In the August 5 issue of Circulation, Dr. N. Zimmerman and his colleagues (University of Heinrich Heine, Dusseldorf) cite the results of their own study of the functional and biochemical response of platelets to aspirin in patients undergoing coronary bypass surgery. Among these patients, resistance to aspirin was quite common.

Plasma images were taken the day before the operation and 1, 5 and 10 days after it. In vitro, aspirin inhibited thromboxane synthesis, aggregation, as well as degranulation of platelet alpha-granules taken before surgery, but not after it. On the 10th day, the sensitivity of platelets to aspirin in vitro was partially restored, but in vivo aspirin at a dose of 100 mg / day per os remained still ineffective.

It was believed that in the development of aspirin resistance, a major role is played by cyclooxygenase-2 (COX-2). As the authors established, the concentration of immunoreactive platelet COX-2 increased by a factor of 16 on the 5th day after the operation. However, the selective inhibitor of COX-2 celecoxib did not affect aspirin-resistant synthesis of thromboxane. On the other hand, the thromboxane-synthase inhibitor and the thromboxane receptor antagonist terbogrel effectively inhibited the formation of thromboxane both before and after bypass.

According to German scientists, "Aspirin resistance is due to platelet dysfunctions both in vitro and in vivo. It is most likely associated with a violation of the suppression of platelet-derived COX-1 by aspirin ".

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