Thank you very, very much, Dr. Verma, for your kind invitation. I'm very, very happy to be with you and to come from Jerusalem, where I'm living now, and to present something on my 40-year journey on the topic of idiopathic ventricular fibrillation. So as I told you, I'm presently in Jerusalem, and because in Jerusalem, there was a big, big, very important king of United Monarchy of Israel and Judah. His name was King David, and King David lived here in Jerusalem about 3,000 years ago. And he composed songs, and I would like to read with you the famous Psalm 121 in the context of the territory we are all facing with the coronavirus. So I'm usually reading it in Hebrew every day. I will do, I would hope not to make big mistake reading it in English for you. I lift up my eyes to the mountains. Where does my help come from? My help comes from the Lord, the maker of heaven and earth. He will not let your foot slip. He who watches over you will not slumber. Indeed, he who watches over Israel will neither slumber nor sleep. The Lord watches over you. The Lord is your shade at your right hand. The sun will not harm you by day, nor the moon by night. The Lord will keep you from all harm. He will watch over your life. The Lord will watch over you coming and going, both now and for evermore. This was King David. Now I'm talking about the survey, what happened with IVF. First of all, I would like maybe a personal survey, and to tell the people who doesn't know that, but I was born in Tunisia, which is a marvelous country. And I was obliged to leave it in 57, to come to Paris with my family, to take my cardiology, all my academic training was in Paris. And I had fantastic chance, a privilege, to meet two people with Professor Gilbert Mottet, who was my mentor, who is one of the father of Long-Quotid Syndrome, and who gave me the love of cardiac electrophysiology and also the love of quinidine. And also Professor Philippe Comel was a very good friend. And all was, in these years, what we discovered was new in cardiac electrophysics. So I moved to Israel in 78. I started to direct the EP Lab there until I retired a few years ago, and I've been starting working with Dr. David Laurier, who is a director of the EP Lab in Hadassah University Hospital from last two years. I'm very happy. It's a fantastic department. And this is my personal story. Now, let us come back. One day, about six months after I moved in Israel, it was this afternoon, I was called to see a patient for admitting for acute MI. So I went, I saw a patient was in the emergency room, and I say the floor, the nurse, okay, we can admit him. But when I come back to go back to the CCU, I saw a tracing, an incision tracing on the floor. I take, I took it, I look to him, and I said, oh, I've never seen that. What kind of VPC you have here with a very short carpal interval? No ischemia, nothing. The KG is normal. The QT is fantastic. But what is this short? I've never seen that. I've seen that when not in normal heart, in patient who in a very few seconds will have a V ventricular fibrillation, and will have acute ischemia or acute MI. So to whom belongs this KG? So the nurse told me, I don't care, Dr. Velazquez, this is not, this is a patient who the neurologist have seen him, and he sent it home now to perform an EG ambulatory. Okay, I say, okay, no problem. Where is the patient? There is guy, I saw a patient, a 28-year-old man with his wife. He told me about three episodes of syncope during the last month associated with short-lasting convulsions. This was witnessed by his spouse. Now the convulsion and the syncope were very short-lasting and with very fast return to consciousness. The patient had no family history of semi-cardiac death. He was a heavy smoker and bronchial asthma. So I called back the nurse in the CCU. I told her we not received, admit, the patient with 70 or patient with acute MI. We are receiving in the department this 28-year-old man. A few hours later, I was called emergently because this nice guy was doing repeated ventricular fibrillation. Now, as you can see here, you have trigeminal with a very short carpal interval here of a VPC. Here you have non-sustainability and this guy developed more than 10 episodes of ventricular fibrillation which were always preceded by this kind of non-sustained VT like polymorphic VT. Most of the VF were required DC cardioversion, of course, but two of them in panel D and panel E were self-terminating about 15 seconds. You see here reorganization of the ventricular activity that most probably explains why the patient didn't die outside the hospital. He had only syncope episodes. Now, the patient's status when he was not in fibrillation, he has no CHF, normal cardiac examination, normal echocardiogram. We did emergency coronary angiogram