The prevention of heart infarction with 100 mg aspirin is common pract
ice in Germany, in spite of the fact that it is based on only two smal
l studies, the results of which are not generalized. Over 14 years, se
veral experimental and clinical studies have shown that 20-30 mg aspir
in/d for pharmacokinetic reason selectively inhibit the thromboxane sy
nthesis while the endogenous prostacyclin synthesis remains intact. Pr
ostacyclin plays an important cardioprotective role for the ischemic h
eart, having antiplatelet and antifibrillatory effects, potentiates th
e antiplatelet effect of the nitrovasodilators and nitric oxide, and i
ncreases the release of adenosine. A superior preventive action and lo
wer side effects of 30 mg/d aspirin in direct comparison with higher d
oses was first proved by the Cottbus reinfarction study. The 30 mg asp
irin tablet per day ought to replace the present prevention with highe
r doses.