-dehydrothromboxane B2 as a marker of acetylsalicylic acid resistance in patients with stable coronary artery disease

Introduction. Acetylsalicylic acid (ASA, aspirin) resistance is the inability to reduce thromboxane A2 synthesis in platelets and inhibit platelets activation and aggregation while taking ASA. Assessment of urinary 11-dehydrothromboxane B2 (11-dhTxB2) levels is one of the methods to identify aspirin resistance. Our research aimed to investigate whether urinary 11-dhTxB2 levels and other clinical and laboratory parameters are associated with a history of major adverse cardiovascular events (MACE) including myocardial infarction and ischaemic stroke in aspirin-treated patients with stable coronary artery disease. Patients and methods. In a cross-­sectional study we investigated 82 patients with stable coronary artery disease who took ASA at doses of 75–150 mg/day. We used the evaluation of the urinary 11-dhTxB2 levels standardized by creatinine as a method to identify aspirin resistance. Statistical analysis was performed using Mann-­Whitney U-test, ROC-analysis and multivariable logistic regression. Results. The medians of urinary 11-dehydrothromboxane B2 level in patients with and without MACE were 587.8 (Q1-Q3 512.8–800.3) pg/mg creatinine and 438.3 (Q1–Q3 337.6–577.9) pg/mg creatinine, respectively (p=0.001). The threshold level of urinary 11-dhTxB2, which predicted a high risk of aspirin resistance, was 521.1 pg/mg creatinine, and in 36 (43.9 %) patients the concentration of the 11-dhTxB2 exceeded this level. The regression model characterising the dependence of the presence of a history of MACE was constructed. It included platelet count, urinary levels of 11-dhTxB2 and the presence of type 2 diabetes. Sensitivity and specificity of the model were 55 % and 88.9 %, respectively. Conclusions. The results of the study demonstrate that the antiplatelet effect of aspirin is weaker in stable coronary artery disease patients with a history of MACE than in those without a history of MACE.

The Effect of the ABCB1(MDR-1) C3435T Polymorphism in Turkish Patients with Aspirin Resistance in Acute Ischemic Stroke.

Recurrence of thrombotic events during aspirin therapy is known as aspirin resistance (AR). This study aimed to investigate the rate of AR, the factors influencing AR in patients with acute ischemic stroke under regular aspirin use, and the relationship between AR and ABCB1 (MDR-1) C3435T (rs1045642) polymorphism. Throughout this multicenter prospective study, 174 patients with acute ischemic stroke who had been prescribed aspirin for at least one month due to the risk of vascular disease, along with 106 healthy volunteers, were included as part of the study group. The results of our study indicate that AR was detected in 21.3% of the patient group. According to the results of an analysis of the polymorphism of the ABCB1 C3435T in patients with AR compared to those with aspirin sensitivity, patients with AR possessed more heterozygous (CT) and homozygous genotypes (TT) than those with aspirin sensitivity (p = 0.001). Based on multivariate logistic regression analysis of factors affecting AR in acute ischemic stroke patients, hypertension (OR: 5.679; 95% CI: 1.144-28.19; p = 0.034), heterozygous (CT) genotype (OR: 2.557; 95% CI: 1.126-5.807; p = 0.025), increased platelet values (OR: 1.005; 95% CI: 1.001-1.009; p = 0.029), and CRP/albumin values (OR: 1.547; 95% CI: 1.005-2.382; p = 0.047) were found to be associated with a greater risk of AR. The presence of heterozygous (CT) genotype in the ABCB1 C3435T gene region in the Turkish population is associated with an increased risk of AR. When planning aspirin therapy, it is crucial to consider the ABCB1 (MDR-1) C3435T polymorphism.

Assessment of the extent, causes and prevalence of aspirin resistance among Saudi and Egyptian patients: A comparative study

Assessment of the extent, causes and prevalence of aspirin resistance among Saudi and Egyptian patients: A comparative study

Potential Aspirin Resistance in Patients with Obstructive Sleep Apnea Syndrome

Potential Aspirin Resistance in Patients with Obstructive Sleep Apnea Syndrome

Short-term efficacy and safety of personalized antiplatelet therapy for patients with acute ischaemic stroke or transient ischaemic attack: A randomized clinical trial.