and we see he had normal coronary arteries but hypokinesia of the left ventricular apex. I think retrospectively that this was due to the multiple shocks he had. Now, the arrhythmia control was difficult and this occurred after 48 hours following a cocktail therapy associating many, many medications, amiodarone IV prokaryotamide. What I think helped a lot in this patient was when we paste the right ventricle at a fast rate and after two days he didn't have any arrhythmic event when he was spaced during amiodarone therapy. What we did is the following. We continue amiodarone peros daily 1,200 and I did an AEP study after 10 days of this therapy. I was unable to induce any arrhythmia but don't forget that we at this time in 70 now we only have stimulation which of including only two extra stimuli. The patient was discharged on 600 milligrams per day. One month later he come back in my office to tell me that he had a recurrent syncope identical to once before and the time of first hospitalization. Oh, what happened here? I took him to a repeat EP study on April 1st and quite easily using double express stimulation with a short coupling interval 200 and 160 milligrams I induced sustained polymorphic VT ventricular fibrillation which required DC shock. Now I have a problem. What to do now? Patient has syncope. We are in 79. No defibrillator, nothing. I remember my previous mentor, my previous boss, Officer Motet loves a lot quinidine. I say why not using additional quinidine to amiodarone? Oh, all the doctors in the department say it's impossible quinidine, long QT, amiodarone. I say okay but we can start, we can see. Okay, I of course succeeded in convincing the doctors. We started quinidine bisulfate. I gave a dose of 1500 milligrams. I achieved a blood serum level of two milligrams per liter. I repeat the study on combination amiodarone and quinidine and I was enabled despite multiple, multiple, multiple repetition of double express stimulation at the shortest coupling interval which resulted in ventricular capture to induce more than these three non-sustained VT beats for the first time. So I discharged the patient on amiodarone. The treatment was perfectly tolerated clinically, only mild QT prolongation, liver and thyroid function were perfect and what's important is that the patient remained asymptomatic during 23 years. I published it for the first time in patient 81, 81 something for Dr. Verma. He told me something about 1981. I will not tell you what he said to me. So first publication and because I tried to to see what happened with quinidine in other patients during a seven-year period, I observed five patients. These five patients with apparently idiopathic ventricular fibrillation. I did an EP study. I was able to induce sustained polymorphic VTBF. I gave quinidine in four patients in one patient in all five patients impossible to induce to reinduce ventricular fibrillation. The patient were placed on chronic antiarrhythmic therapy with this medication and felt perfectly without any recurrence of arrhythmia during a mean of 52 months. What's important is the patient age 24 and the patient age 52 were respectively a woman and a man who were found to have Brugada syndrome only later after Pedro Brugada reported his service. So what happened with our patient? I remember I remind you 23 years asymptomatic. After these 23 years he had a syncopal episode which was 100% of vasovagal. I took him to the lab because I wanted really to see using much more aggressive protocol of stimulation what may happen. So I repeat now the programmed stimulation in this patient with using three extra stimuli and repetition of double and triple extra stimuli impossible to induce more than a few non-sustained VTBF. So I think we can understand that this patient, in this patient quinidine is a fantastic medication for him not only preventing spontaneous occurrence of ventricular fibrillation but also and more importantly prevented the inducibility of ventricular fibrillation at programmed ventricular stimulation. Of course I repeat I reported him again in a heart rate in 2004. What happened with him was unfortunately he had to undergo a heart right lung transplantation in 2012. This was fantastically done almost no complication of course he was treated with anti-rejection drugs and he was fine continuing quinidine only after I stopped amiodarone and of course the quinidine level were always always very well monitored. Unfortunately about six months ago following hemorrhage in the opposite lung and also limited surgical lung resection he died but of course his death was unrelated to any cardiac arrhythmia. Because we were obliged to stop quinidine while he was intubated on medical ventilation interestingly developed atrial fibrillation and shitty brain suggesting