The advance of cardiology has improved the prognosis of atherothrombosis through direct diagnosis and early management, but the global incidence of atherothrombotic events has been modified only slightly. Currently, although the stenosing effect of atherosclerosis is well known and if treated hardly poses a problem, the unpredictable risk of arterial thrombosis continues to cause the seriousness of the disease in as much as it is not linked to the degree of stenosis. The initiation of thrombosis progresses via destabilisation phenomena of atherosclerotic plaques with rupture or erosion of the capsule. The identification of plaques "at risk" of instability, so-called "vulnerable" plaques, is thus now a fundamental concept. Thanks to anatomo-pathology, certain morphological and functional criteria of these vulnerable plaques are better understood and are starting to find a clinical resonance. An inflammatory syndrome scenario, thin capsule, and a large lipidic heart associated with an as yet quiescent atherosclerotic plaque are predictive elements of acute coronary syndrome. These elements show promise and an already combined biological and morphological approach will certainly be at the heart of clinical research for years to come.