"Prevention” does not just mean avoiding exposure to harmful elements, giving up smoking, fatty meals and excessive lounging on the sofa. 
Increasingly coming into play, is a more “positive” approach to preventing an ischemic angiocardiopathy, that is based upon the introduction of pleasant and beneficial habits for healthy arteries (2). Eating foods that are typical of Mediterranean countries, moderately sprinkled with a good red wine, ideally consumed at the table with an adequate amount of time at our disposal and in a relaxing environment, are all also useful in aiding prevention.  
Epidemiological studies have recently highlighted the “anti-infarct” qualities of the Mediterranean diet.  
Olive oil, with a high content of monounsaturated fatty acids, is effective in cutting cholesterol and in increasing HDL (3).  
The consumption of fish carrying high amounts of n-3 series polyunsaturated fatty acids, can reduce platelet aggregation, triglicerides and fibrinogen levels. 
Red wine, if consumed in moderate amounts and during meals, reduces the incidence rate of cardiac infarction (Fig. 1).  
The so-called “French paradox” explains how the widespread habit of a non-exaggerated intake of red wine has determined a low occurrence of ischemic angiocardiopathy in France, in spite of a high consumption of butter and other animal fats (4).  

Traditional risk factors: cholesterol et al 

For a long time it was thought that the level of cholesterol was the single most important marker for the risk of cardiovascular ischemia and so a lot of research was devoted to assessing how much bearing its reduction would have upon this risk.  
It emerged from these studies that intervening with hypocholesterolemizants cuts down the cardiovascular mortality rate but can be accompanied by an increased rate of deaths from other causes. 
From a metanalysis of all these studies, it also emerged that, principally, the employment of a particular family of these cholesterol-reducing drugs is able to reduce significantly the number of deaths due to ischemic angiocardiopathies, whereas working through dietetics or with other classes of drugs is not similarly effective (5, Tab. I). 
We could then ask ourselves if the observed effect might be due to the lowering of the cholesterol level alone, or to a direct action by the drugs in question. Indeed, the statins also possess direct anti-atherosclerotic effects, by inhibiting the proliferation of smooth muscle cells and are able to reduce the levels of coagulation factors VII and fibrinogen, as well as the inhibitor of plasminogen activator (PAI-1), all of these being elements that play important roles in determining the cardiovascular risk.  
That the cholesterol level on its own is insufficient for establishing the ischemic risk was clearly pointed out by the “ECAT” Study, a European effort centered on the predictive value of lipidic and hemostatic parameters on the likelihood of developing a thrombosis (6).  
Patients with a raised cholesterolemia only had a high risk of developing unstable angina if they also presented with a high fibrinogen level; on the contrary, hyperfibrinogenemia constituted a risk factor independently of cholesterolemia.  
It follows that reducing the level of cholesterol, without taking account of the fibrinogenemia, cannot be efficacious in preventing the risk of thrombosis.     
 

Mortality from cardiac infarction in Europe: the making of a new kind of geographical map 

Do the factors mentioned so far have the same bearing in all parts of Europe?  
Or has a rational approach to the prevention of the ischemic disorders (through changing the external variables) to take account of the culture, habits and basic biological order of the diverse European populations?  
The data from the MONICA Study informs us that there is a mortality rate gradient for cardiac infarction running between the Northern and Southern parts of Europe (7, Tab. II).  
In Scotland, or in Finland, there are six times more deaths from infarcts than is the case in Italy or Spain. In between, geographically, there are intermediate incidence rates for Central Europe. 
The distribution of cholesterol levels follows this incidence gradient for infarcts in Europe. 
Once again the people in the Northern European nations, at a high infarction risk, present a greater degree of cholesterolemia than those living in the Southern regions, who are at low risk.  
So, does good prevention mean it is enough to lower the cholesterol level and, in any case, would reducing it in Edinburgh have the same significance as lowering it in Naples? 
The answer has long been thought to have been “yes”, but the diversity in the distribution of risk/protection factors across Europe would, rather, justify differing effects of the corrections in eating habits (through the elimination/introduction of some food items) in the various European countries.  
Furthermore, it appears to be increasingly clear that, in the pathogenesis of the angiocardiopathies, just as in many other multi-factorial conditions, the factors in our surroundings connect themselves onto our genetic backgrounds, that can of themselves differentiate the populations in Europe.  

Genetics/environment interaction: can predestination be influenced? 

The levels of the factors so far mentioned may be genetically determined.  
A polymorphic variation in the gene that codifies for fibrinogen is responsible for a large part of the variability in blood fibrinogen levels within a given population (8, Tab. III).  
Such genic variations could also condition the increase in fibrinogenemia in response to a series of stimuli, such as smoke, diet, inflammation.  
Two polymorphisms of the gene for coagulation Factor VII, are associated with a reduction in the infarction risk (9).  
These alleles, quite frequent in Italian population (35.6% and 21.4%), reduce to a half the risk of infarction. 
They are less frequent in North-Europe population than in the Italian one: this difference could at least partly explain the decreasing gradient of mortality from North to South Europe. 
To a certain extent, cholesterolemia also depends on a polymorphism, in the gene that codifies for alipoprotein E (10).  
The E4 allele is associated with high cholesterol levels, while the E3 allele goes with low levels.  
All these genetic variants have also been associated with the disease risk and could at least partly explain the gradient of mortality due to infarct of the myocardium in Europe.  
The Finlanders, with a high mortality rate for infarcts and with high cholesterol levels, also have the highest frequency of the E4 allele and the lowest frequency of the E3 allele.   
The effects of dietetic and/or pharmacological interventions to reduce cholesterolemia may also be regulated by genetic factors, as in the case of probucol (a hypolipidemic drug) or of a diet with a low content of saturated fats, that have a more significant effect in lowering the cholesterol in individuals carrying the E4 allele, compared to carriers of the E3 allele.  
But does this mean we are saved from an infarct by “works” or by “grace”?  
This  dilemma, at the threshold of the third millennium, spurs on the discussion on risk factors.  
Is it the changes made to the external elements or is it genetic predestination that weighs upon the cardiovascular risk?  
For sure, a more appropriate prevention will, in future, have to take account of how the genetic make-up of individuals might modulate the susceptibility to the external variables in our lives.