recent cardiac embolic stroke was found and it's interesting that it may be that quinidine in this patient by preventing atrial fibrillation also most probably preventing any embolic stroke. Now if I summarize our case we have a 20 year 28 year old man with storm of idiopathic ventricular fibrillation who had no arrhythmic recurrence during more than 40 years of epiguided therapy with quinidine with without amiodarone and don't forget 40 years without ICD. I told the patient I told all the doctors that if we had been the first to implant the fibrillator on his patient in 81 he would have died of complication of infection of all what you want. I'm sure that the fact that he didn't get ICD is the only reason of his 40 years life with quinidine and this is the guy Moshe in Ichilov hospital where I worked until 2015. Now is my case the first case using quinidine in patient if storm of IVF for responses no there is a fantastic when I say fantastic it's really fantastic case published in the American Heart Journal in 49. We are dealing with from Norway from Oslo we are dealing with a 38 year old man with a six month history of short lasting palpitation who was hospitalized for recurrent syncope and seizures on 6 January 1944. He had a total of 10 syncopal episode on the day of admission something very similar to our patient. Now the tracing is not of good quality I agree with you but it is a simultaneous 4-lead tracing I think from Siemens. The mingograv because because fantastic for simultaneous tracing you have here the short coupled VPC the non-sustained polymorphic VT and here you have a sustained polymorphic VT flutter what you want I think completion lasting about 80 seconds before a patient recovers. Now what is interesting in this patient is when you see the onset of the in the onset of the polymorphic VT induction you see that this kind of tracing is now well known in the EP community as a fascicular most probably perkiny potential or ectopic activity arising from the right ventricle most probably. Now what they did with this patient in 44 they gave quinidine which was the only medication gave to which was given to patient with atrial fibrillation at this time and syncopes and vertical relation were abolished using 1000 mg quinidine then only only 200 mg a day. The patient was released home on 200 three times daily one week later all treatment was discontinued because patient request but three months later due to recurrence syncope quinidine at a homeotherapic dose was renewed 100 mg daily. Please compared with the dose I have been using with my patient which was between 1000 to 1500. We are dealing here with a dose of 100 mg daily. Now what happened in the same hospital most probably two doctors who know about this doctor with a patient now reporting because his patient died but he died after 40 years he took quinidine and most probably quinidine at very small dose. Now they showed here tracing which was most probably a which underwent the photoshop photoshop photoshop photoshop photoshop and you say that the the guy we we did the figure here even forgot the one of a curious here that this is very nice tracing so they continue the medication 100 milligram but the patient died very very soon after an extensive lung carcinoma was discovered in 86 and a post-mortem examination the heart was apparently normal with proximal ad but the doctors really thought that the diagnosis the true diagnosis of this patient was a idiopathic ventricular fibrillation and I can tell you I made the calculation this guy most probably received a low dose quinidine of most probably 100 milligram daily during 42 years. Okay this is a fantastic case. Now Dr. Giulio Conte from Lugano in in Switzerland asked me to collaborate to a very important multi-center long-term registry which has been published about six months ago and in this paper which collected the 245 patients from 25 European centers I think we did a fantastic job I did a fantastic job by collecting this experience and we defined idiopathic ventricular fibrillation which everybody know it is a rare condition as a diagnosis when we exclude all the other underlying disease when you have a normal esthetic baseline and during follow-up when you have no organic heart disease demonstrated by 2DTT by coronary angiogram or CT coronary angiogram and now during I would say the last 10-20 years we need absolutely that the MRI was will be strictly normal. Of course we have to exclude the CPVT, early reproduction syndrome, Bourdain syndrome, long QT syndrome and short QT syndrome. Of course also any other cardiac respiratory metabolic and toxicological cause should be excluded. Now what we see in this kind of patient is polymorphic VTVF which occurred on the normal QT with a short coupling of the first VPCs. I