Prevalence Of Aspirin Resistance Research Articles

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

Aspirin resistance: causes, clinical significance, correction

Aspirin is the most frequently prescribed antiplatelet agent today. It exerts its antiplatelet effect by irreversible inactivation of the platelet cyclooxygenase-1, resulting in an irreversible inhibition of thromboxane-A2 formation. The clinical benefit of antiplatelet therapy with acetylsalicylic acid (ASA) in high risk patients has been convincingly demonstrated through the results of multiple placebo-controlled trials. Nevertheless, a large number of patients treated with aspirin suffers an adverse cardiovascular event. This observation led to the concept of ”aspirin resistance“. The mechanisms of aspirin resistance remain to be determined, although different theories are being discussed. Several tests are used to assess resistance to ASA in vitro. Depending on which assay is used and which population is tested, the prevalence of aspirin resistance varies between 5% and 60%. So far, it was not possible to define a clear gold standard for detecting aspirin resistance, which considers both, biochemical data and clinical events, and correlates them in a reproducible way. The clinical implications of aspirin resistance are well-documented through a lot of studies, which conclude that resistance to aspirin in vitro is associated with a significant increased risk for adverse cardiovascular events in cardiovascular patients. Insufficient or excessive antiplatelet effect of acetylsalicylacid may be due not only to changes in the synthesized cyclooxygenase-1, but also to changes in its amount. Literature data on the association of various polymorphic markers of candidate genes with the effectiveness of antiplatelet therapy of ASA are few and contradictory. Therefore, it is currently impossible to identify genetic predictors of the effectiveness of ASA as well as any antiplatelet agent. Continuation of research in this area in the future will predict the patient’s response to a drug and, therefore, individualize the approach to the choice and dosage of antiplatelet drugs, which will reduce the incidence of adverse reactions.

Comparative Study of Ex Vivo Antiplatelet Activity of Aspirin and Cilostazol in Patients with Diabetes and High Risk of Cardiovascular Disease.

Background The role of aspirin in primary cardiovascular disease prevention in patients with diabetes remains controversial. However, some studies have suggested beneficial effects of cilostazol on cardiovascular disease in patients with diabetes. We prospectively investigated the antiplatelet effects of cilostazol compared with aspirin in patients with diabetes and cardiovascular risk factors.Methods We randomly assigned 116 patients with type 2 diabetes and cardiovascular risk factors but no evident cardiovascular disease to receive aspirin at a dose of 100 mg or cilostazol at a dose of 200 mg daily for 14 days. The primary efficacy outcome was antiplatelet effects of aspirin and cilostazol assessed with the VerifyNow system (aspirin response units [ARU]) and PFA-100 (closure time [CT]). Secondary outcomes were changes of clinical laboratory data (ClinicalTrials.gov Identifier: NCT02933788).Results After 14 days, there was greater decrease in ARU in aspirin (–28.9%±9.9%) compared cilostazol (–0.4%±7.1%, P<0.001) and was greater increase in CT in aspirin (99.6%±63.5%) compared cilostazol (25.7%±54.1%, P<0.001). The prevalence of aspirin resistance was 7.5% according to VerifyNow (defined by ARU ≥550) and 18.9% according to PFA-100 (CT <192 seconds). Compared with aspirin, cilostazol treatment was associated with increased high density lipoprotein cholesterol (7.1%±12.7% vs. 4.2%±18.0%, P=0.006) and decreased triglycerides (–9.4%±33.7% vs. 4.4%±17.57%, P=0.016). However, there were no significant changes in total and low density lipoprotein cholesterol, C-reactive protein level, and cluster of differentiation 40 ligand between cilostazol and aspirin groups.Conclusion Aspirin showed better antiplatelet effects assessed with VerifyNow and PFA-100 compared with cilostazol. However, there were favorable changes in atherogenic dyslipidemia only in the cilostazol.

Prevalence of aspirin resistance among the arthroplasty population: A pilot study.

Prevalence of aspirin resistance among the arthroplasty population: A pilot study.

