We're ready for our next speaker, Dr. Xian Chen from Taipei, Taiwan. And I think everybody in this room, as is the case with Mella Scheinman, knows Dr. Xian Chen's work, and we look forward to his presentation. Today, I will talk with the title, Use of Second Average ECG in Prediction of Magnetic Cardio Recurrence after ARVC Operation. As we understand, ARVC is one type of genetically inherited disease. The cardiovascular ARVC, it is a progressive depression by the fibro-fatigue infiltration. Second one, on a clinical picture, it's a syncope, heart failure, may trigger tachydysmia and a sudden cardiac death. We may understand there are three clinical stages of ARVC. First one, it is a subclinical stage. Second one, it is an electrical stage. And the third one, it is a structural change. In my laboratory, we use the revised task force criteria of ARVC. There are a couple of criteria, major and minor, or a major plus a minor. I believe here you understand a couple of those major criteria. It is a regional right ventricular dysfunction, clearly the ECG, depilatation, depilatation, arrhythmia, biopsy, family history, and genetic testing. And today, we will have some electrocardiogram and some electrical, some second average. We focus on the depilatation and the depilatation. We understand that the pathogenesis of ARVC from the genetic testing, the very important one, you need to find a mutation or a PKP2 mutation. This is very important. You give the diagnosis of ARVC. From the second average in a patient with ARVC, I show you one case. For example, in this figure in the left panel, this patient showed a three plus second average. The QIS duration is 165 milliseconds. The duration of terminal QIS duration is 95 milliseconds. Luminal square voltage is 11 microvolts. However, for the other patients, he did not show a single average positive. The QIS duration is only 92 milliseconds. The duration of terminal QIS, it is 26 milliseconds. Luminal square, it is 51 microvolts. After that, clinical value of those single average. In prediction, VT, and the VF recurrence of the catheterization, these are the main issues we will talk in this presentation. In my hospital, we started ARVC ventritic cardiac abrasion from 2010. Total ARVC patient underwent abrasion for VT, VF. It is 93 patients in a recent eight years. We have 48 male. The average age is 46. Epicardial abrasion, we have 38 patients. It represents 40.9% of this cohort study. We know the subject of ARVC. It is different from other tracheal disease. The most significant one is the epicardial scar dominated in ARVC patients. For example, I show in the lower panel, it is extensive scar in this patient with ARVC from the epicardial service area recording. From the non-invasive study, first one, I show that interpericordial QI dispersion can predict the epicardial foresight. In panel A, it is a unipolar body map. From this patient, you see the area of the scar. In panel B, show another patient with a unipolar body map. In panel C, from here, you will see the V4 and V5, V5 and V6, or V6 and V1, you can see the QI dispersion, especially between V6 and V1. In panel D, we show another case with QI dispersion. Between V6 and V1, you will see a significant dispersion of the QI. Horizontal scar, it is very important in ARVC patients because more VT and more VF recurrence in this type of horizontal scar. We defined two types of scars. Transmural scar, it is a bipolar body map in the endocardial area. It's about the same as epicardial. In this case, endocardial, endocardial lobe region, it is 50%. In the epicardial, it is 50%, and almost at the same size. This is the first one type of the transmural scar. The second type is a horizontal scar. You will see in the endocardial recording, lobe region in the endocardial surface is 4.3%, but in the epicardial surface area, lobe region, it is 65%. In this type of the horizontal scar, in the long term, you will see the recurrence of endocardial-ventricular fibrillation. It is much significant compared to the patient with the transmural scar. How is the genetic difference and the data potential in the male and the female predict a poor outcome? You will see the male patients, they have a poor outcome of the castration, and there is a higher percentage of ventricular fibrillation recurrence compared to the female patients. No matter it is VT, VF, or the non-sustained ventricular fibrillation, also from the proportion of the data potential in the endocardial and the epicardial recording, the male, it is a poor outcome compared to the female. Therefore, you understand a lot of the invasive and non-invasive parameters can be used for the prediction of the outcome. This is our total procedure, 91 patients. After the first procedure, the recurrence state, it is 61.5%. After the second procedure, 80.2%. After the first procedure, ventricular fibrillation free rate is 19.1%. That means after the repeated procedure of castration, you can have a lot of ARVC patients with recurrence of VT, VF. So, what is the main kind of ventricular fibrillation recurrence? You will see in the second, third, fourth procedure, the scar progression, it is closely related to the ventricular tachycardia. That means ARVC, it has a natural cause of the scar progression. And we also find that the history of endurance x-ray, it is significantly predicted recurrence from the multivariate analysis. I'll show you one case. This is in the first procedure, the ventricular fibrillation trigger site and the fast VT excision site is in this area, and only this area shows a bipolar scar area. However, in the second procedure, you will see the new ventricular tachycardia isthmus and the larval potential in the larger area. In the third procedure, you will see the new VT isthmus and the larval potential shifting to the posterior