International Circulation: Your investigative efforts have been to understand the relationship between the electrical activation of the heart during atrial fibrillation and the specific gross and microstructures of the left atrium. How do we get a better understanding of these relationships developed in recent years as a physician? Are there any new conceptsto report in this area?

　　《国际循环》：您在理解心房颤动时电激活与左房特定gross及微观结构之间的关系方面开展了很多研究。作为一名临床医生，根据近年来该领域的发展，我们应如何更好地理解上述关系？在该领域有何新概念？

　　Dr Packer: Over the last three or four years， there has been a lot of progress made in understanding the pathophysiology of atrial fibrillation and the role of fibrosis and scarring. There have been new ways developed to identify the mechanisms which is interesting because we went for ten or fifteen years without a lot of progress， but now that we know more about the features we do today， we have a much greater chance of dealing with atrial fibrillation. Let me give a couple of examples. We have a much better understanding of why， when fibrosis occurs， it becomes problematic. It may be an important contributor to the occurrence of atrial fibrillation. Once we knew more about the pathology and pathophysiology， we found that electrical activity actually hinges on that fibrosis. If there is a fibrotic area， the edges of that fibrosis are a nice locale for triggers and rotors. So we don’t only have fibrosis， but we have the mechanism for the electrical part of the arrhythmia. There are several groups working on this concept of rotors. It used to be that we only talked about triggers that start the atrial fibrillation， but now we have the understanding that there are more important (perhaps) activities that occur in these rotors that move around and behave like they have singularity points. This was an idea that Jose Jalife has worked on for years， and now we find these features occur in patients with atrial fibrillation also. So there is an electrical mechanism and you have fibrotic scarring. Some of the work that has been done actually puts those two together so we understand it better now than we did before. We need more work to understand better if the relationship is as good as we think it is. If you look at atrial fibrillation in terms of the way we have being ablating it by isolating pulmonary veins， this suggests there are other factors that will call for linear ablation. The trigger starts or drives the problem. Then there is the perpetuator which keeps it going， the rotor. Then there is the fragmentation of electrical activity， the CAFE activity. This progresses to fibrillatory conduction where there is the maximum amount of disintegration of the normal circuitry and chaotic activity. All of these things we have learned over the past two or three years in terms of the relationships between them. So it is not just a matter of ablating the trigger， it requires understanding of the whole mechanism revolving around the fibrosis.

　　Packer教授：过去3~4年，我们在理解心房颤动的病理生理学、纤维化及瘢痕在心房颤动发病中的作用方面取得了很多进展。虽然我们已经有10或15年时间在该领域没有取得很多进展，但现在我们已经有了识别上述有趣机制的新方法，已经能够更好地了解心房颤动的特征，有更大的机会来治疗心房颤动。我们已经能够更好地理解心脏纤维化可能是导致心房颤动发生的重要因素。一旦对病理学及病理生理学有了更多了解，我们就会发现，电活动实际上在很大程度上受到纤维化的影响。如果心脏中存在纤维化区域，纤维化区域的边缘就成为导致心房颤动的触发器。因此，患者实际上不仅存在纤维化，还存在导致心律失常的电生理机制。有几个研究小组就转子理念进行了研究。过去我们只是讨论和关注能够启动心房颤动的触发器和转子，而现在我们则知道这些转子可以移动，在心房颤动的发病中具有更重要的作用。Jose Jalife等在转子理论方面开展了多年的工作，现在我们已经发现心房颤动患者中确实存在上述特征。因此，若患者存在心脏纤维化瘢痕，则就存在发生心房颤动的电生理机制。有些工作实际上将心脏纤维化与心房颤动更紧密地结合在了一起，因此，与过去相比我们现在对其有了更好的理解。如果纤维化与心房颤动的关系正如我们所认为的那样，我们则需要开展更多的工作去更好地理解。众所周知，通过隔离肺静脉可对其进行消融来治疗心房颤动。这提示心房颤动的发病还存在其他机制或因素，需要进行线性消融。在触发器发挥启动作用后，转子将持续保持其作用，引发碎裂电活动。这将最终导致颤动传导，心房正常电路大量碎裂并出现混乱电活动。在过去2~3年间，我们对电激活与心房微观结构的关系有着上述了解。从现有发现来看，心房颤动的治疗不仅需要对触发器进行消融，还需要对纤维化相关的整个机制有更好的理解。

　　International Circulation: Are there any new developments related to guided ablative therapies for serious ventricular arrhythmias?

　　《国际循环》：严重室性心律失常的消融治疗有何新进展？

　　Dr Packer: Ventricular arrhythmias have been more difficult but we do understand them better than we did. The important issue with ventricular arrhythmias is understanding that most of them are related to underlying anatomy. Whether you are looking at an RV tachycardia， a tachycardia from the aortic cusps， a tachycardia from the pulmonary vessels or a tachycardia coming from the papillary muscle， we understand the mechanisms better. A lot of this depends on our understanding of imaging and being able to identify a particular structure and thus be better able to deal with that structure and the electrical activity that comes from it.  So imaging capabilities are new and important.