AIM The aim of this study was to determine whether the testing strategy for clopidogrel and/or aspirin resistance using CYP2C19 genotyping or urinary 11-dhTxB2 testing has an impact on clinical outcomes. METHODS A multicentre, randomized, controlled trial was conducted at 14 centres in China from 2019 to 2021. For the intervention group, a specific antiplatelet strategy was assigned based on the CYP2C19 genotype and 11-dhTxB2, a urinary metabolite of aspirin, and the control group received non-guided (i.e., standard of care) treatment. 11-dhTXB2 is a metabolite of thromboxane A2 metabolite that can help quantify the effects of resistance to aspirin in individuals after ingestion. The primary efficacy outcome was new stroke, the secondary efficacy outcome was a poor functional prognosis (a modified Rankin Scale (mRS) score ≥3), and the primary safety outcome was bleeding, all within the 90-day follow-up period. RESULTS A total of 2815 patients were screened, and 2663 patients were enrolled in the trial, with 1344 subjects assigned to the intervention group and 1319 subjects assigned to the control group. A total of 60.1% were carriers of the CYP2C19 loss-of-function allele (*2, *3), and 8.71% tested positive for urinary 11-dhTxB2- indicating aspirin resistance. in the intervention group. The primary outcome was not different between the intervention and control groups (P= 0.842). A total of 200 patients (14.88%) in the intervention group and 240 patients (18.20%) in the control group had a poor functional prognosis (Hazard ratio, 0.77; 95% CI, 0.63 to 0.95; P= 0.012). Bleeding events occurred in 49 patients (3.65%) in the intervention group and 72 patients (5.46%) in the control group (hazard ratio, 0.66; 95% CI, 0.45 to 0.95; P= 0.025). CONCLUSION Personalized antiplatelet therapy based on the CYP2C19 genotype and 11-dhTxB2 levels was associated with favourable neurological function and reduced bleeding risk in AIS and TIA patients. The results may help support the role of CYP2C19 genotyping and urinary 11-dhTxB2 testing in the provision of precise clinical treatment.

The Diabetic Platelets.

This communication describes the platelet morphology and physiology noted in persons with diabetes and its complications. It reviews the effects of glucose lowering drugs on platelet function, and summarizes the role of anti-platelet drugs in diabetes management.

286 Genetic, laboratory and clinical factors associated with low-dose aspirin failure in the prevention of preeclampsia

OBJECTIVES/GOALS: Low-dose aspirin is an established treatment to prevent preeclampsia, a leading cause of maternal and perinatal complications. Nevertheless, aspirin failure is not uncommon. We are investigating whether a gain-of-function genetic polymorphism in a platelet thrombin receptor is associated with aspirin failure in the prevention of preeclampsia. METHODS/STUDY POPULATION: Women who had preeclampsia in an initial pregnancy who then received low-dose aspirin in a subsequent pregnancy will be evaluated. We will compare between women who developed preeclampsia despite aspirin (aspirin non-responders) to women who did not develop preeclampsia with aspirin treatment (aspirin responders). Specifically, we will evaluate the allelic frequency of a single nucleotide variant (rs773902) in PAR4 thrombin receptor on platelets. This variant is associated with increased platelet function and potentially aspirin resistance. In addition, we will analyze the platelet response to PAR4 activation before and 1 hour after administering a single 81 mg enteric-coated aspirin tablet. RESULTS/ANTICIPATED RESULTS: We hypothesize that the prevalence of the PAR4 variant will be significantly higher among women who had recurrence of preeclampsia despite aspirin therapy. We also postulate that women who developed preeclampsia despite aspirin prophylaxis and have the polymorphism will have increased platelet aggregation in response to activation of PAR4, either by thrombin or peptides that activate the receptor, both at baseline and 1 hour after aspirin administration. DISCUSSION/SIGNIFICANCE: If our hypothesis that aspirin failure in preeclampsia prevention is associated with the gain-of-function polymorphism in the platelet PAR4 thrombin receptor, there may be justification for additional experimental studies to assess whether better pregnancy outcomes can be obtained by targeting thrombin itself using low molecular weight heparin.

A Review on the Appropriate Dosage of Aspirin as a Prophylactic Agent Against Deep Vein Thrombosis Following Total Knee Arthroplasties

Guidelines regarding Deep Vein Thrombosis prophylaxis following total knee arthroplasties have had conflicting information regarding the use of aspirin as a prophylactic agent in recent years. The National Institute for Clinical Excellence refrains from listing the drug in its guidelines while the American College of Chest Physicians advocates for the drug. Despite the conflicting guidelines, physicians have favored the drug in recent years, with more than 80% utilizing it as a prophylactic agent in total knee arthroplasties. Although a consensus may have been reached by physicians regarding the use of the drug, a consensus has not been reached regarding the preferred dosage. With this in mind, a search of the PubMed database was conducted which yielded six studies that discussed the efficacy of various dose ranges of aspirin. All studies corroborated that not only was aspirin an effective prophylactic agent, but that there was no significant difference between dosages regarding efficacies. Due to factors such as aspirin resistance and the potential of aspirin to cause gastrointestinal injuries, this literature review concludes that the dosage of aspirin given for the prophylaxis of DVT in TKAs should be considered on a patient to patient basis.