think it's important when we are dealing with idiopathic ventricular fibrillation to exclude patients in whom the VF started after about of monomorphic VT. For example if you have a patient with an RVOTVT which is very fast and which degenerated into ventricular fibrillation after one two or three minutes I don't think we have to we should classify it as idiopathic ventricular fibrillation. Now VF affect both genders which is different what you see in Uganda in which more than 90% of patients are male. The age of onset in idiopathic VF is a little bit younger than in patient in Uganda. The episode of IVF frequently occurs during daily activity and not during night as usually we see in Uganda. There is no particular geographic distribution in true IVF. I'm talking about true IVF and no familial form at my knowledge. I don't know about that but we have about 10% of familial history of sudden cardiac death. We have a variable EP inducibility rate of sustained PVT VF 30% in most labs in the world and 90% in my own lab using a special protocol. I will talk about that later and let us see median arrhythmia recurrence in about 22% during a median follow-up of 64 months. I asked yesterday Julio to prepare the slide in which we have the age distribution in the IVF European survey because it was not included in the paper and I remind you 245 patients, 25 centers, 59% male, median age at first VF episode 38. Only to show you that of course as in Bugada the most important age are between 27 and 48 but you have about 6% of patients less than 16 years and quite a few really a few population of patients after 16. We have 6.6% between 60 and 70 and only 2.5% after age 70. Now what's two very important things from this survey is the fact that recurrent arrhythmic event in patient has been documented using ICD at the 22% of a patient at five years and in 33% at 10 years. It means that at 10 years about 70% of patients will not have recurrent episode of five years which is very important. Now another important thing here is the age. When you are young when you are less than 16 the rhythmic recurrence of arrhythmia which will make much more higher than if you are age more than 16. Now age is very critical and this is a big big problem when you have IVF in very young patients. Now let me give you now my point of view on the various possibility how to manage idiopathic ventricular fibrillation. Of course you have the ICD therapy. Old guidelines would talk about ICD therapy. I would try to to show you that we also can use and I used it I used it EP-guided antiarrhythmic therapy for more than 40 years. We also have a possibility of blind kidney therapy. You have seen the report of a patient of case report from Oslo and I will talk about catheter ablation. Now let us start with ICD. Of course for any doctors today in Chicago or in the world you will be told that ICD is considered to be the only proven effective treatment. I completely disagree with that but these are the guidelines. I completely disagree because ICD is expected to treat ventricular fibrillation but it doesn't prevent it. The ideal medication, the ideal treatment should be to prevent the effect and not to treat it. For example please I don't know if you know about this report this case report of a patient in Burgada who had arrhythmic stones and I find that quinidine prevented the inducibility of ventricular fibrillation. So the patient received quinidine several years until one day or somebody told him why don't you implant ICD. Okay he told me I want an ICD. Okay no problem you will get an ICD but never stop quinidine because you had arrhythmic stones and I'm sure that you will have again arrhythmic stones in the future and it's a pity because quinidine suppress prevent arrhythmic stone. He said okay okay we implant defibrillator and of course of course he stopped quinidine and about six months later he had arrhythmic stones but what happened with arrhythmic stones? After one, two, three, four, five ICD discharge, the patient still in ventricular fibrillation and only using the sixth DC shock, the patient was saved. And believe me, but he's now taking his Prenidine, he removed it and of course he has his ICD. I think his ICD is completely superfluous. Complication of ICD, I don't have to tell you how many complications we observed, especially taking into account that you will implant ICD in a young patient, age 20 or 25 or 30, we should theoretically die at age 85, this patient, any patient who will receive an ICD for adiopathic VA for Bugada will have 60 years of implant and of course of complication, extraction, infection, dislodgement, psycho-critical disorder, because nobody even told this patient that maybe there is another solution, maybe you have Quinidine, maybe you have test Quinidine