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To assess the necessity determination of platelet aggregation in patients (pts) with unstable angina (UA) with the performance of subsequent correction of antithrombotic therapy.
The study involved 170 pts with UA and conservative treatment strategy with a low risk on the scale of GRACE. The study group presented 68 pts of the main group (MG) that perform dynamic monitoring of platelet aggregation to identify the primary and secondary resistance to antiplatelet agents with subsequent correction of antiplatelet therapy. The control group (CG) consisted of 102 pts with standard antiplatelet treatment. To assess platelet resistance to antiplatelet agents was performed aggregatogram on the analyzer Multiplate (ASPI-test, ADP-test) on 5-7 day after administration of clopidogrel and aspirin, then at 1, 3, 6, 9 months’ follow-up. Pts were considered resistant to clopidogrel at (AUC) ADP- test (AUC)> 60U (the threshold value calculated earlier for people with NA), aspirin at ASPI- test (AUC)> 52U.
At discharge in MG decreased sensitivity to ASA reported in 13 (19.2%) persons, to clopidogrel in 15 (22%) pts. Of the 102 pts from CG revealed a decrease in sensitivity to ASA per unit dose in 18 (17.6%) persons, to clopidogrel in 22 patients (21.5%) pts. The high residual platelet reactivity (HRPR) was diagnosed in 40 individuals (39.2%) from CG and in MG in 28 (41.2%) pts. Thus, in the initial state, pts with UA angina in MG and KG were comparable in the identified resistance to antiplatelet agents.
In the MG when the detected resistance to the gradual increase in dose of “unprotected” aspirin (75-150 mg) and the correction of concomitant therapy (dyslipidemia, cancellation NSAIDs) allowed overcome pseudo resistance to ASA in 100% of cases.
Reduced HRPR in pts with clopidogrel resistance was achieved by replacing the generic to the original drug or ticagrelor, as well as the correction of concomitant therapy (proton pump inhibitors cancellation, correction of dyslipidemia). If the detected resistance to aspirin and clopidogrel (25.8% of individuals), antiplatelet agents other than the above correction scheme, high-risk individuals administered anticoagulant therapy (rivaroxaban 2.5 mg 2 times a day).
Recurrent angina was developed in 6 (8.8%) persons from MG and in 26 (25.5%) of CG patients (p = 0.001), myocardial infarction recorded in 1 (1.5%) patients in the MG and 3 (2.9%) of the CG individuals. In 3 patients died CG (2.9%) of the acute coronary insufficiency. Deaths were not in main group.
The use of dynamic monitoring of platelet aggregation in patients with UA officials allowed the timely detection HRPR in pts receiving antiplatelet agents and carry out the treatment of the correction, which reduced the number of repeat cardiovascular events.