and the basal area. In the first procedure, it is also in a new area. So, this scar progression is related to the new ventricular tachycardia recurrence in this patient. Now, I will give the answer to the secret energy can be applied in ARVC ventricular tachycardia. I will show you the result from my laboratory. For example, this one patient was 3+, 1+, next year single average ECG. From our analysis, we divided the patient into the single average less than 3 point higher or equal to 3 point. For the long-term follow-up, it is significantly. We also divided the single average 0, 1, 2, 3. You will see the significant difference between the four groups. That means the single average positive number can significantly predict the medical events in the ARVC patient after the cast operation. Therefore, the single average change after operation in the ARVC, what is the result? Pre-procedure single average was performed in all the VT patients. 17 ARVC patients underwent a successful VT operation in the recent five years. Post-procedure single average, no change in 31 patients. Significant change in 39 patients. Single average show you the significant progression in 11 patients. Short of the regression, 28 patients. For example, this is in the right panel, this example of single average progression without single average before the cast operation, but in this patient, even after the cast operation, single average showed a progression of change to the 2 point positive. Therefore, the single average in the ARVC in the current group one, electrical regression. Group two, no change. Group three, electrical progression. The third group with electrical progression would be a higher recurrence state after the cast operation in those ARVC patients. My take-home message, ARVC is a genetic inherited disease. It is a catalyst by the progression of fibrophytic depressment. Many predictor, including a substrate property, voltage map, non-invasive pyramid, T wave alterance, QIS dispersion, and single average, they are associated with future arrhythmia event in patient with ARVC. Patient with 3 point single average was associated with malignant event in ARVC patients. Electrical regression or single average after cast operation in ARVC was found to be associated with fewer ventricular arrhythmia recurrence. Thank you for your attention. Applause Quick question. Some of the ARVDs have LV involvement as well. Did you check for that and see if there is a single average UKG related to the LV involvement as well and sign of worse disease rather than the... And second question is, did you look at the genotypes? Like PKV, you know, which one was, you know, any association with those? Yes, very good question. Letter matrix dominates, or the letter matrix progression to the letter matrix, this is an important issue in ARVC patients. In my group, unfortunately, we only have a limited number. I remember it's only five or six patients with the letter matrix dominant. So it is difficult. We use a single average for the prediction on those patients. Second one, we have a genetic testing for those patients and the PKP, the mutation, it is represent a very high proportion in my laboratory for ARVC patients. Thank you, very nice presentation. Two questions. It wasn't clear to me whether all your patients had epi and endo VT ablations. We have 40%. That's what I thought, 40% were epi. Yes, you are necessary to use epicardial ablation. But in your data, you lumped them all together. Is that correct? In the data, looking at signal average ECG, you included those who had. Yes. But there may be a problem because we all know that the endo ablations alone are very poor. So I think you have to split out your data to better. Yes. So that's one thing. The other thing is in patients with ARVC, not infrequently you'll have right ventricular conduction delay or even frank right bundle. What did you do? How did you use the signal average in those patients? Yes. This signal average is only part of our study. We also have another paper already submitted for the review. It is we measure right ventricular conduction time, left ventricular conduction time, and my ventricular conduction time to correlate with signal average. And we find some significant correlation between our conduction time and the signal average. Thank you for that talk. I was curious about the description of the scar which you categorized as vertical versus horizontal. So when you say horizontal scar, it's basically a distribution in the inferior aspect of the RV, which is an unusual presentation for ARVC. So how confident are you, number one, that that is ARVC? Because our own experience is that this distribution of scar is atypical. But oftentimes you can get extensive epicardial scarring without much on the endocardium. So would that be also something you would call a horizontal scar? Yes, this is... In that paper we published in Europe, we have a definition of the difference between endocardia and epicardia. If the difference is higher than 50%, and the other is in a different area, and the epicardia is more predominant compared to the endocardia, we divide it into the horizontal scar. Of course, I understand it is complete identically because we cannot see the voltage between endocardia and epicardia. I just have a question for the audience. In decades past, at Cedars, you were very involved in measuring late potentials. I don't know if I can actually find our instruments and software, so I was particularly interested in your presentation. So my question to the audience is, who's doing late potentials anymore? And we should be, but who is? Right, but there's more to it than that, of course. So I got no response. I'm afraid that's what I expected.

second average ECG

ARVC operation

ventricular arrhythmias

genetic differences

poor outcomes