A brief review on high on-aspirin residual platelet reactivity

Moldovan

Acta Medica Marisiensis

2016

Objective: The aim of this study was to evaluate the prevalence of aspirin non-responsiveness using whole blood multiple electrode aggregometry and to investigate the role of different clinical and laboratory variables associated with the lack of response. Methods: The present study included 116 aspirin treated patients presented with acute coronary syndromes or stroke. Response to aspirin was assessed by impedance aggregometry using arachidonic acid as agonist, in a final concentration of 0.5 mM (ASPI test). Results: In our data set 81% (n=94) were responders and 19% (n=22) non-responders showing high-on-aspirin platelet reactivity. Correlation analysis showed that the ward of admittance, low-density lipoproteins (LDL), concomitant antibiotic treatment, beta-adrenergic receptor blockers, history of myocardial infarction as well as PCI performed on Cardiology patients have different degrees of association with aspirin response. Conclusion: Concomitant treatment with beta-adrenergic receptor inhibitors, history of myocardial infarction and Cardiology ward admittance significantly increased the chance of responding to aspirin treatment whereas antibiotic therapy and low-density lipoproteins cholesterol seemed to increase the risk of high-on-aspirin residual platelet reactivity.

Section: Platelet Function Assessmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

High-on-Aspirin Residual Platelet Reactivity Evaluated Using the Multiplate^® Point-of-Care Device

Moldovan

Acta Medica Marisiensis

2016

Encyclopedia of Life Sciences

Haemostasis: General Pathways

Balduini

2018

Haemostasis protects the organism from bleeding due to tissue and vascular injury. It is a complex system of interconnected mechanisms that have the purpose of halting blood loss and reconstituting the integrity of the damaged tissue. The haemostatic process begins with a vascular damage that results in the exposure of the subendothelial collagen; this component is recognised by platelet receptors that initiate a series of events resulting in platelet aggregation with the formation of the primary unstable thrombus. Tissue damage also sets off the activation cascade of the coagulation factors, which results in the transformation of fibrinogen into fibrin, stabilising the thrombus. The final phase of haemostasis is the removal of the fibrin clot by plasmin, followed by wound healing of the damaged tissue. In normal conditions, haemostasis is controlled by sophisticated mechanisms that trigger the activation of the coagulation process to block blood loss, preventing unnecessary thrombus formation. Key Concepts Haemostasis is a system of highly interconnected mechanisms aimed at protecting the organism from blood loss. Four phases occur in haemostasis: (1) tissue and vessel wall damage, (2) platelet activation, (3) blood clotting and (4) fibrinolysis and wound healing. Injury of the vessel wall initiates the mechanisms responsible for platelet activation and coagulation factor activation. Coagulation factors are plasma proteins that in the absence of tissue damage circulate in blood in an inactive form. Tissue lesion provokes a proteolytic cascade that sequentially activates all the factors, resulting in the formation of the stable fibrin clot. The haemostatic mechanisms are limited to the area in which tissue injury and platelet adhesion occurred. Upon definitive arrest of bleeding, the fibrin network is dissolved by plasmin deriving from proteolytic activation of plasminogen. Plasminogen activation is strongly stimulated by fibrin, and therefore plasmin is active only in the areas in which fibrin is present. Alterations of the different haemostatic mechanisms result in severe pathologic conditions that represent one of the main causes of death in modern society. The haemostatic process is controlled by sophisticated mechanisms aimed at maintaining a functionally correct balance between prothrombotic and antithrombotic pathways.

Effects of Aspirin on Endothelial Function and Hypertension

2016

Purpose of reviewEndothelial dysfunction is intimately related to the development of various cardiovascular diseases, including hypertension, and is often used as a target for pharmacological treatment. The scope of this review is to assess effects of aspirin on endothelial function and their clinical implication in arterial hypertension.Recent findingsEmerging data indicate the role of platelets in the development of vascular inflammation due to the release of proinflammatory mediators, for example, triggered largely by thromboxane. Vascular inflammation further promotes oxidative stress, diminished synthesis of vasodilators, proaggregatory and procoagulant state. These changes translate into vasoconstriction, impaired circulation and thrombotic complications. Aspirin inhibits thromboxane synthesis, abolishes platelets activation and acetylates enzymes switching them to the synthesis of anti-inflammatory substances.SummaryAspirin pleiotropic effects have not been fully elucidated yet. In secondary prevention studies, the decrease in cardiovascular events with aspirin outweighs bleeding risks, but this is not the case in primary prevention settings. Ongoing trials will provide more evidence on whether to expand the use of aspirin or stay within current recommendations.