Aspirin effectiveness in patients with rheumatoid arthritis and coronary heart disease who receive non-steroidal anti-inflammatory drugs

• Main Authors: T. V. Kropotina, N. A. Morova
• Format: Article
• Language: Russian
• Published: «FIRMA «SILICEA» LLC 2013-04-01
• Series: Российский кардиологический журнал
• Subjects: rheumatoid arthritis; chd; nsaid; platelet aggregation
• Online Access: https://russjcardiol.elpub.ru/jour/article/view/367

Aim. To study coagulation and vascular-platelet haemostasis in patients with rheumatoid arthritis (RA) and coronary heart disease (CHD), who receive various non-steroidal anti-inflammatory drugs (NSAID) in combination with low doses of aspirin. Material and methods. The study included 79 patients (59 women and 20 men; mean age 61,0 years; mean disease duration 8,5 years) with confirmed RA diagnosis. All participants received disease-modifying anti-inflammatory therapy and NSAID, as well as standard pharmacological CHD therapy. The parameters of coagulation and vascular-platelet haemostasis were compared by the type of administered NSAID (diclofenac, tenoxicam, nimesulide, or meloxicam). In total, 40 patients with increased platelet aggregation but no previous antiaggregant therapy were administered aspirin (100 mg/day). Platelet aggregation was reassessed at Day 7–8 of aspirin therapy. The control group included 25 untreated healthy men (mean age 55 years). Results. Activated coagulation haemostasis was observed in 58,2% of patients with RA and CHD, as manifested in increased levels of fibrinogen, soluble fibrin monomer complexes (SFMC), factor XII-dependent fibrinolysis, and von Willebrand factor, compared to controls. The therapy with most NSAID was linked to similar changes in coagulation haemostasis. The patients receiving diclofenac, nimesulide, and meloxicam demonstrated an activation of vascular-platelet haemostasis, as manifested in a significant increase of spontaneous platelet aggregation and ADPinduced platelet aggregation, compared to controls. Among patients receiving tenoxicam, there was a tendency towards a reduction in ADP-induced platelet aggregation (aspirin-like effect). Among patients already receiving diclofenac, nimesulide, or meloxicam, aspirin administration typically resulted in reduced platelet aggregation. In total, 42,4% of the patients did not respond to aspirin therapy. Conclusion. Patients with RA and CHD who receive NSAID are also in need of antiaggregant therapy. The latter should be administered under control of vascularplatelet haemostasis, as in a substantial proportion of these patients (42,4%), aspirin effectiveness is not adequate.