Dept. of Cardiac Radiology
AIIMS , Delhi
Sr.Consultant & Head Dept. of Nuclear Medicine
Seven Hills Hospital, Mumbai
President, Cardiological Society of India
</b> Dear Friends, we just had a very, very important information about the imaging and I have two more personalities again from the same field of imaging how we can enhance the potential of imaging has to be very well understood. I have with me Prof. Dr. Priya Jagia, professor of imaging from All India Institute of Medical Sciences, New Delhi and I have with me Prof. G. N. Mahapatra who is a great nuclear imaging personality from Mumbai. We will have some discussion in reference to the cardiology. Dr. Priya, my first question to you is, we see so many patients coming to us with the coronary artery disease. They have underlying viable or nonviable myocardium. At times, it is very difficult. We do a lot of dobutamine test with a low dose and high dose and see what is the ischemic response but with a low dose we can find out the viability of response. We would like to ask you if you were to choose one technology of the two, what is your preference, if there is a preference of CT, why CT? Why not echo?
</b> For the viability imaging, I think MRI is the investigation of choice. It is the investigation of choice for evaluation of ventricular viability. After you have done echo you have seen dyskinetic segment or you have seen akinesia and you want to assess for viability I think I ideally go for MR viability. Viability actually means to see whether the tissue is viable that is whether it can be revived or not. It is a tissue which has undergone some damage, but whether it is reversible or not. So when you are seeing some abnormality in the regional wall motion abnormality in the echo, you are not sure whether you want to revascularize the vessel, whether the ventricular wall will bounce back, whether it will recover or not, so viability is the testing which we do on MRI to see whether after revascularization there will be an improvement in the function or not, so, that we do after giving the contrast and we see after sometime how the ventricle, how the contrast remains. We can tell how much is the degree of fibrosis. If there is a lot of fibrosis, if say, see the entire thickness of the ventricular wall is fibrosed then we say the viability is almost nil. But if the thickness involving of the fibrosed myocardium is say 50% or 25% then there are more chances that this tissue will you know bounce back after revascularization and we say yes there is a viability there.
</b> Dr. Priya, I think that is very important information you are giving. There are number of times a patient comes to us walking in the clinic and we really have to assess the viability. MRI may be a good modality. But in Intensive Care Unit, when a patient comes in emergency, they are in a state of cardiogenic shock or they are in a multisystem involvement, to assess viability it is very difficult. The reason is patient needs to go to an MRI center. So, I feel the mobile echo is more superior there.
</b> Definitely, we cannot replace echo. Echo is something which is available all the time. It is available in most of the hospitals. Cardiologists are familiar with it though it is an operator dependent modality but you are very, very familiar with it, so your screening has to be always with echo and then only when you think that this patient can undergo MRI, then only you can send the patient for an MRI.
</b> So, I think Dr. Priya has given a very clearcut answer that so far as the Intensive Care is concerned or in emergency when the patient comes and you really want to know about the viability, echo is definitely superior, but the otherwise when the patient comes in the clinic I think the right way is to send the victim to the MRI. That will give you a better idea and give you a better information.
</b> CT can also be used for viability purposes, but then the amount of radiation involved you give contrast twice over for the coronary also and also for the viability, so MRI is the investigation of choice.
</b> I think the MR is going to be superior. I think both the ladies are talking of MRI, the future is going to be MRI. That is what I feel and I really love MRI more than the CT because of its positive potentials as compared to CT. We see a lot of hypertrophic cardiomyopathy these days and even those who are not cardiomyopathy but they are hypertrophic because of hypertension. Do you think MR is again the better modality.
</b> Yes, yes definitely, not only for diagnosing the hypertrophic cardiomyopathy, but for you know having a baseline reference because, all said and done, echo is an operator dependent. Today you are measuring it at some point, next day you are measuring it at some other point. So, if you want a reference point for the myocardial thickness then MR is the way to go. It can also help you prognosticate the treatment. You can see the amount of thickness even after you have done alcohol ablation. You can see how the patient has responded. You can again measure the wall thickness. So MR is advisable not only for the diagnosis, for prognostication, for followup after the ablation and also for followup over the year how the patient has faired.
