Resistência à aspirina: realidade ou ficção?

Abstract

more circulating platelets, which contribute to the formation of the thrombus 5,6 . At this moment, the platelets activate and secret several substances such as ADP, serotonin, fibrinogen, von Willebrand factor, fibronectin, growth factors (platelet-derived growth factors, alpha-growth factor, beta-growth factor), procoagulants (platelet factor 4 and factor V) and TXA2 .Another relevant event for the formation of the thrombus is platelet aggregation, that is, the binding of platelets. The final pathway for platelet aggregation is the glycoprotein IIb/ IIIa receptor, which is also the main adherence receptor. The fibrinogen also has an important role in this process, considering that it stabilizes the platelet thrombus and functions as bridge between platelets 5,6 . The vascular endothelium controls platelet reactivity through three main mechanisms: the arachidonic acidprostacyclin pathway, the L-arginine nitric oxide and the endothelial ectoadenosine diphosphate (Ecto-ADPase) 5,6 . Endothelial cells convert the arachidonic acid into prostacyclins through the action of cyclooxygenase 1 (COX1), cyclooxygenase 2 (COX 2) and prostacyclin synthetase. The prostacyclins inhibit platelet function, increasing the levels of intracellular cyclic adenosine monophosphate (cAMP) 5,6 . The nitric oxide diffuses into the platelets and stimulates the production of guanosine monophosphate, causing a decreased intracellular calcium flow. Such calcium reduction modifies the conformation of the glycoprotein IIb/IIa, allowing the formation of fibrinogen bridges and platelet aggregation 5,6 . The Ecto-ADPase limits the plasma level of nucleotides. The activity of this enzyme annuls the critical phase of recruitment of platelet reactivity, as it removes the nucleotides from the fluid environment 5 . Platelet antiaggregationThe blocking of platelet aggregation is considered an effective strategy for the prevention and treatment of cardiovascular events caused by atherosclerotic disease 7 .The search for therapeutic strategies capable of blocking platelet aggregation in patients with atherosclerotic disease, with the objective of decreasing the occurrence of clinical events, has been the objective of several studies [8][9][10] . Due to the fact that aspirin inhibits cyclooxygenase 1, which prevents the formation of thromboxane A2, is considered an excellent platelet antiaggregant drug 11 .The effectiveness of aspirin in preventing cardiovascular events has been demonstrated by a meta-analysis that AbstractA meta-analysis of clinical studies of patients with cardiovascular disease demonstrated that the use of aspirin was associated with a 22% decrease in death rates and relevant ischemic vascular events. However, clinical studies demonstrated that patients that regularly took aspirin presented recurrence of cardiovascular events. Such observation led to the question whether, in some patients, the aspirin was not effective in blocking platelet aggregation and these patients were called unresponsive to aspirin or aspirin-resistant.The clini...

Avaliação do cálculo de dose para transfusão de plaquetas

“…A via final para a agregação plaquetária é o receptor da glicoproteína IIb/IIIa, que também é o principal receptor para adesão. O fibrinogênio, por estabilizar o trombo plaquetário e servir de ponte entre as plaquetas, também tem importante participação nesse processo(OLIVEIRA et al, 2010).…”