Prevalence of aspirin and clopidogrel resistance in neurovascular stenting: a single-center experience

Objectives: The objective of this study was to determine the frequency of aspirin and clopidogrel resistance of patients undergoing neurovascular stenting procedure in the interventional radiology unit. Methods: The Multiplate® Analyzer (Roche Diagnostics, Germany) test data of 250 patients who underwent carotid or intracranial artery stenting due to atherosclerotic stenosis or treatment of intracranial aneurysms between 2013-2017 in the Interventional Radiology Unit of our hospital were evaluated retrospectively to detect the aspirin and clopidogrel resistance. Aspirin or clopidogrel resistance defined as the higher AUC value than 40U and 46U, respectively. The patients who did not have a result of the Multiplate® test; had anemia, known coagulation disorder or thrombocytopenia were excluded. Results: Among the 172 patients who met the inclusion criteria, 59 (34.3%) were those who had an intracranial stent during aneurysm treatment, and 113 (65.7%) had carotid stenting due to atherosclerotic stenosis. The prevalence of aspirin resistance was 9.4% (16/170) whereas that of clopidogrel resistance was 23.8% (41/172). Among the patients with atherosclerotic stenosis, aspirin resistance accounting for 3.6%, and clopidogrel resistance was 23.0%. Furthermore, the resistance in the patients with stent-assisted coiling for aneurysm treatment was 20.7% for aspirin and 25.4% for clopidogrel. Conclusions: In our study, the prevalence of aspirin resistance was found 9.4% and clopidogrel resistance 23.8% in patients who had neurovascular stenting. The effect of this condition on clinical outcomes in these patients should be investigated by randomized controlled trials.

A Pilot Study Of Aspirin Resistance In Obstructive Sleep Apnea Patients.

Purpose: Obstructive sleep apnea (OSA) leads to endothelial dysfunction and platelet hyperactivity, which are linked to increased risk of cardiovascular disease and implicated in the development of aspirin resistance. We hypothesized that aspirin resistance is prevalent among OSA patients and aimed to explore effects of continuous positive airway pressure (CPAP) therapy on aspirin responsiveness. Methods: In Phase 1, prevalence of aspirin resistance was determined cross-sectionally in a group of OSA patients (n=59) on daily low-dose aspirin (81 mg) taken before entering the study, for primary or secondary prevention. In Phase 2, aspirin responsiveness before and after initiation of CPAP therapy was compared and stratified by endothelial function in a cohort of aspirin-naïve patients with newly diagnosed OSA (n=18). Results: In Phase 1, prevalence of aspirin resistance was 17%; most patients (56%) were on CPAP therapy. In Phase 2, initiation of CPAP therapy was associated with significant improvement in endothelial function (p=0.03). The mean pre-CPAP aspirin resistance units (ARU) was 569 (SD=75). In subjects with endothelial dysfunction (44%), the mean decrease after initiation of CPAP therapy was 43 ARU (SD=81, p=0.18). In contrast, subjects with normal endothelial function experienced the mean decrease of 8 ARU (SD=116, p=0.83). Conclusion: Aspirin resistance may be prevalent among OSA patients. After initiation of CPAP therapy, we observed a trend towards improvement in aspirin responsiveness among patients with endothelial dysfunction. The role of endothelial dysfunction and aspirin resistance should be explored in further studies that focus on the effect of CPAP on cardiovascular outcomes.

Aspirin Resistance in Children with Congenital Heart Disease and Its Relationship with Laboratory and Clinical Parameters

Background: Patients with congenital heart disease (CHD) are more prone to thromboembolism. Aspirin is the most commonly used medication around the world to prevent thrombosis in cardiovascular diseases. Objectives: This study aimed to define the frequency of aspirin resistance in pediatric patients with CHD and to evaluate the correlation of clinical and laboratory parameters with aspirin resistance. Methods: The study population consisted of 103 patients using aspirin, including 53 cases of cyanotic CHD and 50 cases of non-cyanotic CHD. Platelet aggregation was measured by the AggreGuide A-100 ADP Assay. Results: The prevalence of aspirin resistance was 36.9% in children with CHD. Although aspirin resistance in cyanotic CHD patients (41.5%) was higher than in non-cyanotic patients (32%), the difference was not statistically significant (P = 0.414). There was no significant association between aspirin responsiveness or resistance and the patient’s sex, age, duration of aspirin use, and concomitant medication use. Comparison of the laboratory data of aspirin-responsive and -resistant patients showed no significant difference between these groups, except for albumin (P = 0.032) and serum fibrinogen (P = 0.0001) levels. The fibrinogen level and thromboembolism history were independent risk factors for aspirin resistance. Also, there was a significant correlation between platelet aggregation in peripheral blood smears and aspirin resistance (P = 0.0001). Conclusions: Our findings suggest that measurement of the serum fibrinogen level and platelet aggregation in blood smears may be the first step to predict aspirin resistance.