</b> I think that Dr. Priya has mentioned a very important point that the MR modality is a very important modality not only for diagnosis of hypertrophic cardiomyopathy, but also seeing the therapeutic response. If the patient has undergone radiofrequency ablation or alcohol ablation or even after myomectomy, if you really want to see the regrowth of the septal growth or prognostically is there worsening or there is an improvement , I think that can be easily assessed by MRI. Though, as an echo cardiologist, I also believe that the echo is also a very important modality for hypertrophic cardiomyopathy, because we see the important ingredients in the form of systolic anterior motion or the mitral valve apparatus as well as we find the asymmetry of the interventricular septum and we can see the hemodynamics better, like we see the mid cavitary obstruction or we see even the LVOT obstruction and we can easily asses the reduction of the LVOT gradient as well as the mid cavity gradient which really helps us in deciding which patient has to undergo what device or which patient does not need a device.
</b> So, let me tell you, the systolic anterior motion of the mitral valve, the LVOT gradient can all be measured on the MR. See MR is all the more important for the cardiac diseases because it has got a very high temporal resolution.
</b> Will you see the mid systolic closure of the aortic valve.
</b> Yes, yes that also we can see. We can measure the gradient across if you have a mid cavity obstruction. Yeah, MR is taking. See it is not the goal standard as yet. I would say, you know the measurement of gradients and all, but yes we can give you an idea about how much obstruction.
</b> I find only the potential of echo is it can be done within 2 minutes.
</b> Sir, MRI can never replace echo. Echo is something which is so easily available, when I talk about MR we are trained people. It is not easy to do cardiac MR, needs personnel who are specifically trained for cardiac MR, cannot be done by each and every person.
</b> So I think it is very important if we can do an MRI right at the emergency, right in the OPD, and I just take 2 minutes to find out how much is the gradient and I can see the concentric LV or asymmetrical hypertrophy of the LV. I feel very, very satisfied in my approach, but I am sure sometime when I have difficulty I refer my patient to Dr. Priya or Mona Bhatia to help me, so that I can delineate the information required in the reference to the therapeutic intervention and prognostic in reference to the device they use, because we find so much of significant gradient from one portion to another. If a guy is lying down his gradient is very different, guy sits his gradient is different. When he walks on his feet there is tachycardia, there is increased sympathetic activity and we find a very significant gradient. Even we see post ventricular ectopic, just one ectopic can usually increase the gradient and patient may collapse. So I think sudden cardiac death can be prevented to a very large extent if we use a multimodality. I think there should not be a conflict, no fight between the echo and the MRI.
</b> No, these are complementary.
</b> It is a complementary and multi-modality approach is the answer. Thank you very much Dr. Priya for your insight to the hypertrophic cardiomyopathy. I have with me Prof. G. N. Mahapatra and I know him for the last so many years now. He is coming regularly for this conference. Dr. Mahapatra why you choose to come in a conference like this with a lot of spirituality and science. You are not a spiritual guy. You are clearly dealing with the nuclear imaging. Do you think there is some mingling of spirituality with the nuclear imaging?
</b> Thank you very much for inviting me to this conference Dr. Chopra. I just want to tell you that nuclear imaging as such also yogic exercise, meditation and other things, it can monitor how much the effect after the yogic exercise, after the meditation and after the righteous changes. So, Then after a certain time, you can repeat and see the improvement that is a thing.
</b> Dr. Mahapatra, what I am asking is when you talk of spiritually and tries to work on the spirit. When you talk of spirit is a consciousness based and every consciousness control the protons and the neutrons and electrons. So, you see the movement of atoms by nuclear cardiology or nuclear medicine or like molecular level. What level do you work?
