International Circulation: As a senior investigator in the Thrombolysis in Myocardial Infarction (TIMI) studies， you have published on the use of serum cardiac markers for the diagnosis and prognosis of patients with unstable angina and acute myocardial infarction， and antithrombotic therapy for acute coronary syndromes. Can you give us a review of these findings and what new data has been presented at this meeting?

　　《国际循环》：作为心肌梗死溶栓（TIMI）研究的首席研究者，您已经发表了有关血清心脏标志物用于不稳定性心绞痛和急性心肌梗死患者诊断和预后，以及急性冠脉综合征抗栓治疗的文章。您能否回顾一下这些结果，本次会议上报告了哪些新数据？

　　Dr Antman: We have been using serum biomarkers in the diagnosis and evaluation of patients who have various forms of cardiovascular disease. One of the first biomarkers that I personally got involved with was a replacement for CKMB (creatinine kinase muscle-brain fraction). That biomarker was a cardiac-specific troponin. The troponins are part of the regulatory apparatus that help to control the sliding filaments of the myocardium， actin and myosin. When the myocardium is damaged by a thrombotic occlusion of a coronary artery and there is necrosis developing， biomarkers are released from the dying heart cells. The beauty of the cardiac-specific troponins is that we can say this biomarker actually came from cardiac muscle as opposed to skeletal muscle. The reason for that is that there are three different kinds of troponins – troponin I， C and T. Troponin C has the same amino acid structure in heart muscle and skeletal muscle， but troponin I and troponin T have different amino acid structures in the cardiac muscle as opposed to skeletal muscle. So it is possible to set up a biomarker assay for cardiac-specific troponin I and cardiac-specific troponin T. We now use these assays to detect even small amounts of myocardial necrosis. That has profound implications. We can overlook CKMB as a marker that tells us whether a patient has had a myocardial infarction and can now use cardiac-specific troponins. We can detect even smaller amounts of myocardial necrosis with these biomarkers， which allows us to refine our therapy for patients who are releasing cardiac-specific troponins. We know from that information that they have sustained myocardial damage. Another biomarker we have had some experience with is an indicator of hemodynamic stress on the ventricles - B-type natriuretic peptide (BNP). When that goes up， it is an indication that the patient has hemodynamic stress on their ventricles. It is an important and helpful marker because patients who are dyspneic， may be short of breath as a consequence of lung problems or cardiac problems. This allows us to tell the difference. If a patient has an elevated BNP level， we can say that the patient’s dyspnea is related to the heart. At the various meetings we go to throughout the year， there is new information that becomes available concerning these biomarkers each time.

　　Antman教授：我们已经将血清生物标志物用于各种心血管疾病类型患者的诊断和评估。我个人涉及的第一种生物标志物是CKMB的替代指标即肌酸激酶肌肉-脑分数。该生物标志物是心肌特异性的肌钙蛋白。肌钙蛋白是帮助控制心肌滑动长丝（肌动蛋白和肌球蛋白）的调节装置的一部分。当冠状动脉血栓性闭塞时，心肌受损且有坏死发生，濒死的心脏细胞就释放生物标志物。心肌特异性肌钙蛋白的美妙之处在于，我们能够说这个生物标志物实际上就是来自心肌，而不是骨骼肌。其原因在于，有三种不同的肌钙蛋白 ——肌钙蛋白I、C和T。心肌和骨骼肌中，肌钙蛋白C有着相同的氨基酸结构，但心肌和骨骼肌的肌钙蛋白I和肌钙蛋白T有着不同的氨基酸结构。因此，有可能建立心脏特异性肌钙蛋白I和心脏特异性肌钙蛋白T的生物标志物测定法。现在，我们利用这些测定法可以检出即使少量的心肌坏死。这有着深远的影响。我们可以忽略将CKMB作为一种告诉我们患者是否有过心肌梗死的标志物，现在可以采用心肌特异性肌钙蛋白。用这些生物标志物，我们甚至可以检出更少量的心肌坏死，这使得我们能够改善在释放心肌特异性肌钙蛋白的患者的治疗。从这些信息中我们得知心肌损害已经发生。另一种我们已经取得一些经验的生物标志物是心室血液动力学负荷指标——B型利钠肽（BNP）。当BNP上升时，提示患者存在心室血液动力学负荷。这是一个重要且有益的标志物，因为呼吸困难的患者可能由于肺部问题或心脏问题而表现出气促。这一标志物使我们能够对此加以分辨。如果患者BNP水平升高，我们可以说，患者的呼吸困难与心脏相关。在我们全年所去的各种会议上，每次都有关于这些生物标志物的新信息出现。