The prevalence and associated factors of aspirin resistance among prophylactic aspirin users

Background. Aspirin is an antiplatelet used for the secondary prevention after vascular events. It is also suggested for the primary prevention of vascular events in high risk people, however, despite using standard prophylactic doses, aspirin resistance may result in therapeutic failure and arterial thrombosis. Since the prevalence of aspirin resistance and its associated factors were heterogeneous in different studies, this study was conducted to determine the prevalence and associated factors of aspirin resistance in an Iranian population under aspirin for primary prevention of vascular events. Methods. 264 patients without documented vascular disease with 80 mg daily aspirin consumption for at least one month enrolled in this cross-sectional study. Aspirin resistance was assessed by the measurement of thromboxane B2 in the urine samples using the enzyme-linked immunosorbent assay method. Aspirin resistance was defined as a urine level of thromboxane B2 ≥ 1700 ng/dl. Results. The prevalence of aspirin resistance in this study was 9.8%. Age (OR = 0.935, 95% CI: 0.880-0.993, P = 0.028) and geographical regions (OR = 0.117, 95% CI: 0.014-0.958, P = 0.045) showed independent correlation with aspirin resistance. No significant association observed between aspirin resistance and gender, diabetes mellitus, hypertension, hyperlipidemia, smoking, duration of aspirin use, body mass index, and drug history. Conclusions. Despite the standard daily dose of aspirin for primary prevention of vascular events, some of our patients exhibited aspirin resistance that was directly related to a higher age and geographical region. More studies are required to clarify the beneficial role of aspirin resistance test before planning a preventive strategy in high risk individuals.

ASPIRIN RESISTANCE IN PATIENTS WITH OSA: ARISA TRIAL

SESSION TITLE: New Insights Into the Relationship Between OSA and Cardiovascular Disease SESSION TYPE: Original Investigations PRESENTED ON: October 18-21, 2020 PURPOSE: Obstructive sleep apnea (OSA) is one of the leading independent risk factors associated with cardiovascular events. Untreated OSA is associated with endothelial dysfunction and platelet hyperactivity through multiple metabolic, thrombotic and inflammatory pathways linked to development of cardiovascular disease. Patients with concomitant OSA and cardiovascular risks are routinely prescribed aspirin for primary and/or secondary prevention; however, it is proposed this population carries higher risk of aspirin therapy resistance. Proposed mechanisms of aspirin resistance include increased platelet turnover, gene polymorphisms (COX-1, COX-2, GPIIb/IIIa), decreased aspirin-mediated acetylation, and prothrombotic effects of leptin – all shared mechanisms with OSA. We hypothesized that compliant use continuous positive airway pressure (CPAP) therapy, which is known to improve endothelial function and decrease platelet hyperactivity may improve endothelial function and aspirin responsiveness in this population. METHODS: In Phase 1, prevalence of aspirin resistance was determined in a group of OSA patients (n=59) on daily low-dose aspirin utilizing the VerifyNow Aspirin laboratory test. Aspirin resistance was defined as aspirin reaction units (ARU) ≥ 550. In Phase 2, aspirin responsiveness, stratified by pre-CPAP endothelial function determined by two methods, the VerifyNow Aspirin laboratory test and the non-invasive EndoPAT200. The measures were obtained before and after initiation of CPAP therapy in a cohort of aspirin-naïve patients with newly diagnosed OSA (n=18). Statistical significance was set as p<0.1. Aspirin resistance was defined as aspirin reaction units (ARU) ≥ 550. Endothelial dysfunction was defined as RHI <1.67. RESULTS: In Phase 1, aspirin resistance occurred in 17% of study subjects. In Phase 2, utilization of CPAP therapy was associated with significant improvement in endothelial function (p=0.03). In subjects with endothelial dysfunction pre-CPAP (44%), initiation of CPAP therapy was associated with significant decrease in mean ARU from 563 to 520 (p=0.09). Meanwhile, in subjects with normal endothelial dysfunction, ARU decreased insignificantly, from 574 to 566 (p=0.4). Control group was not part of data analysis due to limited number of subjects. CONCLUSIONS: Although a limited study due to sample size, aspirin resistance was prevalent among our cohort of OSA patients. Initiation of CPAP therapy was associated with significant improvement in aspirin responsiveness when endothelial dysfunction was present pre-CPAP therapy. CLINICAL IMPLICATIONS: The role of endothelial dysfunction and aspirin resistance should be explored in further studies that focus on the effect of CPAP and cardiovascular outcomes. DISCLOSURES: No relevant relationships by Rakhee Agarwal, source=Web Response No relevant relationships by Jose Mendez, source=Admin input No relevant relationships by Maria Scinico, source=Web Response No relevant relationships by Oleg Sostin, source=Web Response

