Российский кардиологический журнал (Aug 2012)

ANTIAGGREGANT THERAPY AND REDUCTION OF HIGH RESIDUAL PLATELET REACTIVITY

  • N. A. Mazur,
  • A. A. Lomonosova,
  • E. A. Zolozova,
  • E. A. Sayutina,
  • V. V. Chigineva

Journal volume & issue
Vol. 0, no. 4
pp. 74 – 78

Abstract

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Aim. To assess the levels of residual platelet reactivity (RPR) and its potential correction by antiaggregant therapy in patients with angina. Material and methods. The study included 40 patients with coronary heart disease (CHD), aged under 70 years, with adequate blood pressure control and no contraindications for antiaggregant therapy. All participants underwent general clinical examination, general blood assay, blood biochemistry, and platelet aggregation assessment (blind method). ADP (5 mkmol/l) was used as an aggregation inductor. The patients were randomised into two groups, to compare the antiaggregant activity of aspirin (thrombo ASS 100 mg) vs. plagril (clopidogrel 75 mg), and plavix (75 mg) vs. plagril (75 mg). Platelet aggregation was assessed at baseline and at least three weeks later. After three weeks of the initial therapy, the patients were switched to another therapy arm (cross-over). Finally, all patients were receiving two antiaggregants (thrombo ASS and plagril). Results. During the therapy with enteric coated aspirin (100 mg), RPR above the target level (>46%) was observed in 72,5%. After switching to clopidogrel therapy, target RPR levels were achieved in almost 50% (n=16). Among remaining resistant patients (n=13; 32,5%), 8 achieved target RPR while receiving a combination of aspirin and plagril. Therefore, only 5 patients (12,5%) were resistant to both medications. Clopidogrel monotherapy did not reduce RPR to target levels in 14 patients (35%). In this group, aspirin was effective only in one patient. Conclusion. High RPR levels were more prevalent during the treatment with enteric coated aspirin (72,5%), compared to clopidogrel therapy (plagril or plavix; 35%; p<0,001). Only 12,5% of the participants were resistant to both medications (aspirin and clopidogrel). Overcoming this resistance could be possible with the use of new thienopyridine antiaggregants (prasugrel) or glycoprotein IIb/IIIa inhibitors.

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