Inhibition of different isoenzymes of COX and a decrease in prostaglandins at the inflammatory sites increase thromboxane A2 (COX-1) and decrease prostaglandin I2 (COX-2) production, which may lead to vasoconstriction, platelet activation, hypertension, accelerated atherosclerosis, renal sodium retention with peripheral edema, and heart failure [92]. This evidence concerns the gene PTGS2 and heart failure.