with EPI study as somebody from Israel pretend that it may be the solution. Now, the big problem with ICD and IVF are the pediatric group because the high incidence of ICD related complication, and it is very important to try to avoid ICD until the child grows sufficiently, this is important in this kind of patient to eat Quinidine if possible. And also the elderly group, because it's very rare to have the first IVF after age 70 years. And also because the arrhythmic risk recurrence decreases with age. So nobody addresses the question, what should be the age limit at which ICD will not be replaced? Don't you think that this may result in some medical legal problem, if we say to your patient who is now age 75, that okay, he did his first IVF when he was 30 years, but now he's 75, maybe you're not obliged to replace it, especially that he get a lot of complication. Of course, the patient will agree, but if, for example, he died of any other reason, okay, non-arrhythmic reason, after six months, what will happen? I'm sure that his son will say, oh, he was so fine. My father was so fine with his ICD, but some doctor didn't want to replace it, okay? And I think the suite will only a matter of time. Now, as I told you, I love, I think, EP-guided therapy with Clonidine is a fantastic option, but we need some requirements. We need that the VF will be inducible at baseline EPS. We need that the patient will accept, will even prefer enterythmic medication over ICD. We need that the medication will be tolerated. We also, that the patient will show an excellent drug compliance. We need that the patient will have a good psychological profile, not to stop medication after six months. And also, we need to check that EPS will show after five, 10 years, that the ventricular fibrillation of drug is not inducible more. Now, for that, have been used, what I call an aggressive protocol of programmatic ventricular stimulation. This protocol is usually the standard one, okay, that you are all using, but if this protocol is negative, what I'm doing is to repeat it using stimulus current of five gastric threshold, but always less than three milliampere. I do not limit copying interval. It's very important for this patient to give extra stimulus copying interval as short as possible. And also very important, if you want to induce VF in this patient, to repeat extra stimulation at the shortest copying interval associated with ventricular capture. And I usually do it 10 times for double extra stimulation and five times for triple extra stimulation, of course, for the RVA, for RVOT, at the cycle of 600. So I only prolonged by no more than 10 minutes, the protocol, but I increased dramatically my chance to have a positive inducible electrophysiologic study. When I reported my results on IVF and some patient got it was in 99, I can tell you that the follow-up, I had inducible VF in 80% of this patient and the patient using quinidine was no longer inducible in 96%, almost 100% of patient. I'm also using high doses. I'm not using one milligram because I think it's very important if you decide not to implant an ICD, to have a patient non-inducible with quinidine. So I'm sure that a patient with 100 milligrams of quinidine, of course, will be inducible. So the dose are not the same. The dose we stops, we prevent an arrhythmia clinically and the dose we prevent the induction of an arrhythmia is completely different. And also very important, I talk to you about that to repeat, to test the reproducibility of electrophysiologic efficacy of quinidine. I will show you a fantastic case in 97, 57 year woman who had a lot of syncope episodes, which were related to non-sustained and even sustained polymorphic VT with short coupling interval, normal heart. I did a baseline electrophysiologic study. I was able to induce sustained polymorphic VT-VF with three extra stimuli from the apex. And I gave during the same session IV prokaryotamide that was enabled to induce sustained polymorphic VT. This is an excellent sign. When you use low dose of prokaryotamide, 500 milligrams is very low dose. And we are enabled to induce VF. This will be a good, good indication that you will be very effective also with quinidine. And exactly what happened after giving quinidine orally, you see that I'm enabled with using even four extra stimulation, not two, not three, not five, four, what you want. Impossible to induce, to reproduce the induction of VF with quinidine. But about 10 years later, where quinidine was not available in our country. So I have to take the silico from Sanofi from France. So I repeated the study using the new salt of quinidine, salt of quinidine, which is an hydrochloric salt instead of a bisulfate, what I was using previously. And you see again, using the apex repetition, what you want, impossible to induce, nothing more than a single VPP. The patient died of unrelated cardiac arrhythmia about 28 years later, about last year. Now, what is my experience with quinidine? 