Renu Vermani， MD， FACC：国际知名的心血管病理学家。是2005年成立的CVPath研究所所长，是ACC、AHA和加拿大病理学院成员。Renu Vermani教授负责心血管病理学领域的多项研究资金的评选，在动脉粥样硬化、易损斑块、支架和其他心血管疾病领域的同行评审期刊作为作者和共同作者发表600多篇文章。
　　International Circulation: You just gave a presentation on how disease is special involving bifurcations with the left main coronary artery.  Could you give us a short overview of your presentation?
　　Prof. Renu Vermani:  What I really showed in my talk is when we look at bifurcation in atherosclerosis where do bifurcation lesions develop and what the relationship is of the lesion.  Firstly， it makes a difference where it develops.  The left main artery is much more elastic when compared to muscular arteries like the left anterior descending (LAD) or circumflex arteries.  Because it arises from the aorta it therefore is not surprising that it is a transitional artery and has more elastic fibers than other arteries do.  I also talked about the length of the left main artery， whether it is small (less than 10 mm)， medium (10-15 mm)， or large (greater than 15 mm).  I showed that， from our experience， the atherosclerosis seems to appear more in the longer length lesions than in the shorter length ones.  Calcification is also more pronounced and developed in the longer lesions than in the shorter lesions.  If there is greater calcification or greater atherosclerosis in terms of length of lesion， it tends to go along with the LAD and not so much with the circumflex artery.  We often see a particular type of disease in the left main artery in both early and late disease in over 300 cases of patients who were dying suddenly of left main artery disease.  We asked the question: what type of disease are we seeing here?  The vast majority， that is greater than 30% of those with greater than 50% narrowing， have fibrous plaques and fibrous calcified plaques.  The rest overall had cases of plaque eruption more frequently than plaque erosion.   Plaque erosion is extremely rare in the left main artery.  We also found that roughly 6% of the cases had healed plaque ruptures， so even in the left main 1-40% of cases progress to atherosclerosis and continue to thrombosis.  This also affects the left main artery.  One of the things that determine where the plaque develops is the flow dividers.  Where you find flow dividers， at the corina for instance， you do not find atherosclerosis.  Atherosclerosis usually develops in places like the lateral wall， which is the low share regions that have more turbulent blood flow and therefore result in more development of atherosclerosis， plaques， and necrotic cores.  Bifurcation lesions are essentially spared of the area of the corina in coronary arteries.  One of the reasons why left main bifurcation disease when it was originally described included plaques in the corina， it was because angiography could not discriminate the area.  Further studies have broadened our understanding of plaque development and these findings have now been proven.  For instance， Gary Mince showed data very similar to the data we have.  The angle of the left main artery also makes a difference.  The shorter the left main artery is the less the disease is going to be in the corina and the less disease will be overall in the left main.  The more severe the angle is the more likely it is to have corinal plaques.  This is something that I did not show in my talk but is something we have observed in our cohort of cases.  I also showed cases of bare metal stents 30 days post-implantation and found that overall these stents tend to do very well.  The reason is that it is more because of the bigger size of the artery.  Once there is a bigger sized artery there is less likelihood of having problems because the trauma to the artery is less and there is less re-stenosis.  Out of the 10 cases only 2 required re-stenosis.  I showed about 10 stenosis cases using drug-eluting stents and 5 had thrombosis.  I believe that has to do with the fact that in the flow divided regions there is much more delayed healing and therefore have uncovered struts that tend to form thrombi due to the turbulent flow of blood.  It was predominantly in taxis stents that this occurred because we had first generation pathology only.  The one case we showed from CIPHER that had thrombosis also had hypersensitivity reaction.  The case involved a 39 year old woman who， five years earlier， had had the stent implanted and due to a loss of health insurance took herself off of the dual anti-platelet therapy resulting in episodes of chest pain and subsequently led to her death.  There was another case involving the patients deciding to stop dual anti-platelet therapy and developed thrombosis within days.  With drug-eluting stents， if the cardiologist is going to put it into high-share regions of bifurcation， it is important to make sure that the patient is covered with dual anti-platelet therapy for a much longer period than you would otherwise in cases of more stable plaques.

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