Evaluation of inflammatory conditions associated with aspirin resistance

Yalcinkaya, Emre; Çelik, Murat

doi:10.3109/03009734.2014.918679

Cited by 6 publications

(6 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 11 Catecholamine burst, as a compensatory mechanism and systemic inflammatory response syndrome, may directly activate platelets that are non‐sensitive to aspirin. 12 …”

Section: Pathophysiologymentioning

confidence: 99%

“…Systemic inflammatory response syndrome may significantly affect the response to aspirin by alternative pathways of platelet activation with hyperproduction of thromboxane A2 regardless of the arachidonic acid pathways 11 . Catecholamine burst, as a compensatory mechanism and systemic inflammatory response syndrome, may directly activate platelets that are non‐sensitive to aspirin 12 …”

Section: Pathophysiologymentioning

confidence: 99%

See 1 more Smart Citation

Antithrombotic and anticoagulation therapies in cardiogenic shock: a critical review of the published literature

et al. 2021

View full text Add to dashboard Cite

Cardiogenic shock (CS) is a complex multifactorial clinical syndrome, developing as a continuum, and progressing from the initial insult (underlying cause) to the subsequent occurrence of organ failure and death. There is a large phenotypic variability in CS, as a result of the diverse aetiologies, pathogenetic mechanisms, haemodynamics, and stages of severity. Although early revascularization remains the most important intervention for CS in settings of acute myocardial infarction, the administration of timely and effective antithrombotic therapy is critical to improving outcomes in these patients. In addition, other clinical settings or non‐acute myocardial infarction aetiologies, associated with high thrombotic risk, may require specific regimens of short‐term or long‐term antithrombotic therapy. In CS, altered tissue perfusion, inflammation, and multi‐organ dysfunction induce unpredictable alterations to antithrombotic drugs' pharmacokinetics and pharmacodynamics. Other interventions used in the management of CS, such as mechanical circulatory support, renal replacement therapies, or targeted temperature management, influence both thrombotic and bleeding risks and may require specific antithrombotic strategies. In order to optimize safety and efficacy of these therapies in CS, antithrombotic management should be more adapted to CS clinical scenario or specific device, with individualized antithrombotic regimens in terms of type of treatment, dose, and duration. In addition, patients with CS require a close and appropriate monitoring of antithrombotic therapies to safely balance the increased risk of bleeding and thrombosis.

show abstract

“… 11 Catecholamine burst, as a compensatory mechanism and systemic inflammatory response syndrome, may directly activate platelets that are non‐sensitive to aspirin. 12 …”

Section: Pathophysiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

Antithrombotic and anticoagulation therapies in cardiogenic shock: a critical review of the published literature

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Oxidative stress may result in the hyperproduction of thromboxane-A2 regardless of the arachidonic acid pathways. Catecholamine burst during inflammation and oxidative stress may directly activate platelets that are non-sensitive to aspirin [ 20 ].…”

Section: Factors Contributing To a Low Biological Response To Antimentioning

confidence: 99%

Multifactorial Background for a Low Biological Response to Antiplatelet Agents Used in Stroke Prevention

Wiśniewski

2021

Medicina

View full text Add to dashboard Cite

Effective platelet inhibition is the main goal of the antiplatelet therapy recommended as a standard treatment in the secondary prevention of non-embolic ischemic stroke. Acetylsalicylic acid (aspirin) and clopidogrel are commonly used for this purpose worldwide. A low biological response to antiplatelet agents is a phenomenon that significantly reduces the therapeutic and protective properties of the therapy. The mechanisms leading to high on-treatment platelet reactivity are still unclear and remain multifactorial. The aim of the current review is to establish the background of resistance to antiplatelet agents commonly used in the secondary prevention of ischemic stroke and to explain the possible mechanisms. The most important factors influencing the incidence of a low biological response were demonstrated. The similarities and the differences in resistance to both drugs are emphasized, which may facilitate the selection of the appropriate antiplatelet agent in relation to specific clinical conditions and comorbidities. Despite the lack of indications for the routine assessment of platelet reactivity in stroke subjects, this should be performed in selected patients from the high-risk group. Increasing the detectability of low antiaggregant responders, in light of its negative impact on the prognosis and clinical outcomes, can contribute to a more individualized approach and modification of the antiplatelet therapy to maximize the therapeutic effect in the secondary prevention of stroke.

show abstract

“…Inflammatory cytokines contribute to the formation of AR through platelet transformation, activation, and adhesion processes (Du et al, 2016). The pre-thrombotic state can be generated by the production and release of thromboxane A2 due to the increased expression of cyclooxygenase-2, which is associated with inflammation (Yalcinkaya and Celik, 2014). Reactivity to aspirin therapy may be reduced by inflammation-induced AR (Shan et al, 2010).…”

Section: Inflammationmentioning

confidence: 99%

Mechanism of Improving Aspirin Resistance: Blood-Activating Herbs Combined With Aspirin in Treating Atherosclerotic Cardiovascular Diseases

Zhao

Yang

2021

Front. Pharmacol.

View full text Add to dashboard Cite

Atherosclerotic thrombotic disease continues to maintain a high morbidity and mortality rate worldwide at present. Aspirin, which is reckoned as the cornerstone of primary and secondary prevention of atherosclerotic cardiovascular diseases (ASCVDs), has been applied in clinics extensively. However, cardiovascular events continue to occur even though people utilize aspirin appropriately. Therefore, the concept of aspirin resistance (AR) was put forward by scholars, which is of great significance for the prediction of the clinical outcome of diseases. The pathogenesis of AR may be incorporated with low patient compliance, insufficient dose, genetic polymorphism, increased platelet transformation, inflammation, and the degenerative changes and calcification of platelets. The improvement of AR in the treatment of ASCVDs has gradually become a research hot spot in recent years. Traditional Chinese medicine (TCM) regards individuals as a whole and treats them from a holistic view, which has been found to have advantages in clinical studies on the treatment of AR. Many kinds of blood-activating TCM have the effect of improving AR. The potential mechanism for the improvement of AR by blood-activating herbs combined with aspirin was explored. The combination of blood-activating herbs and aspirin to improve AR is likely to turn into a hot topic of research in the future.

show abstract

Evaluation of inflammatory conditions associated with aspirin resistance

Cited by 6 publications

References 8 publications

Antithrombotic and anticoagulation therapies in cardiogenic shock: a critical review of the published literature

Antithrombotic and anticoagulation therapies in cardiogenic shock: a critical review of the published literature

Multifactorial Background for a Low Biological Response to Antiplatelet Agents Used in Stroke Prevention

Mechanism of Improving Aspirin Resistance: Blood-Activating Herbs Combined With Aspirin in Treating Atherosclerotic Cardiovascular Diseases

Contact Info

Product

Resources

About