40 year experience, drug discontinuation about 30%. Never QT prolongation requiring drug discontinuation, never. When you have a normal ECG, no familial history of low QT syndrome, the probability of patient would develop low QT problem associating with another point and VF is zero. The side effects are transient, always resolving after drug discontinuation and no long-term circular. The limitation of quinidine therapy, of course, are the drug-related side effects. The late drug intolerance with refusal for getting ICD, this is a problem. A patient told you that, okay, he's agreed to take medication. After two years, he stopped medication. He doesn't want ICD and you cannot, you know, it's difficult to convince now, he doesn't want ICD. But if I had implanted ICD before 40, would be much more better. But now I have a problem with a patient who doesn't want ICD, maybe danger. And also another limitation is very late for patient compliance. A patient took medication five years. He said, I'm okay with medication now. I want to try to stop. This is a big problem. I have to recognize this is a big problem. This is a real problem because I'm selecting the patient. Psychological profile here is very, very, very important. Now, thank you, Sami Viskin, for telling us that coronary virus has been in red, but also in red are, I'm joking here. In red are all the countries in which quinidine is not available. So this is another big, big problem. Now, blind quinidine therapy. I show you the case from Oslo. This is a possibility. I think a doctor today should tell his patient there is a case in the literature in Oslo described, published, and okay, that there is a possibility. I will give you quinidine, two tablets. You may die at age 90 from something else than recurrent idiopathic metamorphosis. I think we should be honest and we should tell that to our patient. And Dr. Basil Redesky, who died only a few months ago, wrote in chest, in a paper entitled Quinidine as an Antirhythmic. He wrote, be not the first on whom the new are tried, but not the last to lay the old aside. Now, management of idiopathic fibrillation also include catheter ablation. And this is mainly due to a final work of the genius. I call him the genius. Dr. Michele Sager from Bordeaux, my good friend. And this is based mainly on the important role of the Purkinje system as the predominant source of triggers for the nation of idiopathic metamorphic fibrillation. And now everybody knows who working in this field, but there are three zones of predilection of triggers of VPC. The first is on the right ventricular Purkinje, you see here, right ventricular Purkinje. The second is the left ventricular Purkinje. It may be the, let us see, the left posterior fascicle or the left anterior fascicle. Okay, excuse me, left anterior fascicle. Both are here, are located here. Also the F is the papillary muscle also may be involved. Myocardium, much more rarer. And of course, the RVOT and the LVOT. But I would say that 70% of the cases came from a Purkinje system on the right apical site and the left side of left posterior fascicle of left anterior fascicle. This is very important. I will show some case. And this is the demonstrative curious morphology of this VPC for RVOT, this is well known for RV Purkinje. And for the LV Purkinje, you see, you have a lot of VPBs with the right from the branch block pattern with various axis. You have here the Bellasend curious morphology. Okay, it's okay to give Bellasend RVBB left anterior. It's okay. I do agree with this classification, but you also have the RVBB right axis and many intermediate morphology between both. Now, Michele Sager reported on the very nice Purkinje electrogram recorded here in a patient and here in the left ventricular Purkinje, look to that and look to this one. Thank you, Michele Sager. Now, I would like to conclude. I know we have additional time, maybe, maybe, because I have here a case, fantastic case, because it had been done one in February and the other one a few days ago. And this case has been performed in Adassa when I'm working, but I was at home when it was done. This is terrible for me, terrible. So I didn't attend the case. The first tabulation was done by Dr. Bitton and Dr. Elitzur in February of this year, two months ago. And the second case was made by Professor David Luyer and also Dr. Bitton a few days ago. Now, we are dealing with a young 14-year-old boy without any family history and apparently no obvious channelopathy. This patient at age six years old underwent ASD surgery and he developed later some kind of