This delay can be explained by previous lack of knowledge of the precise molecular mechanisms involved in the inflammatory processes in atherosclerosis, lack of selective inhibitors and scepticism of this approach arising from poor outcomes when non-specific anti-inflammatory agents such as corticosteroids have been used in the setting of acute myocardial infarction [33], and increased incidence of cardiovascular events in individuals treated with anti-inflammatory inhibitors of cyclooxygenase 2 (Cox-2) [34]. Here, PTGS2 is linked to acute myocardial infarction.