Jason Bradfield, MD, discusses ventricular tachycardia and catheter ablation.
Thank you all for being here and thank you to the organizers for having me. My topic for today is to trick your tech cardia catheter ablation. Who when and how my name is Jason Bradfield from U. C. L. A cardiac arrhythmia center. Have no disclosures. So we're gonna talk a little bit today about VT ablation. I realize this is a mixed audience of folks interested in cardiology. Not necessarily all electro physiologists. We'll talk about who we oblate both idiopathic and empathic patients and those with cardiomyopathy when we intervene. Generally, this is when meds fail or not desired by the patient and we'll talk a little bit about the techniques we use, which varies depending on the substrate idiopathic PVCS or BT occur in patients with structurally normal hearts. We treat them predominantly for one of two reasons, either symptoms or a high burden of PVCS that leads to a risk of PVC induced cardiomyopathy. Typically in the 15 to 20% or more range on a 24 hour. Holter monitor any empathic PVCS and VT typically are focal and origin as opposed to structural VTS which are more typically reentry in origin in terms of their mechanism. So when we're doing an ablation for a patient with idiopathic PVcs, we're typically looking for electrical signals that are early relative to the beat that we're mapping. So we use electron atomic maps to localize the earliest sign of activation. So the earlier earlier you are with these local signals on the ablation catheter or on a mapping. Catheter. The more likely you are in the site of origin. And then we can use both the three D. Map and flores coptic images as shown here. And this is the ablation catheter in the right ventricular outflow track to map and oblate those vocal arrhythmias. We can also use pace mapping where we pace at the site of early activation and see if that matches the clinical PBC. So this is pacing and this is the clinical PVC and they're very similar to suggest we're in the right place. Idiopathic arrhythmias tend to cluster in certain regions of the heart. We typically think of the right ventricular outflow tract is the most common side of origin. Some of that may be an over representation of early studies that were successfully a bladed in the R. V. O. T. P. V. C. S in reality can come from a variety of different regions but they tend to cluster in what we call the superior subtle process and the inferior septal process that includes areas like the R. V. O. T. The aortic root, the LV summit and that are kind of different regions within what we would call the superior septal process. And then the inferior process process includes things like the cardiac crux often involving the venous system in other areas when you're mapping idiopathic ventricular arrhythmias. The key is really to be comprehensive and your mapping and not assume that you're always going to be coming from one place. These are very highly related and closely related anatomical regions in this image. You see an aortic root shot with a simultaneously with an R. V. O. T. Angiogram. And you can see how anatomically close these regions are with a coronary sinus and A I. V. Catheter as well as his catheter and RV catheter by mapping comprehensively in a number of different regions we can hone in on the area of the earliest activation. A lot of these arrhythmias come from the left side of the heart. It probably more than was originally thought. This is an example of a map of the aortic root as you see here. And these are the coronary cusp in the L. B. Body or risk optically superimposed is an eric route shot onto that map again with the coronary sinus catheter in place. And by mapping retrograde through the aorta, we can put a catheter into the coronary cusp of late successfully. Many arrhythmias that come from this region anatomically, as I mentioned, the arctic route as shown here and the post here right ventricular outflow tract are highly related and only separated by a very small wall thin wall. And so sometimes people think that something's coming from the RV. O. T. But in reality it may be coming from their root coronary cusp region because they're so anatomically close and you can see that from this pathologic specimen coronary customs are here. Our bot is here in this thin walled structure of P. V. C. Or V. T. Could be coming from anywhere on either side of this and what you label it as really depends on where you were successful at blading it and sometimes the PVCS can exit on different sides of this wall. So in this case this PVC was a bladed successfully in the R. V. O. T. And a similar but slightly different PVC a bladed across that wall in the coronary cusp. We're learning a lot about idiopathic PVcs and that there are some circadian or diurnal variations that occur in this patient population. And this helps us understand which patients are likely to respond to certain medications like beta blockers but also helps us understand when we're doing a PVC or Bt ablation and empathic patient. What drugs will likely help us bring out those extra beats. Because in this patient population it is often true that the PVCS are hard to elicit and bring out and we use medications like ice april to bring those PVcs out for sufficient mapping. Knowing their diurnal variation helps us determine which drugs will be successful. And that's something that we published a while back moving towards structural meaty again, typically occurring in patients with underlying karma empathy. The mechanism is re entrant because of scars as shown in this MRI you get areas of slow conduction through the scar which allow for re entrance circuits to occur. All Vts and structural heart disease have some form of substrate. Whether that's systemic heart disease or infiltrated disease or some other substrate. But they also often have triggers whether that's changes in autonomic tone related to their karma apathy. Whether it's some stimulant or drug, whether it's an electrolyte abnormality that combined with the substrate to cause VT and sometimes VF. And in the worst case scenario said cardiac death when it comes to ablation of structural heart disease, we know that it works. The international matricular cardio ablation center collaborative group which we run out of U. C. L. A. Showed in retrospective data. Multi center international data that the success rate at one year. VT freedom was approximately 70% in all comers. That includes a skeptic and non ischemic retinopathy. What we also know from numerous studies is that patients need to be referred earlier in their disease course to have the best chance of success if we wait too long. Their crime apathy may progress to the point that ablation may be less likely to be