bradycardia, bradytachycardia and tachycardia bradytachycardia with a lot of episode of atrial fibrillation. CRTD was implanted after he already had also a ventricular retina. So this is a guy who had CRTD. He had apparently normal RV and apparently normal LV and a lot, a lot of episodes, short, longer episode, many shocks of VTVF. Most of VT are polymorphic and this VF are refractory to high dose of colidin. I'm very surprised, but I also seen a Bugada patient, a young patient who was refractory to quinidine and who had been obliged to make epicardial ablation. But this patient also, maybe the age plays a big factor also in quinidine inefficacy. So he received a lot of medication, all is ineffective. He was even placed in high priority in the list for heart transplant. So this guy should have undergone heart transplant three months ago, but he was referred to Dr. David Luria from ablation, maybe ablation. And in February, you see that this patient had this biventricular pacing and a lot of monomorphic here, looks monomorphic ventricular tachycardia triggered by this kind of VPC. This kind of VPC has an right for the branch block pattern and apparently right axis deviation. Now the patient arrives in the hospital and almost no sustained or even short lasting polymorphic VT, only a few VPBs, which apparently were clinical. What do at the same time, it was during the night, Dr. Bitto and Dr. Elitsu, they tried to make base mapping of these VPBs and they obtained a good base mapping, a fantastic base making, I think 89% correlation with the spontaneous VPBs at an area that the thing is the anterior lateral, not far from the left anterior fascicle. And interestingly, during the ablation pulse, they obtained some ventricular activity. The ventricular activity obtained during the pulse was almost identical to the spontaneous recorded VPCs. So I think they did a fantastic job and really all the episode disappeared. We are happy that the two months, three months, the patient had no other episode. But what happened after two months against ICD storms, that of course ventricular fibrillation, but if you look very, very closely now, you see something that I think fantastic. You have a whole terminatory of 12 lead. This 12 lead shows that you have pacing here, pacing here. I think this complex here is a spontaneous complex of aberration bead, because you have sometime rapid atrophy relation. This may be also a fusion bead. Personally, I think this is an aberrant bead because here I think is the initiation of a ventricular fibrillation here with a complex, which has a very short carbon interval, but has a right bundle branch block pattern. You see the RSO prime here on V1, but here you have a left axis. And presently in two months ago, we had the right axis. So we are dealing with some different focus. And now Dr. David Luria takes the patient as emergency case also, and also find and ablate several areas in the areas of left posterior fascicle. After he recorded some fascicle here at the very close to the left posterior fascicle, which was preceded by 24 millisecond, the onset of a curious complex of a first initiating bead of a ventricular fibrillation. I'm personally surprised, I told it yesterday when the case was presented, that the coupling interval here was long. Personally, I believe there is something else in other location, which is blocked. It means we are not here at the best location of the initiation. Maybe we have something here with a peculiar potential, which is blocked, but in another area. I don't. So of course, I didn't tell you the end. The patient had abolition of his ventricular fibrillation, has been doing very well, and had been released with VCRTD, and no arrhythmias. Really, congratulations to all the staff of ADASA. Now, I think I will stop here, and maybe we can discuss, if you want me to show you a fantastic case of a woman who had Bourgada syndrome and diagnosed as idiopathic ventricular fibrillation, and was inducible with one single ventricular extracystal, I will do it. It was in 87. Now, excuse me. Yes, 85, but first of all, maybe you have some important question, and I'm ready for the question. Thank you, Professor Belhazen. There are a couple of questions that have come through. You said you were going to go against the grain and guidelines, and we got a sense of that with your thoughts on ICD. There was a question about your thoughts on subcutaneous ICD versus transvenous ICD. Do you have any thoughts on that? I think in ADASA, and also in NIHILO, where I was working, we don't have a lot of experience with subcutaneous. I don't know. I cannot comment on something where I have no personal experience. I saw in the literature, but maybe some problems with, I cannot connect. I prefer not comment the field which I'm not, you