For years, nonsteroidal anti-inflammatory drugs that target the cyclooxygenase 2 (COX-2) enzyme have been linked to increased cardiovascular risks. New research indicates that these elevated risks occur because COX-2 inhibitors suppress prostacyclin—a vasodilator and platelet inhibitor with heart-protecting properties—in vascular cells (Yu Y et al. Sci Transl Med. 2012;4:132ra54).
A team led by researchers in Pennsylvania confirmed that COX-2 is expressed in cells lining blood vessels and revealed that selectively removing it from the mouse vasculature reduced urinary excretion of the major metabolite of prostacyclin. This predisposed mice to thrombosis and hypertension. Urinary excretion of the metabolite varied inversely with blood pressure across all mutant mice.
Hampton T. COX-2 Inhibitors and Heart Risks. JAMA. 2012;307(21):2247. doi:10.1001/jama.2012.5731