Aspirin Resistance: Current Status and Role of Tailored Therapy

Grinstein, Jonathan; Cannon, Christopher P.

doi:10.1002/clc.22031

Cited by 56 publications

(58 citation statements)

References 80 publications

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“…Increasing the dose of aspirin to ≥300 mg has been shown to improve the laboratory response to aspirin [17,19,59,60]. In that regard, it has been proposed that certain high-risk patient populations, such as those with obesity, diabetes, post-ACS and a history of stent thrombosis, might benefit from diagnostic platelet function testing and dose adjustments based on the results [61]. Algorithms have been developed to tailor aspirin therapy based on platelet function testing [62].…”

Section: Future Perspectivementioning

confidence: 99%

Optimal Aspirin Dose in Acute Coronary Syndromes: an Emerging Consensus

et al. 2014

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Numerous clinical trials testing the efficacy of aspirin for the secondary prevention of cardiovascular disease have been published. We reviewed the literature pertaining to aspirin dose in acute coronary syndrome patients. Clinical trials assessing the comparative efficacy of different doses of aspirin are scarce. This complex antiplatelet therapy landscape makes it difficult to identify the best aspirin dose for optimizing efficacy and minimizing risk of adverse events, while complying with the various guidelines and recommendations. Despite this fact, current evidence suggests that aspirin doses of 75-100 mg/day may offer the optimal benefit:risk ratio in acute coronary syndrome patients.

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Section: Future Perspectivementioning

confidence: 99%

Optimal Aspirin Dose in Acute Coronary Syndromes: an Emerging Consensus

et al. 2014

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“…The effect of aspirin is achieved by suppressing thromboxane production and further by inhibiting platelet activation and aggregation 3. Substantial number of patients on aspirin therapy fails to reach this desired effect, and then they experience major adverse vascular events, a phenomenon known as aspirin resistance (AR) 4. Since the discovery of this phenomenon, to unravel the mechanisms of aspirin insensitivity so far remains a daunting task.…”

Section: Introductionmentioning

confidence: 99%

Association of GPIa and COX‐2 gene polymorphism with aspirin resistance

Wang

Sun

Dong

et al. 2017

Clinical Laboratory Analysis

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ObjectiveThis study aimed to explore the association between GPIa, COX‐2 gene polymorphisms and aspirin resistance in the ischemic stroke patients from the southern part of Jiangsu province.MethodsIn all, 97 patients with acute ischemic stroke were enrolled in the study. GPIa gene polymorphism at 807C>T (rsl126643) locus and COX‐2 gene polymorphism at ‐765G>C (rs20417) locus were genotyped by PCR pyrosequencing technology. Patients were divided into the aspirin sensitivity (AS) group and aspirin resistance (AR) group according to the platelet aggregation rate. The relationship between the two gene polymorphisms and aspirin resistance was investigated and analyzed.ResultsThe distribution of the genotype (CC, CT, TT, CT + TT, and CC) and the frequency of allele T of GPIa gene at 807C>T locus were significantly different in AS and AR groups in female patients (P < .05). Logistic regression analysis showed that the genotype of CT+TT at 807C>T locus was significantly correlated with AR after adjustment for relative factors (P = .047, OR = 4.856, 95% CI: 1.020–23.108). There were no significant differences in the genotype distribution and allele frequency of the COX‐2 gene ‐765G>C site between two groups (P > .05).Conclusion GPIa gene polymorphism at 807C>T locus was associated with AR in Chinese Han females, and the expression of allele T increased the incidence of AR. The gene polymorphism of COX‐2 gene at ‐765G>C locus was not significantly correlated with AR.

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“…But despite the enormous amount of clinical and experimental studies on this issue over the past decade, there is currently no consensus on mechanisms, resistance, and ways to overcome resistance to antiplatelet agents [12]. It is believed that resistance to antiplatelet may have multifactorial nature.…”

Section: Introductionmentioning

confidence: 99%

Genetic Features of Resistance to Antithrombocytic Drugs in Patients With Ischemic Heart Disease After Conducted Percutaneous Coronary Intervention

Liakhotska

2017

EUREKA: Health Sciences

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The aim of the study: To study and evaluate platelets aggregation activity as primary phase of haemostasis and anti-platelet therapy in IHD patients after PCI, depending on the polymorphism of the gene ITGA 2 - C 807T. Materials and methods: 54 patients who were on a treatment at the clinical hospital "Feofaniya" (Kyiv) and at the Kyiv Clinical Hospital on railway transport №2 were examined: 20 women and 34 men (mean age - 67.8 ± 7.46 years). The study involved patients with stable forms of coronary artery disease (stable angina pectoris II-III) and acute coronary syndrome, with a history of percutaneous coronary intervention (PCI). All patients received antiplatelet therapy: acetylsalicylic acid (3.7%), clopidogrel (9.3%) or a combination of them (87%). Functional activity of the platelets was studied on a Biola Aggregation Analyzer laser agrometer. The response to antiplatelet therapy was confirmed by the Aggredyne test. The polymorphism of the C807T of the ITGA2 gene was determined by polymerase chain reaction (PCR). Based on the results of the aggregation ability, antiplatelet therapy sensitivity, the patients were divided into two groups: group I - individuals with varying degrees of insensitivity to antiplatelet drugs (35 patients), group II - susceptible to treatment (19 patients). In each group was analyzed the polymorphism of the gene ITGA2 and features of the functional activity of the platelets, depending on the genotype. Results: In 50% of patients receiving ASA there was a different degree of non-sensitivity, with respect to thienopyridines - this figure was 20%. Among patients who received dual antiplatelet therapy did not match at least one of the drugs - 83.3%. Among the "non responders" 78.9% had a mutated T-allele, and a homozygous variant for the T allele was recorded in 53.15% of patients, while "respondents" - 15.8%. Most in the group of "respondents" was the group of the native genotype - C / C. The most pronounced tendency to influence the genotype on spontaneous aggregation was observed in relation to the T-allele, in particular in the homozygote (genotype T / T). The significant difference between the groups was obtained from the platelet response to ADP. Thus, the reaction of carriers in the T-allele, as homo- and heterozygotes, was significantly different. Conclusions: In 64.8% of patients with coronary heart disease after PCI was observed a decrease in antiplatelet sensitivity, which has a clear link with the polymorphism of the gene ITGA 2. The presence of the T-allele in the genotype of patients with IHD is associated with a less adequate platelet response in patients receiving dual antiplatelet therapy for ASA and thienopyridines on ADP, which may have an effect on the sensitivity to thienopyridines.

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Aspirin Resistance: Current Status and Role of Tailored Therapy

Cited by 56 publications

References 80 publications

Optimal Aspirin Dose in Acute Coronary Syndromes: an Emerging Consensus

Optimal Aspirin Dose in Acute Coronary Syndromes: an Emerging Consensus

Association of GPIa and COX‐2 gene polymorphism with aspirin resistance

Genetic Features of Resistance to Antithrombocytic Drugs in Patients With Ischemic Heart Disease After Conducted Percutaneous Coronary Intervention

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