Evaluation of the efficiency of dual antiplatelet therapy in patients with acute coronary syndrome who underwent percutaneous coronary intervention

Objective. To evaluate platelet function and the efficiency of antiplatelet therapy, by using clinical data and spontaneous platelet aggregation indicators in patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI). Subjects and methods. The study involved 154 people, including 104 patients with ACS (82.7% men; 17.3% women; mean age, 60.7±10.4 years), who underwent emergency coronary intervention. The patients received dual antiplatelet therapy. Spontaneous and induced platelet aggregations were studied by the turbidimetric method. The ACS patients (n=104) were divided into 3 groups: acute ST-elevation myocardial infarction (MI) (STEMI), non-ST-elevation MI (NSTEMI), and unstable angina (UA). A control group included 50 healthy individuals (14% men; 86% women; mean age, 41.7±14.9 years), who did not take antiplatelet drugs. Results and discussion. During 12 months, spontaneous platelet aggregation decreased by 5–20% in patients with STEMI, by 30–40% in those with NSTEMI, and 14–21% in those with UA. The indicators of spontaneous and induced platelet aggregation did not depend on the presence or absence of the loading dose of an antiplatelet drug at the prehospital stage or on age and gender. This indicator significantly reduced within 24–48 hours after disease onset; i.e. the decrease in platelet aggregation began no earlier than 24 hours after disease onset. The indicators of platelet aggregation did not differ in ACS patients on admission and in the control group (p>0.05). The ACS patients (n=15) who did not receive the loading dose of antiplatelet agents at the prehospital stage were found to have higher induced platelet aggregation rates than the patients in the control group. In patients with platelet hyperaggregation, ticagrelor was more effective in reducing spontaneous platelet aggregation, while in those with normal and low aggregation of platelets, ticagrelor and clopidogrel had the same effect on their function. In inpatients with ACS, spontaneous platelet aggregation decreased by 23.9% during antiplatelet therapy (p=0.0001); by 36.8% when using the inducer adenosine diphosphate (ADP) at a concentration of 0.1 mmol/ml (p=0.0001); by 62.5% when applying ADP at that of 1.0 mmol/ml (p=0.001); by 47.2% when employing ADP at that of 5.0 mmol/ml (p=0.001). Platelet aggregation returned to the baseline level in 80.3% of patients at 6 months and in 86.9% at 12 months. The patients with platelet hyperagregation developed cardiovascular events (UA, recurrent MI, stent thrombosis) developed in 100% of cases; 33% had normal aggregation and 14% had hypoaggregation.