By J. Knoll and K. Kelemen (Eds.)
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Extra resources for Advances in Pharmacological Research and Practice. Proceedings of the 4th Congress of the Hungarian Pharmacological Society, Budapest, 1985
Commun. , Solomon D. : A phospholipase A9 inhibitory protein in rabbit neutrophils induced by glucocorticoids, Proc. natn. Acad. Sei. , Asano T. : Alterations of eicosanoid synthetic capacity of rat brain microvessels follo wing ischemia: relevance to ischemic brain edema, J. Neurochem. , Nemecz Gy. Pharmac. , Tósaki Α . , Nemecz Gy. : Prevention by macrocortin of global cerebral ischemia in Sprague-Dawley rats, Eur. J. Pharmac. , Tósaki Α . , Leprán I. : Glucocorticoids in myocardial and cerebral infarction.
Such large numbers are required in order to show a 20% difference when the end point is survival. Thus, to demonstrate a 20% difference between treatment and placebo, there would have to be a total of 400 - 600 deaths in the trial, and no single trial of such scale has been carried out with beta-blockers. Thus the pooling of data from 24 trials has been necessary to demonstrate the significant effect. The question naturally arises as to how does beta blockade reduce the incidence of sudden death and myocardial reinfarction?
Therefore, it seemed highly probable that by reducing both these effects by means of the specific actions of beta-blocking drugs, as first pro posed by Black /1962/, there would be a beneficial clinical effect on AMI. The results of the first study by Snow /1966/ demonstrating a reduction in mortality in AMI from 29 % to 16 ^ appeared to confirm Black's hypothesis. ". Six years later this statement is no longer true. 000 patients /Yusuf et al. 1985/. /Figure 1/. I. 5 - 7 days/ or postinfarction /8 days - 3 years/ period results in a 20% reduction in mortality, compared with placebo, b/ The effect is achieved by a 30% reduction in sudden death, c/ There is a 25% reduction in myocardial reinfarction rate.