The predisposing and precipitating causes of acute myocardial infarction Ml
) are multiple; furthermore, different individuals may have different susce
ptibility, to a large extent genetically determined, to each of them. in sp
ite of the complex aetiology of Mi and of our limited knowledge of the caus
es responsible for the formation of persistent occlusive thrombosis in epic
ardial coronary arteries, the achievements obtained by controlling traditio
nal risk factors are remarkable. Traditional risk factors, however, have a
limited sensitivity among subjects with low/moderate levels of risk. Furthe
rmore, in particular among subjects at medium risk, current preventive stra
tegies are limited by the low incidence of preventable events which makes i
t necessary to also treat the vast majority of subjects who would not devel
op cardiac events even without any treatment. An improvement in preventive
strategies for HID can be achieved with the identification of: (1) new risk
factors; (2) genotypes enhancing the susceptibility to specific risk facto
rs; (3) phenotypes and genotypes making patients susceptible to specific pr
eventive strategies; (4) genotypes protecting from risk factors. Although a
word of caution is necessary as a number of recent studies on genetic mark
ers, on new risk factors and on the interaction between genetic markers and
environment have failed to withstand the rigour of population-based studie
s, the early findings available to date suggest that cost-effective prevent
ive strategies based on individual susceptibility to specific predisposing
and precipitating causes of MI may become a reality in the foreseeable futu
re.