ABSTRACT
The examination of 194 patients with coronary heart disease concurrent with clinical manifestations of angina pectoris established that the development of coronary atherosclerosis was accompanied by suppressed prostacyclin (PGI2) synthesis and increased thromboxane A2 (TxA2) leukotriene (LT) synthesis. The activation of synthesis of the vasoconstrictor and proaggregate TxA2 depended on the severity of clinical signs of angina pectoris. The imbalance of PGI2 to- TxA2 metabolite ratios was associated with dyslipidemias and the extent of coronary atherosclerosis. Bicycle ergometry testing resulted in prostanoid imbalance. The determination of the dynamics of prostanoids was used to check the efficiency of antianginal therapy. The concomitant application of inhibitors of thromboxane synthetase and LT synthesis was recommended for secondary prevention of thrombotic complications in patients with coronary atherosclerosis.