Resistance of aspirin during and after pregnancy: A longitudinal cohort study.

The objective of this study is to investigate possible changes in aspirin resistance during and after pregnancy over time. A longitudinal cohort study in obstetric high risk women with an indication for aspirin usage during pregnancy to prevent placenta mediated pregnancy complications. Aspirin resistance measured in the first, second and third trimester of pregnancy and at least three months postpartum by four complementary test: PFA-200, VerifyNow®, Chronolog light transmission aggregometry (Chronolog LTA) and serum thromboxane B2 (TxB2) level measurements. Correlation between the devices was investigated. In total, 23 pregnant women participated in the present study. Aspirin resistance according to the PFA-200, VerifyNow®, Chronolog LTA and serum TxB2, was 30.4%, 17.4%, 26.1% and 23.8% respectively. Resistance by any device was 69.6%. Aspirin resistance measured by the VerifyNow®, Chronolog LTA, serum TxB2 and aspirin resistance by any device during pregnancy was demonstrated more frequently than aspirin resistance after pregnancy. Correlation between the different devices was weak. Aspirin resistance was found in a considerable part of the participants. Considerable variation between participants, within participants over time and between the different devices was found. Prevalence of aspirin resistance during pregnancy differs from after pregnancy. More research on aspirin resistance and clinical obstetric outcome is needed.

Platelet Surface CD62p and Serum Vitamin D Levels are Associated with Clopidogrel Resistance in Chinese Patients with Ischemic Stroke

Background: To explore the association of platelet activation markers, vitamin D, and antiplatelet drugs resistance in ischemic stroke patients. Methods: A total of 230 patients with ischemic stroke were enrolled in this study. Platelet aggregation, platelet activation marker (CD62p), and vitamin D were measured after 7-14 days of dual antiplatelet treatment (aspirin + clopidogrel). All individuals were divided into a drug resistance group and a drug sensitive group according to the platelet maximum aggregation rate induced by antagonist adenosine diphosphate or arachidonic acid. Results: In this study, the prevalence of aspirin resistance was low (1.2%), while the prevalence of clopidogrel resistance (CR) was 24.8%, so we focused on CR. The percentage of CD62p on activated platelet [(25.74 ± 4.61) versus (12.41 ± 3.93), P < .001] and the prevalence of hypertension [93.0% (53) versus 79.8% (138), P = .021] in CR group were significantly higher than those in clopidogrel sensitive (CS) group, while the vitamin D concentration [(8.96 ± 4.41) versus (13.9 ± 4.84) ng/mL, P = .003] in CR group was significantly lower compared with the CS group. No significant difference was found in soluble P-selectin between these 2 groups [(56.2 ± 16.13) versus (54.2 ± 14.87) ng/mL, P = .258], neither in calcium [(2.29 ± .12) versus (2.33 ± .13) mmol/L, P = .821]. Logistic regression analysis showed that hypertension (odds ratio [OR] = 5.348, 95% confidence intervals [CI] 1.184-23.350, P = .026), expression of platelet CD62p (OR = 1.095, 95% CI 1.052-1.201, P = .018) and vitamin D level (OR = .832, 95% CI .763-.934, P = .005) were associated with CR in ischemic stroke patients. Conclusions: CR in ischemic stroke patients is associated with several independent predictors, including increased platelet activation marker CD62p, decreased vitamin D level, and hypertension.

