[Physiopathology of myocardial infarction: the acute coronary occlusion]

Rupture of the atheromatous plaque, thrombosis and local vasoconstriction are involved in the genesis of acute myocardial infarction. The vulnerability of the plaque depends on its histological structure. Its fragility is related to the size of the lipid core, the thinness of the fibrous capsule and the inflammatory reaction. External aggression favourites rupture. This triggers both thrombogenesis by bringing the blood cells into contact with thrombogenic subendothelial factors and local vasoconstriction due to endothelial dysfunction. Although rupture of the plaque is an unpredictable event, there is a circadian variability the highest incidence of infarction being between 6 a.m. and midday. Comprehension of the physiopathology of myocardial infarction has opened up new therapeutic approaches which should reduce the incidence of plaque rupture. Prevention is based on stabilisation of the plaque by dietary hygiene, lipid-lowering drugs and, maybe, in the future, by local application of antisense oligonucleotides. Finally, anti-aggregant therapy (aspirin or anti-GIIb-IIIa) could prevent the formation or extension of the thrombus.