　　Packer教授：室性心律失常的治疗比较困难，但是我们确实要比之前要做的更好一些了。就室性心律失常而言，最重要的就是要知道大多数室性心律失常都存在潜在的解剖学基础。就右心室心动过速、起源于主动脉尖部的心动过速、其余肺血管的心动过速以及起源于乳头肌的心动过速而言，我们对其发生机制更了解。对室性心律失常发生机制的了解在很大程度上取决于我们对心脏影像的了解以及识别特定结构的能力。只有做到这些才能更好地针对相应的结构及其所引发的电活动进行处理。因此成像方面的研究是严重室性心律失常消融治疗的新内容、也是非常重要的内容。

　　International Circulation: Would you give us a brief introduction to the latest developments in atrial fibrillation treatment in recent years?

　　《国际循环》：能够请您给我们简要介绍一下近年来心房颤动治疗领域的最新进展？

　　Dr Packer: Part of that is our better understanding of the things that create atrial fibrillation including hypertension， sleep apnea， obesity， stress and other factors. We also have a better understanding of where it resides. We have known about pulmonary veins and their involvement in atrial fibrillation for a while， but we now know that you can have drivers and rotors outside of the pulmonary veins if there is scarring alongside the vein. So it starts with an initiating trigger that develops into a rotor and then to something more chaotic and fractionated with fibrillatory conduction. It is not a perfect understanding but it gives us a better idea because it gives us a sense of where it is coming from. We ablate by targeting the focus. One of the complications of course is pulmonary vein stenosis due to heat injury to the vein setting off an inflammatory cascade， which includes fibroblast migration， which leads to scarring. We avoid that by keeping a safe distance from the pulmonary veins and by being aware of the heat generation that is used.

　　Packer教授：就进展而言，其中之一就是我们对高血压、睡眠呼吸暂停、肥胖、应激及其他因素导致心房颤动有了更好的了解。此外，我们对心房颤动源于何处也有了更好的了解。既往我们知道肺静脉参与心房颤动的发生，现在我们进一步知晓“若肺静脉周围存在疤痕，则肺静脉周边存在可促进心房颤动发生的驱动因素及转子”。因此，触发器会启动转子，进而引发更多混乱和颤动传导。虽然这并非是对心房颤动相关机制的最完美理解，但却让我们对其有了更好的理解，让我们知道心房颤动发生的源头。这样一来，我们就可以针对相关焦点进行消融。消融治疗的并发症之一是静脉热损伤可导致炎症级联反应，促进成纤维细胞迁移进而导致疤痕形成最终造成肺静脉狭窄。在行环肺静脉消融治疗时我们需要意识到消融治疗时会产生热量，与肺静脉保持一定的安全距离。

　　International Circulation: Five years from now， what do you think will be involved in the management of non-valvular atrial fibrillation?

　　《国际循环》：未来五年，您认为有哪些内容将被纳入至非瓣膜性心房颤动的管理中来？

　　Dr Packer: There are a couple of things I see coming in the next three or four years building on what we are already doing now. We will build on the concept of triggers and rotors and fractionated activity. We will do a better job of preventing atrial fibrillation in the first place by treating sleep apnea better， monitoring hypertension and so on. Then there will be new energy forms in the treatment of atrial fibrillation. For example， CRAB balloons have improved. They are larger and place better. The energy is directed more towards the tissue than out into the left atrium. I think laser balloons will be helpful. One of the things we are working on in the research lab is carbon particles or hadron therapy. We take a carbon atom and accelerate it via an accelerator to about the speed of light which then goes through the chest wall and ablates cardiac tissue without the need for catheters. So in that five-year time frame， particularly for ventricular tachycardia， we will be using that kind of energy therapy to do these procedures a lot less invasively. If we can deliver carbon atoms straight through the skin then that could be tremendously important because the risk may be substantially less. So new energy forms， preventing atrial fibrillation in the first place and a better understanding of the mechanisms of atrial fibrillation provide a bright future for the management of atrial fibrillation in that five-year time frame. I think we will be doing a lot more， a lot more effectively， with a lot less risk.

　　Packer教授：根据我们现在正在开展的相关工作，我认为未来3~4年内将有很多内容被纳入至非瓣膜性心房颤动的管理中来。我们将创建触发器、转子及碎裂电活动的概念，能够通过治疗呼吸睡眠暂停、更好地进行血压监测等措施更好地开展心房颤动的一级预防，心房颤动的治疗也将有更多的能量形式可供选择。例如，CRAB球囊已经得到了改善与提高，变得更大、更好放置。消融能量更具有组织针对性，而非直接伸入左心房。我认为，激光球囊非常有助于实现这一点。目前我们正在实验室中开展有关碳粒子或质子治疗的研究，应用一个碳原子并通过加速器使其加速至接近光速水平然后穿透胸壁从而在不需要导管的情况下实现对心脏组织的消融。因此，在未来5年中，我们将能够应用这种能量治疗相对更无创地开展上述消融治疗，尤其是在预防室性心动过速方面。如果我们能够直接让碳原子穿透皮肤，则能显著降低消融治疗风险，因此对治疗而言具有极其重要的意义。新的能量形式、做好心房颤动的一级预防、更好地理解心房颤动的发病机制均有助于我们在未来5年内更好地实现对心房颤动的管理。我认为，我们将能更多、更有效地做好心房颤动的管理，并降低其风险。