Prevalence of aspirin resistance by thromboelastography plus platelet mapping in children with CHD: a single-centre experience.

RationaleAspirin resistance has been reported in up to 80% of children with cardiovascular defects undergoing surgery. Because of a patient who had embolic stroke while on therapeutic aspirin dose but in whom aspirin resistance was present on his thromboelastography platelet mapping, we chose to obtain thromboelastography platelet mapping on cardiac patients on aspirin to assess their risk. OBJECTIVES: This study evaluates aspirin resistance noted in these patients and their characteristics.Methods and resultsThis is a retrospective study of 25 patients taking aspirin for a month at therapeutic dose. In total, 11 female patients were enrolled. Ages in all subjects were 5 months to 27 years. A total of 19 patients had a Fontan surgery. Three had a cavopulomanary anastomosis, one had a hybrid procedure, and two had coronary anomalies. Compliance was assessed at the time of the clinic visit. Aspirin resistance was defined as platelet inhibition below 50%. Variables evaluated were level of platelet inhibition, age, body mass index, and gender.

Prevalence of aspirin resistance in patients with type II diabetes: a descriptive-analytical study .

Aspirin resistance is one of the most important factors for arterial thrombotic events in diabetic patients. This study aimed to evaluate aspirin resistance in diabetic patients. In this cross-sectional study, 180patients who received 80mg of aspirin daily for at least 10 days were studied, and their urinary 11-DH-TXB2 was measured. Those with 11-dehydro-thromboxane B2 above 1,500pg/mg creatinine were considered aspirin resistant. Data with significance level of 5% were analyzed in SPSS-16. The mean±SD of patient age was 60.22±9.59 years and 50% (n=90) were male. BMI was normal in 29.4% of the patients (n=53), the others were overweight or obese. Aspirin resistance was observed in 33 (18%) patients. The relationship between aspirin resistance and gender, age, and BMI was not significant (p>0.05). There is a high prevalence of aspirin resistance in diabetic patients and given that such patients are at risk of arterial thrombotic events, evaluation of aspirin resistance is suggested for those at a high risk of cardiovascular events or recurring events despite the use of aspirin. .

Prevalence of Aspirin Resistance among Jordanian Patients with Cardiovascular Disease

Introduction: Despite the wide range of aspirin indications, there is a considerable amount of patients do not respond to aspirin, who also are referred to as aspirin non-responders or aspirin resistant patients. Aims and objectives: This study was carried out to prospectively evaluate the prevalence of aspirin resistance in Jordanian patients with cardiovascular disease and further clarify the clinical predictors of aspirin resistance. Materials and methods: Biochemical aspirin response was assessed based on the measurements of urinary11-dehydro thromboxane B2 (11-dhTxB2) levels using FDA approved diagnostic kit. Patients taking aspirin (75-325mg) for at least 7 days were prospectively enrolled from all stable cardiac patients presenting at Jordan University hospital outpatient clinics. Results: Eighty six (86) patients were enrolled in this study. Another twenty four healthy individuals were enrolled to function as a control group. The mean urinary levels of 11- dhTxB2/creatinine were significantly lower almost 3- times in patients in the primary and secondary aspirin prevention group compared with the control group (1567.58 vs. 4236.19 pg/mg, p-value &gt;0.005). Thirty-one patients were found to be aspirin resistant with a prevalence of 36%. Conclusion: Our findings of aspirin resistance are particularly important given the large number of patients using this medication for prevention of atherothrombotic events. These results indicate that aspirin resistance should be diagnosed so that individuals with no response to aspirin can receive an alternative or an additional antiplatelet therapy.