Abstract Number: LBA21 Platelet Function Assays for Aspirin and Ticagrelor are More Reliable When Compared with Clopidogrel

Introduction The most common antiplatelet agents administered for neurovascular disease treatment and prevention are aspirin, clopidogrel, and ticagrelor. The utility of monitoring various platelet function assays (PFAs) in relation to neurovascular disease is unclear and variability exists in clinical practice. The aim of this study was to evaluate reliability of PFAs as a biomarker of the platelet inhibition in aspirin, clopidogrel, and ticagrelor in patients on antiplatelet agents for a broad range of neurovascular indications. Methods We conducted a retrospective chart review of prospectively collected data on patients who presented to our comprehensive stroke center and had PFAs drawn. PFAs utilized include Aspirin VerifyNow test, measured in aspirin resistance units (ARU) and Plavix VerifyNow test, measured in P2Y12 reaction units (PRU). Values less than 550 ARU are consistent with aspirin‐induced platelet inhibition. Similarly, values less than 197 PRU are indicative of platelet inhibition in clopidogrel or ticagrelor. Compliance and incidence of intracranial hemorrhage (ICH) and other adverse bleeding events were assessed. Social science statistics software was used for data analysis. Results From January to June 2022, a total of 297 patients had platelet function assays drawn for neurovascular indications. Average age was 69.96 (95% CI 68.31, 71.61). One hundred and eighty nine subjects were on aspirin. Mean ARU was 448.73 (95% CI 438.53, 458.93). One hundred twenty three subjects were on clopidogrel. Mean PRU for clopidogrel was 162.84 (95% CI 147.33, 178.35). Fifteen subjects were on ticagrelor. Mean PRU for ticagrelor was 73.27 (95% CI 34.62, 111.91). There was a significant difference in therapeutic platelet inhibition between clopidogrel and ticagrelor in subjects who were compliant (n = 105 clopidogrel complaint; n = 14 ticagrelor complaint) (z‐score 3.63, p‐value 0.00028). Of the patients that were compliant none had a non therapeutic platelet inhibition on aspirin and ticagrelor. Of the 123 patients that were compliant on clopidogrel 76% had non therapeutic PFA (n = 8 clopidogrel and ICH; n = 1 ticagrelor and ICH) (Fisher value = 0.0205). Conclusions Our study suggests that platelet inhibition of aspirin and ticagrelor may be more reliable when compared to that of clopidogrel. Significant limitations include the discrepancy in respective sample sizes. Larger studies are needed to validate our results.

Abstract Number: LBA20 Platelet Function Inhibition is superior with ticagrelor with a lower incidence of Intracerebral Hemorrhage

Introduction The most common antiplatelet agents administered for neurovascular disease treatment and prevention are aspirin, clopidogrel, and ticagrelor. The utility of monitoring various platelet function assays (PFAs) in relation to neurovascular disease is unclear and variability exists in clinical practice. The aim of this study was to evaluate PFAs as a biomarker of the platelet inhibition in aspirin, clopidogrel, and ticagrelor in patients on antiplatelet agents for a broad range of neurovascular indications. Methods We conducted a retrospective chart review of prospectively collected data on patients who presented to our comprehensive stroke center and had PFAs drawn. PFAs utilized include Aspirin VerifyNow test, measured in aspirin resistance units (ARU) and Plavix VerifyNow test, measured in P2Y12 reaction units (PRU). Values less than 550 ARU are consistent with aspirin‐induced platelet inhibition. Similarly, values less than 197 PRU are indicative of platelet inhibition in clopidogrel or ticagrelor. Compliance and incidence of intracranial hemorrhage (ICH) were assessed. Social science statistics software was used for data analysis. Results From January to June 2022, a total of 297 patients had platelet function assays drawn for neurovascular indications. Average age was 69.96 (95% CI 68.31, 71.61). One hundred and eighty nine subjects were on aspirin. Mean ARU was 448.73 (95% CI 438.53, 458.93). One hundred twenty three subjects were on clopidogrel. Mean PRU for clopidogrel was 162.84 (95% CI 147.33, 178.35). Fifteen subjects were on ticagrelor. Mean PRU for ticagrelor was 73.27 (95% CI 34.62, 111.91). There was a significant difference in therapeutic efficacy between clopidogrel and ticagrelor in subjects who were compliant (n = 105 clopidogrel complaint; n = 14 ticagrelor complaint) (z‐score 3.63, p‐value 0.00028). There was a significant difference between incidence of ICH in subjects compliant and therapeutic on clopidogrel as compared to ticagrelor (n = 8 clopidogrel and ICH; n = 1 ticagrelor and ICH) (Fisher value = 0.0205). Conclusions Our study suggests that platelet inhibition of ticagrelor may be superior to that of clopidogrel with a lower incidence of intracranial hemorrhage as a complication of therapy. Significant limitations include the discrepancy in respective sample sizes. Larger, prospective studies are needed to validate our results.