Evidence map›Paper›PMID 40192046›Full record

ReviewCardiovascular & hematological disorders drug targets2025

The Impact of Single Nucleotide Polymorphisms and Other Mechanisms on Aspirin Resistance.

Natalia Sergeevna Nuzhdina, Aleksei Vitalievich Kurguzov, David Sergeevich Sergeevichev

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Review in Cardiovascular & hematological disorders drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Natalia Sergeevna NuzhdinaE. Meshalkin National Medical Research Center of the Ministry of Health of the Russian Federation, Rechkunovskaya Str., 15, 630055 Novosibirsk, Russia.ORCID 0000-0002-0634-8820
Aleksei Vitalievich KurguzovE. Meshalkin National Medical Research Center of the Ministry of Health of the Russian Federation, Rechkunovskaya Str., 15, 630055 Novosibirsk, Russia.
David Sergeevich SergeevichevE. Meshalkin National Medical Research Center of the Ministry of Health of the Russian Federation, Rechkunovskaya Str., 15, 630055 Novosibirsk, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis and ischemic events play a pivotal role in the pathogenesis of several cardiovascular diseases (CVD). The primary aim of preventing recurrent thrombosis in patients who underwent cardiovascular surgery is the antiplatelet agent administration. Nevertheless, despite the aspirin therapy or double (aspirin plus clopidogrel) therapy, the effectiveness of antithrombotic treatment remains controversial. In recent years, we have learned that some percentage of patients still demonstrate no clinical response to aspirin treatment and may experience a vascular complication. This article provides an overview of recent scientific studies that have focused on experimental detection and genotyping of single nucleotide polymorphisms (SNPs) in patients, involving the main therapeutic target genes: cyclooxygenase COX-1 and COX-2, guanylate cyclase GUCY1A3, the glycoprotein complex GPIIb-IIIa, and the platelet receptor protein PEAR1." The aspirin resistance (AR) ranges considerably from 0 % to 66% in patients with ischemic heart disease (IHD) and relatively healthy people (control group). SNP distribution analysis has been proposed to explain the inadequate high platelet reactivity (HPR) among patients with IHD under aspirin treatment. Various SNPs have been proposed to explain the development of CVD and the persistent HPR under aspirin treatment widely used in the prevention of recurrent cardiovascular thrombotic events. Meanwhile, the efficacy of aspirin therapy in secondary thrombosis prevention in patients with IHD is not strongly associated with known SNP. The inconsistent results of different AR clinical trials are likely due to the design of the experiments and methodological and quantitative issues; therefore, careful interpretation of the SNP genotyping results is necessary.

Indexed as

AspirinDrug ResistancePlatelet Aggregation InhibitorsPolymorphism, Single NucleotideCardiovascular DiseasesHumansThrombosisAspirinPlatelet Aggregation Inhibitorsacetylsalicylic acidaspirin resistance.Ischemic heart diseasepharmacogeneticssingle nucleotide polymorphismsthrombosis

Identifiers

PMID40192046

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.