However, the inhibition of COX-1 in cells of the gastrointestinal (GI) system and COX-2 in vascular cells translates into increased risk of serious GI adverse events and atherothrombosis and hypertension, respectively.
The role PGI(2) in the physiology and pathophysiology of vascular diseases is reviewed and the recent findings linking PGI(2), COX-2 and atherothrombosis are summarized.
In this review, we discuss the different expression profile of COX-2-related enzymes in the cells actively involved in atherothrombosis, the role of these enzymes as cause of plaque "instability", and the clinical consequences of their inhibition.
The critical role of prostacyclin in many pathophysiological conditions, such as atherothrombosis, has only recently become appreciated (through receptor knockout mice studies, selective cyclooxygenase-2 inhibition clinical trials, and the discovery of dysfunctional prostacyclin receptor genetic variants).
There is concern that cyclooxygenase (COX)-2 inhibitors may promote atherothrombosis by inhibiting vascular formation of prostacyclin (PGI2) and an increased thrombotic risk of COX-2 inhibitors has been reported.