The year 2002 in interventional cardiology was monopolised by the concept of the active stent. Each step of the restenosis process can be targeted by the active principle: platelet thrombosis, inflammation, smooth muscle cell migration, smooth muscle cell proliferation. At this stage, only sirolimus and paclitaxel have successfully completed the clinical validation process in simple lesions. Certain questions remain unresolved: far from 0% restenosis, why are these devices less effective in lesions at high risk of restenosis? Why does sirolimus stent usage create effects of restenosis on the edges and why is it present in cases of positive remodelling of the artery for which the clinical role is still unknown? Above all, will the late escapement of the restenotic process observed in the animal model have a clinical correlation when there is a longer follow up? It is still too soon to know if paclitaxel will raise the same questions. Indications not yet completely validated for the metallic endoprosthesis are disappearing little by little: acute infarction, long lesions. At last restenosis has been put in its proper place: the rate of re-intervention at 9 months remains less than 15% in the whole of the Presto study; systematic angiographic follow up at 6 months in the Trends study shows a restenosis rate of 13% on average. So the boundary between active stent and metallic stent seems more blurred than in 2001 when the results of the sirolimus studies were not available. The detection of ruptured or about to rupture plaque is a challenge which seems to be in hand now with techniques such as endocoronary echography or even more emergent techniques such as thermography, optical coherence tomography, or elastography. Which plaques should be treated? With medication? With mechanical tools? The work of the Lyon team on the clinical follow up of unstable plaques reveals a good prognosis for these plaques once the "guilty" lesion has been treated. The future of these techniques is thus perhaps more orientated towards primary prevention than towards secondary prevention.