<International Circulation>: we have many techniques to identify vulnerable plaque and with the development of new technologies， there is the potential for discovering new characteristics of vulnerable plaque. Can you tell us about these new characteristics?

    Prof.Mintz: I am not so sure there are any new characteristics. Vulnerable plaques have been reasonably well characterized by the pathologists: a large necrotic core; the neovascularization; inflammation and macrophages in the fibrous cap. There are some theories with respect to what stimulates plaque rupture， but those theories are just theories. There are some biomechanical models that seem to suggest that there may be microscopic amounts of calcium in the fibrous cap that forms a point of defect or vulnerability which may lead to rupture， but they are not things we are detecting with imaging. These are things that have been modeled in the laboratory. Imaging is still focusing on its ability to detect and predict events by detecting vulnerable plaques. The major finding in the last year of course which is the results of PROSPECT， showed that one of these technologies， virtual histology， can detect thin cap fibroatheromas which have a higher risk of being associated with events. There is no similar data with the other imaging modalities. Exactly which modality would be the best， I don’t think anybody at this point is prepared to say and it may just be that the entire field is going to fizzle at least in terms of a primary invasive imaging approach， simply because the event rate in PROSPECT was so low.

   <International Circulation>:  And this new technology for identifying vulnerable plaque - what are they and how are they applicable in clinical practice?

    Prof.Mintz: None of them are applicable in clinical practice right now. The technologies besides virtual histology are: optical coherence tomography (OCT) or its newer generation， OFDI， which can detect a thin fibrous cap and may be able to detect macrophages and inflammation in the fibrous cap and it can detect a lipid-rich plaque close to the surface， but again， there is no predictive data with it; the newest technology is near-infrared spectroscopy which is a technique that assesses the chemical composition of plaque and an algorithm has been developed that predicts a large amount of lipid core plaque relatively close to the surface. Neither of these techniques is currently clinically indicated for imaging to identify and then treat vulnerable plaques.

   <International Circulation>: we know the rupture of vulnerable plaque will lead to acute cardiovascular events， even death. If we can treat vulnerable plaque early， favorable outcomes may be achieved， so what early intervention therapies for vulnerable plaque would you advocate?

    Prof.Mintz: At this moment， with respect to mechanical or catheter-based intervention – none - and for a number of reasons. The major one is because the event rate is low. Most vulnerable plaques do not rupture to cause events. Most， when they rupture， probably do so silently and then heal， and some even heal spontaneously without rupturing. So to go into the coronary arteries looking for vulnerable plaques to throw in stents， makes absolutely no sense. I also think that any therapy should be advanced pharmacological intervention. It was surprising that the death from MI rate from PROSPECT was only 1% per year， but in retrospect， that is probably not so surprising， as these patients were treated with excellent medical therapy – aspirin， Plavix and statins. When PROSPECT was planned， and that was as long as seven years ago， these therapies were not routine.