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Adverse cardiovascular events have been associated with cyclooxygenase (COX)-2 selective nonsteroidal anti-inflammatory drugs (NSAIDs) and, subsequently, with traditional NSAIDs. The underlying mechanism is unclear, but this association has been postulated to result from a change in the balance between the prothrombotic and antithrombotic effects of prostanoids through inhibition of prostaglandin production.
Now, investigators in Canada have reviewed studies of inflammatory mediators in atheromatous plaques and have noted that cytokines produced by different T-cell responses (Th1 and Th2) have opposite effects on plaques: Cytokines that affect plaque remodeling and increase plaque instability and risk for rupture are mediated through Th1, wh…