Title: The assessment of antiplatelet activity of aspirin among survivors of myocardial infarction treated with PCI in six months obsen/ation - preliminary results
- Marta Kamińska, Joanna Osada, Milena Dąbrowska, Janusz Kłoczko, Karol Kramkowski, Włodzimierz J. Musiał
- Original articles
- Polish Journal of Cardiology
- Start page:
- Final page:
- ASA-resistance, type 2 diabetes, obesity
Introduction: The antiplatelet therapy with acetylsalicylic acid (ASA) is the firstline treatment in secondary prevention of coronary heart disease. There is accumulating evidence for occurrence of ASA - resistance phenomenon. The identification of the factors affecting an individual response to ASA therapy seems to be of the paramount importance.
Aim of study: The assessment of antiplatelet activity of ASA among survivors of myocardial infarction (Ml), treated with percutaneous coronary intervention (PCI), in six months observation. Evaluation of potential riskfactors ASA-resistance phenomenon in this group of patients. Material and methods: 27 survivors of Ml treated with PCI were enrolled in the study. Platelet aggregation (impedance) induced by arachidonic acid (AA) and collagen (col), flow cytometric measures of platelet P-selectin expression were performed in purpose to evaluate the antiplatelet activity of ASA. Ali parameters were assessed 2 months after Ml in group without history of diabetes mellitus (non DM group; n= 17) and 6 months after Ml in all studied patients.
Results: ASA-resistance defined as the presence of platelet aggregation induced by AA despite ASA therapy was diagnosed in 5 participants (29%), 2 months after Ml, while platelet aggregation was successfully inhibited in the same group 4 months later (p=0.026). 4 diabetic patients (33%), studied 6 months after Ml, were ASA resistant (p=0.033 vs non DM group). In comparison to control group, ASA significantly decreased col induced platelet aggregation (0.5 Mg/ml and 1 ug/ml) 2 and 6 months after Ml both in diabetic and non-diabetic patients. ASA treated patients had similar expression of P-selectin 2 months after Ml and markedly Iower 4 months later, when compared to the control group. The obesity, disturbances of glucose metabolism, higher concentration of total cholesterol and LDL-cholesterol were obsen/ed more often among patients with ASA-resistance. During one year follow-up period we observed 3 major adverse clinical events (MACE) among patients with diagnosed ASA-resistance, whereas in group with successful ASA therapy there was none.
Conclusions: Early post-infraction period is characterized by Iower antiplatelet efficacy of ASA in comparison with six months observation. Obesity, disturbances of glucose metabolism and higher level of lipids can limit the antiplatelet activity of ASA among patients after Ml. The ASA-resistance phenomenon can worsen prognosis among the survivors of Ml.