Optimization of antiaggregant therapy in rheumatoid arthritis and coronary heart disease patients receiving nonsteroidal anti-inflammatory drugs

Abstract

Objective: to study coagulative and vascular-thrombocytic hemostases in patients with rheumatoid arthritis (RA) and coronary heart disease (CHD) depending on therapy with different nonsteroidal anti-inflammatory drugs (NSAIDs) alone and in combination with low-dose aspirin. Subjects and methods. The trial enrolled 58 patients (43 women and 15 men) with a valid diagnosis of RA. The patients' mean age was 61.2 years; the disease duration averaged 10 years. All the patients received therapy with disease-modifying antirheumatic drugs (DMARDs) and NSAIDs. All had CHD; 52 of the 58 patients presented with arterial hypertension; 30 had noncoronary atherosclerosis. Cardiovascular diseases were first identified in 18 patients. All took heart medications. Coagulative and vascular-thrombocytic hemostases were studied in all the patients and the results were compared depending on to the taken NSAID (diclofenac, tenoxicam, nimesulide, meloxicam). Thirty-seven patients who had not previously received antiaggregant therapy were given aspirin in a dose of 100 mg when they were found to have platelet hyperaggregation and aggregation was restudied on aspirin therapy days 7-8. A control group consisted of 26 healthy men (mean age 55 years) who received no medications. Results. In patients with RA and CHD, activated coagulative hemostasis was identified in 65.5% of cases. The signs of hypercoagulation were observed in 35 of the 58 patients. When different NSAIDs were used, the coagulative hemostatic changes were unidirectional and no statistically significant differences were found between the groups. The patients taking diclofenac, nimesulide, or meloxicam were found to have activated vascular-thrombocytic hemostasis. Those receiving tenoxicam showed a tendency towards decreased adrenaline-induced platelet aggregation (the drug's aspirin-like effect); however, no statistical processing was made because of few cases. The use of aspirin in the patients taking diclofenac, nimesulide, or meloxicam resulted in lower platelet aggregation in the vast majority of cases despite NSAID intake. No adequate aspirin response was obtained in 32.4% of the patients. Conclusion. Aspirin is indicated in RA and CHD patients receiving NSAIDS. Antiaggregant therapy should be used under control of vascular-thrombotyc hemostasis as aspirin is insufficiently effective in one third of cases in this group.