　　International Circulation: As the President of the AHA， what is of particular interest for you at this ACC meeting? And what are the differences between the AHA and ACC meetings?

　　《国际循环》：作为AHA主席，您对ACC会议的哪些内容尤为感兴趣？AHA会议与ACC会议有哪些不同？

　　Dr Antman: The American Heart Association was founded in 1924 by six cardiologists who met in Chicago and decided there was so much ignorance about heart disease both in the general public and amongst health professionals. They decided to found an organization that was dedicated to promoting the health of the public and conducting research to find out how to improve the health of the public. That is what the AHA stands for. It is a mission-based organization and our goal is to build healthier lives free of heart disease and stroke. We hope by the year 2020， w  e will be able reduce cardiovascular mortality by 20% and improve overall cardiovascular health for all Americans. Our colleagues at the American College of Cardiology share the same goal as the AHA. We all want patients to do better. Their approach is to talk to members of the cardiology profession and community – physicians， physician assistants， and nurse practitioners. Together， the AHA and the ACC are covering everything we need to improve the overall state of delivery of care for patients with heart disease in the United States. My colleague， Dr Pat O’Gara， is the current President of the ACC and we both work at the same institution in Boston and we have had a wonderful time this past year travelling the world and talking about our experiences in the United States and how we can learn from you in China and exchange information on improving the care of heart patients around the world.

　　Antman教授：美国心脏协会（AHA）于1924年由6位在芝加哥相聚的心脏病学专家成立，当时无论公众还是医疗专业人员都对心脏病所知甚少。他们决定成立一个致力于促进公众健康以及开展寻求如何提高公众健康的研究的组织。这是AHA的奋斗目标。它是一个基于使命的组织，我们的目标打造没有心脏病和卒中的更为健康的生活。我们希望，截至到2020年，我们能够将心血管疾病死亡率降低20％，并改善所有美国人的整体心血管健康。我们ACC的同僚们有着与AHA同样的目标。我们都希望患者可以更好。他们的做法是与心脏病学同行及社会团体——医生、医生助理以及执业护士等进行交流。总之，AHA和ACC都涵盖了我们改善美国心脏病患者诊疗服务整体状态所需要的一切。我的同事Pat O’Gara博士是ACC的现任主席，我们在波士顿的同一个机构工作，去年我们周游世界，谈论我们美国的经验，以及我们如何从中国吸取经验教训，并在世界各地交流有关改善心脏病患者诊疗的信息。

　　International Circulation: Which of the late-breaking clinical trials presented at this conference have impressed you?