</b> No, we do not see proton, neutron or electron. We see the injected radiotracer. The radiotracer emits Gamma rays and Gamma rays are picked up by our scanner like Gamma camera or scanner and then it formulates the image. So, we do not see any electron or proton.
</b> In other words, what I am trying to ask you is what you see is just a cellular insult but what is causing the cellular insult is not known because cellular insult is ultimately caused at the level of the quantum or at the level of what you call is disorderliness of the protons, neutrons and electrons. When there is a disorderliness, then only cellular damage takes place. So, it is quite late at that time when we are doing it and I think we may have some information but if we have something before that that may really help like molecular biology or we talk of an atomic biology then we understand, PET scan for example. When the patient in clinical practice we see at the cellular level, cellular integrity and lot of new molecules have come and already it has come and giving more and more informations at the cellular level.
</b> I talked with Jagat Narula who is an imaging guy from US. In fact, he presented a data in our CSI conference on so called energy imaging. I personally feel energy imaging is at that level much beyond the atoms and much beyond the molecules. We talk of energy. Energy, I am sure we all know it. It is basically at the level of the protonic energy or electronic energy and if we are able to control at that level it is very, very good. What do you think the role of PET scan in today’s armamentarium so far as the cardiac physiology or cardiac pathology is concerned. PET scan.
</b> Yeah, definitely the PET scan tells about the metabolism of the cells or tissue at a particular level when there is an ischemic insult or previous myocardiac infarction, we can detect at a cellular level the metabolism. Metabolism is done by the PET scan.
</b> Does the metabolism really change with the medications or with interventions.
</b> Yes, definitely. So, if there is a metabolism persist, for example we do a as I showed you today in my presentation we do two-phase study at same-day protocol. First we do a resting perfusion scan, find out the area of the muscles not getting blood supply and then in the afternoon we do a PET imaging using a affetimal every thing and then it shows metabolism or it still persist. It is called mismatch. Perfusion absent and metabolism present that is called hibernating myocardium or ischemic myocardium. If it is a matched defect, perfusion absent and metabolism absent, it is called a matched defect for scar tissue.
</b> Dr. Mahapatra, I just want to ask you a very important state forward question. We see a lot of pulmonary embolisms and just now you heard a speaker. He said it is a ventilation perfusion scan but CT is also very-very good as compared to a nuclear scan. What is your view on this?
</b> We have been doing regularly at Seven Hills Hospital where I am heading the department. We do clear-cut perfusion and ventilations. So, the indications are where CT angio is without differential diagnosis of lower segmental region or where CT cannot diagnose. So we do the first perfusion, see a perfusion defect and if interesting in that area at that is called perfusion, there is a mismatch. So we can detect that and end a trouble. So, I was asking that how soon you can repeat after detecting a lesion give thrombolytic therapy and what is the minimum time required. So as long as we have done so many cases as early as three weeks after the thrombolytic therapy then you can detect and see the beautiful come back of the perfusion effect.
</b> Unbiased, what is your recommendation when a patient has got pulmonary embolism. What will be your first preference? CT or a nuclear scan?
</b> In my opinion, if the facilities are available, nuclear perfusion scan is available then I would definitely go for perfusion can. Just give an injection and see that whether the perfusion is normal. If the perfusion is normal, then I do not think there is any embolism and again there are two types of perfusion mainly which we do is called Plaint perfusion and the SPECT perfusion. So, we rotate that and see the slices in coronal, sagittal and transverse, which improves the detection of the perfusion abnormality.
</b> Thank you very much Dr. Mahapatra. I think you have brought a very important point that we can see the pulmonary embolism and perfusion deficit not only by one technology but we can see by two technologies and we can easily see with a great deal of confidence if there is a pulmonary perfusion deficit or if there is no deficit. I think both the speakers have done a wonderful job and I am sure this would create a huge impact in understanding the cellular 07