Antiplatelet drug resistance did not increase the thromboembolic events after stent-assisted coiling of unruptured intracranial aneurysm: a single center experience of 99 cases.

We aimed to evaluate the correlation between aspirin or clopidogrel resistance and the risk of thromboembolic events (TEs). Between June 2011 and April 2015, we reviewed clinical and angiographic characteristics, and TEs in the patients undergoing stent-assisted coil embolization (SAC) of unruptured intracranial aneurysms (UIA) at our institution. We did not modify antiplatelet medication in patients with resistance. The relationships between antiplatelet resistance and the occurrence of acute symptomatic TEs, any diffusion-positive lesions, multiple diffusion-positive lesions, or delayed TEs were investigated. Ninety-nine endovascular treatments with stent-assisted technique were performed on 99 patients. The prevalence of aspirin resistance was 12% and clopidogrel resistance was 62.6%. Acute symptomatic TEs were demonstrated in 4 patients (4%). Diffusion-positive lesions were found in 82 patients [82.1%; 36 patients were group I (≤5) and 46 patients were group II (>5)]. Delayed TEs were demonstrated in 10 patients (10.1%). Neither aspirin resistance nor clopidogrel resistance was relevant to the development of acute symptomatic TEs, any diffusion-positive lesions, multiple diffusion-positive lesions, and delayed TEs (P logistic=not available, 0.448, 0.362, and 0.829 for aspirin resistance and P logistic=0.607, 0.367, 0.278, and 0.245 for clopidogrel resistance). Without modification of antiplatelet medication, we demonstrated 4% of acute symptomatic TEs and 10% of delayed TEs. Aspirin or clopidogrel resistance did not show significant relationships with acute and delayed TEs in the SAC of UIA.

Rs5911 and rs3842788 Genetic Polymorphism, Blood Stasis Syndrome, and Plasma TXB2 and hs-CRP Levels Are Associated with Aspirin Resistance in Chinese Chronic Stable Angina Patients.

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-PGF1α, 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-PGF1α 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.

Post-pregnancy aspirin resistance appears not to be related with recurrent hypertensive disorders of pregnancy

ObjectiveThe FRUIT-RCT concluded that low-molecular-weight heparin added to aspirin compared to treatment with aspirin alone is beneficial in the prevention of early-onset hypertensive disorders of pregnancy (HD) in women with inheritable thrombophilia and prior HD and/or a small-for-gestational age (SGA) infant leading to delivery before 34 weeks gestation. The aim of this study is to answer the question whether aspirin resistance is associated with recurrent HD. Study designWomen with and without recurrent HD matched for age, study arm, and chronic hypertension were invited for this follow-up study 6–16 years after they participated in the FRUIT-RCT. Aspirin resistance was tested after 10days of aspirin intake using three complementary tests: PFA-200, VerifyNow® and serum thromboxane B2 (TXB2). An independent t-test, Mann-Whitney U test, Fisher’s Exact test and Chi2 test were used for the statistical analyses. ResultsThirteen of 24 women with recurrent HD and 16 of 24 women without recurrent HD participated. The prevalence of laboratory aspirin resistance was 34.5% according to the PFA-200, 3.4% according to the VerifyNow® and 24.1% according to TXB2. The prevalence of aspirin resistance by any test was 51.7%. Aspirin resistance per individual test did not differ between women with and without recurrent HD. Aspirin resistance measured by any test occurred more frequently in women without recurrent HD (p<0.01), irrespective of low-molecular-weight heparin. ConclusionsNo relation could be demonstrated between recurrent HD and aspirin resistance per test, measured up to 16 years after pregnancy. On the contrary, complementary aspirin resistance measurements were encountered more frequently in women without recurrent HD.

