In animal studies, COX inhibition decreased myocardial infarct size [24], produced scar thinning [31, 32], attenuated cardiopulmonary dysfunction during endotoxemia [31, 32] and prevented angiotensin II-induced production of superoxide in cardiovascular tissue, together with the decrease in systolic blood pressure and cardiac hypertrophy in vivo [33]. This evidence concerns the gene AGT and infarction.