Although different NSAIDs have different structures, they all work by blocking cyclo-oxygenase (COX) enzymes. There are two main types of COX enzymes: COX-1 and COX-2. Both types produce prostaglandins; however, the main function of COX-1 enzymes is to produce baseline levels of prostaglandins that activate platelets and protect the lining of the gastrointestinal tract, whereas COX-2 enzymes are responsible for releasing prostaglandins after infection or injury. Prostaglandins have a number of different effects, one of which is to regulate inflammation.
"It's very frightening. There seems to be no safe treatment window" for NSAIDs once you've had a heart attack, said Anne-Marie Schjerning Olsen, a cardiologist at Copenhagen University Hospital Gentofte who, along with colleagues, reviewed the records of nearly 100,000 patients who had suffered a heart attack between 1997 and 2009. About 44 percent of them received at least one prescription for an NSAID. Among people who didn't take NSAIDs, Olsen says, the cardiovascular risk after a first heart attack declines rapidly during the first year. "After five to 10 years it's almost the same" as the general population, she says. But heart attack survivors who took any NSAID other than low-dose aspirin had a higher risk of having a second heart attack or dying. The overall death risk rose 59 percent one year after the heart attack and 63 percent five years after, she said. Similarly, the risk of coronary death or a second heart attack rose 30 percent one year after the initial heart attack and 41 percent five years after.
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