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	Cardiovascular Norway- ASA reduces infarct size and improves ECG findings After monitoring the progress of 753 patients following acute myocardial infarction, M. Abdelnoor and K. Landmark came to the conclusion that ASA reduces the severity of myocardial infarction when they found that peak creatine kinase and lactate dehydrogenase levels were lower and ECG evidence of the milder, "non-Q-wave", type of infarction more common in ASA users than in people who did not use ASA (odds ratio = 2.63). The latter effect was even more pronounced in patients receiving thrombolytic therapy in addition to taking ASA. On the other hand, ASA does not inhibit the rise in enzyme levels in patients receiving concomitant thrombolytic therapy. ASA was administered in a dose of 75 or 160 mg in a sustained-release formulation. In the opinion of the authors, ASA is capable of exerting a positive effect on the outcome of myocardial infarction . Abdelnoor, M., et al.: Infarct size is reduced and the frequency of non-Q-wave myocardial infarctions is increased in patients using aspirin at the onset of symptoms. Cardiology 1999 (91) 119-126 2. Cardiovascular Iceland- Drastic reduction in myocardial infarction mortality within 10 years is largely attributable to ASA In 1986, 26.3 percent of patients admitted to hospital in Reykjavik (Iceland) following myocardial infarction died within a year. In 1996 (i.e. 10 years later), this figure had dropped to just 19.7 percent, as was discovered by J. M. Kristjansson and Karl Andersen in a comparative study. They pointed out that the use of ASA during this period increased from 11.3 percent to 76.3 percent. According to the researchers, this six-fold increase has contributed considerably to the improvement in prognosis. In 1996, the odds ratio for one-year mortality calculated for infarct patients receiving ASA when they were discharged from hospital was just 0.13 compared with patients not taking ASA. However, taking ASA before the infarct did not affect the prognosis. Kristjansson and Andersen attribute this to the fact that the patients concerned probably had a very high cardiovascular risk which "neutralised" the protective effects of ASA. Kristjansson, J. M., et al.: Improved one-year survival after acute myocardial infarction in Iceland between 1986 and 1996. Cardiology 1999 (91) 210-214 Pain Great Britain- Efficacy of a single dose of ASA in postoperative pain Single doses of 600/650 mg, 1,000 mg and 1,200 mg ASA are significantly more effective than placebo in the treatment of postoperative pain. In order to demonstrate a 50 percent reduction in pain, results are needed from 4.4, 4.0 or 2.4 patients depending on the dosage. Even at the lowest of the three doses mentioned, drowsiness and stomach irritation were significantly more common than on placebo. The analgesic effect of ASA gives rise to a clear dose-effect relationship. The analgesic effect is equivalent to that of paracetamol on a milligram basis. These results were arrived at by J. E. Edwards et al. on the basis of a systematic evaluation of all randomized, controlled studies carried out so far on the treatment of postoperative pain with ASA. 72 studies involving a total of 3,253 patients on ASA and 3,297 patients on placebo fulfilled the inclusion criteria. With their study, the British researchers hope to set a standard against which other analgesics can be measured. It also facilitates the "benchmarking" of analgesics. Edwards, J. E., et al.: Oral aspirin in postoperative pain: a quantitative systematic review. Pain 1999 (81) 289-297