　　《国际循环》：对这次会议上公布的最新临床试验，您印象最深刻的是哪些？

　　Dr Antman: Here in San Diego， we have seen some very interesting late-breaking clinical trials being presented. Like every meeting， there is the latest information available and we rush to join these sessions. We heard two very interesting papers on Saturday. The first was looking at two different strategies for cardiac imaging to evaluate patients with chest pain and chest pain that occurred relatively recently where there was a concern on the part of the treating physician that the chest pain was related to coronary artery occlusion. The imaging strategies included CT angiography compared to functional testing such as an exercise echocardiogram or a pharmacologic stress test. They compared these two strategies using a composite endpoint (death， myocardial infarction， hospitalization for unstable angina， the need for revascularization) and it turned out that the two strategies were very similar in their ability to actually identify patients who might need a catheterization and to protect patients from the further development of those events. The CT imaging is associated with more radiation exposure compared to an exercise echo， but is associated with less radiation exposure compared to a pharmacologic stress test done with nuclear imaging. So it is a very similar result and the good news for us as clinicians and for patients， in that we have an array of different imaging modalities that we can use to evaluate patients. The second study that was presented was the PEGASUS-TIMI 54 study. This study looked at long-term treatment with dual antiplatelet therapy in patients who had a myocardial infarction one to three years earlier and who were quite stable at the time. It is stable ischemic heart disease that is being studied in PEGASUS-TIMI 54. They compared two treatment strategies – aspirin alone versus aspirin plus ticagrelor， an oral P2Y12 receptor antagonist. This dual antiplatelet regimen blocks platelet aggregation through two different molecular pathways. It turned out that giving dual antiplatelet therapy was better than aspirin alone over a follow-up period of up to three years in protecting patients against a composite endpoint of death， myocardial infarction or stroke. This comes at a cost of an increase in serious bleeding but there was no difference in intracranial bleeding or bleeding that resulted in a patient’s death. It’s a very interesting study that now adds to the body of evidence that chronic treatment with dual antiplatelet therapy is helpful in patients with stable ischemic heart disease. A lot of interesting questions arose after the study was presented and one of the most important questions is how long this therapy should be continued? Some suggest that it is so protective over the three years of follow-up of the study and because the curves began to separate and continued to separate over the course of the study， maybe dual antiplatelet therapy should be continued lifelong in patients with coronary artery disease even if they are in a stable situation.

　　Antman教授：在圣地亚哥，我们已经看到了一些令人非常感兴趣的最新临床试验汇报。跟每个会议一样，在这个环节可以了解最新的信息，很多人都急切地参与这一环节。我们在周六听到了两个令人非常感兴趣的文章。第一个是观察两种不同评估胸痛患者的心脏成像策略，对最近发生的胸痛，负责治疗的医师会担心胸痛与冠状动脉闭塞有关。成像策略包括CT血管造影和功能检测如运动超声心动图或药物负荷试验。他们采用复合终点（死亡、心肌梗死、不稳定心绞痛住院、血运重建需求）比较了这两种策略，结果发现，这两种策略在实际确定可能需要导管插入术以及保护患者免于进一步发生这些事件的能力方面非常相似。与运动超声心动图相比，CT成像有更多的辐射暴露，但其辐射暴露低于采用核成像的药物负荷试验。因此，这是一个非常相似的结果，对我们临床医生和患者而言，好消息是我们有一批可用来评估患者的不同成像方式供选择。第二项研究是PEGASUS-TIMI 54研究。这项研究探讨了在1~3年前有过心肌梗死、当时相当稳定的患者中双重抗血小板治疗的长期应用。PEGASUS-TIMI 54研究的是稳定性缺血性心脏病。他们比较了两种治疗策略—— 阿司匹林单用于阿司匹林加替格瑞洛（口服P2Y12受体拮抗剂）。这种双重抗血小板治疗方案通过两种不同的分子途径阻止血小板聚集。结果发现，长达3年的随访期间，双重抗血小板治疗在预防患者发生死亡、心肌梗死或卒中的复合终点上优于单用阿司匹林。代价是严重出血增加，但在颅内出血或导致患者死亡的出血方面无差异。这是一个令人非常感兴趣的研究，为长期双重抗血小板治疗对稳定性缺血性心脏病患者有益增加了证据。在该研究汇报之后，引发了很多有趣的问题，其中最重要的问题之一是，这种治疗应该持续多久？有些人认为，在研究的3年随访期间，它具有如此好的保护作用，且因为曲线开始分离，并在研究过程中继续分离，因此，在冠状动脉疾病患者中，或许双重抗血小板治疗应当持续终身，即使他们处于稳定状态。