Prévalence et valeur pronostique de la résistance à l’aspirine chez les patients en ischémie critique chronique des membres inférieurs

To assess the prevalence and the association between aspirin resistance in critical limb ischemia patients using the VerifyNow® bed-side platelet test, and occurrence of cardiovascular morbidity and/or death at one year. National multicenter prospective observational study related to COPART II centers. From 2010 through 2014, 64subjects hospitalized for critical limb ischemia and already treated by aspirin before the VerifyNow® test were included. A VerifyNow® test>550 ARU was defined as aspirin resistance. Critical limb ischemia was defined according to the TASC I criteria. The primary outcome was a composite including death, acute coronary syndrome, stroke and major amputation during the one-year follow-up period. In all, 9/64patients were aspirin resistant, the status was confirmed in one case. The prevalence of aspirin resistance was 14.06%. There was no significant difference between aspirin resistant and aspirin non-resistant groups in terms of cardiovascular history and glycemia status. Neither was there significant difference between the two groups in terms of survival. Aspirin resistance was not predictive of poorer survival in critical limb ischemia patients. However, our population was limited. Considering that a clear definition of aspirin resistance and standardized diagnostic tests are lacking, complementary studies might be useful.

Aspirin resistance in cerebrovascular disease and the role of glycoprotein IIIa polymorphism in Turkish stroke patients.

Aspirin resistance occurs in 5-45% of high-risk patients, with various mechanisms proposed for its development. This study aimed to determine the relationships among aspirin resistance, aspirin dosage, type of aspirin and glycoprotein IIIa P1A1/A2 polymorphism in patients with vascular risk factors. Two hundred and eight (75 symptomatic, 133 asymptomatic) patients with vascular risk factors who were using aspirin for primary or secondary prevention were prospectively included. The symptomatic group was further classified into two groups according to aspirin use at the time of stroke. Aspirin resistance was measured by the PFA-100 system (collagen/epinephrine cartridge) and glycoprotein IIIa P1A1/A2 polymorphism was determined by PCR. The overall prevalence of aspirin resistance was 32.2%. The mean age of patients with aspirin resistance was significantly higher than that in those who did not have resistance (P = 0.009). The prevalence of aspirin resistance was similar for the symptomatic and asymptomatic under aspirin therapy groups. The resistance rate was found to be highest with 100 mg enteric-coated preparation use (39.3%). Increasing the aspirin dosage and/or shifting to uncoated preparations caused a change in aspirin sensitivity of 36-60%. Repeated measurements showed development of aspirin resistance in 14% of patients who were sensitive to aspirin in previous measurements. Glycoprotein IIIaP1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke were not significantly related. The effect of aspirin can change by time, dosage and type of preparation used. There are no relationships among glycoprotein IIIa P1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke.

FREQUENCY OF ASPIRIN RESISTANCE IN PATIENTS WITH TYPE 1 AND 2 DIABETES MELLITUS AND ITS ASSOCIATION WITH METABOLIC PARAMETERS

Objectives: In the present study, we aimed to determine the prevalence of aspirin resistance in patients with Type 1 and 2 diabetes and to study its association with metabolic parameters. Methods: Aspirin resistance of patients (n=158) with Type 2 Diabetes Mellitus (DM) who presented to the center after 7 days of regular aspirin use were compared to age-mathced (55±19) healthy controls (n=164). Similarly, aspirin resistance of patients (n=30) diagnosed with Type 1 DM were compared to age-matched (27±7) healthy subjects (n=41) as the control group. Platelet Function Analyzer (PFA)-100 was used to evaluate the efficacy of aspirin. Results: Aspirin resistance was identified in 72 of 158 patients with Type 2 DM (45.6%) and in 47 of 164 healthy controls (28.6%) (p=0.001). Aspirin resistance had a prevalence of 50% in patients with Type 1 DM and was significantly higher compared to the control group of 41 healthy subjects (12.2%) (p=0.001). No correlations were noted between aspirin resistance and sex, smoking, HbA1c, hypertension and aspirin dose. There was a significant relation between aspirin resistance and LDL-cholesterol in patients with Type 2 DM (p=0.020). Conclusion: Patients with Type 1 and Type 2 DM had a higher frequency of aspirin resistance than the control group. Therefore, treatment choices including administering higher doses of aspirin or using other antiplatelet agents such as clopidogrel should be considered to prevent thrombocytic events in diabetes mellitus.