NSAIDs have anti-inflammatory (reduce inflammation), analgesic (relieve pain) and antipyretic (lower temperature) effects. Although different NSAIDs have different structures, they all work by blocking cyclooxygenase (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. Most NSAIDs inhibit both enzymes, although a few are available that mainly inhibit COX-2. The pain-relieving and anti-inflammatory effects of NSAIDs are mainly due to inhibition of COX-2, and their unwanted side effects are largely due to inhibition of COX-1.
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We identified 28 947 persons with OHCA during 2001–10 and matched 115 788 controls with cases on age and sex. Within the 30-day case period, 3376 (%) persons were treated with an NSAID. Compared with non-users, NSAID users were more often women, had generally less cardiovascular diseases, such as ischaemic heart disease, myocardial infarction, and heart failure, but were more likely to have cancer and rheumatic diseases ( P for all <, Table 1 ). Moreover, NSAID users were more often treated with morphine, diuretics, and psychiatric medication ( P for all < ). Table 1 Baseline characteristics of subjects with out-of-hospital cardiac arrest divided into NSAID users and non-users