know, fluent of it. So- If you give an ICD, you routinely give quinidine? What does it mean routinely? If a patient receives an ICD, is your antiarrhythmic drug of choice for a patient with the ICD to get quinidine? I think it's a good question. I think if a patient, we have two kinds of patients, which is the same with Bugada and with idiopathic VF. If a patient has arrhythmic strokes, now I'm trying to be a US doctor here, okay? I'm a US doctor. Of course, I will implant an ICD and so on. Okay. So if a patient has arrhythmic stroke of idiopathic ventricular fibrillation or Bugada, and of course we implant an ICD, I will absolutely give additionally quinidine. Absolutely. If not, I have to explain to the patient that he may have arrhythmic stroke. So if you want to be in danger of arrhythmic stroke, this is his problem. But I think it's important the patient will be discharged on quinidine. Sometimes small dose. I'm not talking here of giving 1,500 milligram. He has an ICD. So I think sometimes one tablet to two tablets a day of quinidine, which are perfectly tolerated, will be effective. Now, if a patient has an ICD implanted, but only a single episode of ventricular fibrillation, of course, I will not give quinidine. Of course, quinidine is reserved only for those patients who will accept not to get an ICD and will be agree to make EP studies and so on, as I told the EP guy to repeat quinidine. Okay, only this kind of patient will receive quinidine at usually much more larger dose than 100 or 300 milligram. Yes. And then the other drugs that you use in those countries where you can't use- Okay, this is important. You know, in countries where quinidine is not available, I'm not sure that disoperamide is available, okay? I think disoperamide should not be available. So I think here's the problem. The problem is if the patient receive quinidine, he's very happy with quinidine, but he develops side effects due to quinidine, but he doesn't want an ICD. What to do? Very simple. I think we can try the second class 1A agent that can be tried here is disoperamide. Disoperamide, unfortunately or fortunately, I have experienced only in three patients, it works exactly as quinidine works. Exactly as quinidine works. The only problem is in male patient, prostatic problems, you know, only problem, but no problem usually observing in females. So I think should be an excellent medication. Now, I will not give disoperamide without doing repeat EPS, okay? So I will do EP guide therapy with disoperamide. I will never give a medication without ICD if I'm not sure that the medication will not be effective in the cardiac lab in preventing ventricular fibrillation. I saw another question, is it sending genetic testing on any of these patients? First of all, I want to tell you the truth. We have been exposed to genetic testing only during the last year. So I will see my 90% of my patients in Ichilov has no genetic testing. According to genetic testing, I think there is a very nice paper, I think it came from Canada. And in Canada, they discovered, I don't think Canada or think maybe from Holland, excuse me, I think from Holland, in which they showed that a small proportion of patients in whom a diagnosis of ventricular fibrillation was done, IVF was done, were in fact genetic disorders and so on. So I personally completely agree today, genetic testing should be a part of that. It's not a matter, I think you have excellent genetics testing with $300 or $400 or $500. I think it's nothing today. So it's not a problem. I strongly in favor of doing genetics testing to any patient who had ventricular fibrillation and apparently normal heart. Now, other questions? Yeah, there were a couple on whether you're doing serial EP testing at various doses of quinidine. Fantastic question. Because my experience on the field, for example, when I was using bisulfate quinidine, I know that when I tested first 1,000 quinidine, I was a little bit disappointed and I have to move to 1,500. So what I was used to do is first to try the maximal, not maximal, the tolerated dose of quinidine the patient may suffer, okay? And usually with 1,500, which was fine. And I'm doing the study. Now, if some patient would develop some inconvenience with drug, of course I will propose them to repeat the study using 1,000 milligram. And I found this 1,000 milligram was effective, okay? But usually I prefer to start with a maximal tolerated dose and decrease it and not to do the inverse. Because if a low dose is negative, you know, it's not effective, I have to repeat the study, it's a problem. I prefer to make only one drug study and not two.

IVF

quinidine

accurate diagnosis

antiarrhythmic therapy

programmed ventricular stimulation

ICD therapy

subcutaneous ICDs

catheter ablation

genetic testing