successful. So referring when they have their first event as opposed to when they've had recurrent admissions for VT storm is in the patient's best interest additionally adding more than one anti arrhythmic drug rarely is beneficial. And ablation has been shown to be superior to adding a second drug as in the banished trial ablation doesn't work as well for non ischemic as it does for ischemic patients. And there's high variability in the success rate for non ischemic patients. But the way we like to look at non ischemic cardiomyopathy is there are certain patient populations within the non ischemic cohort that do very well with ablation, RBC and sharks disease. Or two of those. They have success rates that are very similar to patient population with ischemic heart disease. There are some patients that have less predictable substrates but still highly beneficial results from ablation such as myocarditis. It's chronic sarcoidosis without inflammation, et cetera. There are others that are even more challenging, like hypertrophic cardiomyopathy, amyloid heart or if there's active inflammation of any kind. Those patients have a much lower success rate in each of these patient populations. To be taken into consideration as you're determining the best treatment course and likelihood of success and the non ischemic patient population. Epic cardio mapping where we stick a needle in like a parakeet synthesis but without any fluid around the heart and put catheters into the pericardial space. And you can see the needle down here tempting of the pericardium here with a little bit of contrast and the wire going in and around the heart safely to allow for catheter manipulation in the pericardial space. We determine in a lot of these patients what the best treatment modality is or mapping technique is based on preoperative imaging. So M. R. I. Is done frequently at our institution looking for the scar that is associated with the patients VT if they have septal scar. As shown here. Perhaps epic are real mapping wouldn't be a benefit because the epic cardio surface is not an issue. It's the septal surface. If we're seeing trans mural or epic cardio or mid myocardial scar then having both endo karniol inside of the heart mapping and epic are ideal outside of the heart mapping can be beneficial in terms of treatment outcomes. But again, knowing the substrate matters because the central substrates wouldn't be benefited. Likewise, sometimes patients can even have scars on their popular muscles which is an inter caboto restructure. And again, knowing where you're going in terms of your mapping strategy is highly important. So imaging it plays a key role. We've done a lot of work with pet scans. So in the non ischemic patient population, understanding if patients have an inflammatory cardiomyopathy and if that inflammatory cardiomyopathy is active. So if there's active inflammation on a pet scan, patients do very poorly with ablation and they should be treated with anti inflammatory drugs and then considered for ablation. If they have matricula arrhythmias despite control of the active inflammation inflammation on an electron atomic map during VT mapping and ablation looks very much like scar and therefore differentiating your target becomes very challenging and information cannot be easily a bladed. In our experience we find about a 25% hit rate in the non ischemic population for active inflammation for patients presenting with V. T. V. T. Or B. T. Storm. And we find that by treating that inflammation, those patients do approximately as well as someone without inflammation treated with ablation. So we can avoid ablation in some patients simply by treating the active inflammation. When we do map any of these patients, the techniques involved looking for these areas of slow conduction that I mentioned and we do that by looking at the local electro graham signals. So we make scar maps as shown on the top right here, grading scarf purple, being normal tissue. And we make functional maps which are maps that look at slow areas of slow conduction. So we can assign a color to timeframe of activation and see that when we see bunching of colors that shows areas of slowing of conduction and that suggests areas of functional delay that may lead to re entering arrhythmias. This is an epic arial maps a scar map again grading scar probably being normal. And so these maps can be made on either surface and this is an example of a functional map where we see this bunching of colors and the target is where these colors come together because that's where the areas of slow conduction reside. This is an example of a scar map with activation where you can see the activation into that scar and then the activation into the area of slow conduction. We use newer technology has very high density multi polar mapping which can be very advantageous for quickly obtaining thousands of points on an activation map and decreasing the duration of the procedure for patients that are often very sick. And in this case you see the grid map of the grid catheter here on that Bacardi um and we can quickly map this VT. And we're seeing what we call diastolic potentials, which is slow conduction between the QRS complexes that suggest the area of the isthmus of the VT or the critical region. That needs to be a bladed for control of the ventricular. With me by using this newer technology, we can, in addition to making our scar map here of an inferior basal inferior scar. BTS induced. We see the late potentials that I mentioned that that suggests areas of slow conduction in sinus rhythm that then translate to potentially areas of critical slow conduction during VT. The mid diastolic potentials. Most BTS are not well tolerated for patients with cardiomyopathy because there have low ejection fractions that are quite sick. And so by using all that data that is showing the scar maps the functional maps. Even though we can't map up the entire circuit of the BT because the patient becomes hypertensive, we can get a quick activation map in the critical area and we can see the conduction coming through this little isthmus here and that allows us to target the appropriate area without keeping the patient in VT for very long so that they don't decompensate ablation in that region of the scar and the critical isthmus makes the patient non irreducible and it's a good end point for VT ablation. Now there is a lot of art to the that goes with the science of VT ablation. Many things can't be completely studied in large numbers due to the you know how sick these patients are. So we will often map patients in VT if they can tolerate it. But that often may depend on the injection fraction. Well others we will just look at the substrate in the functional maps. Some patients need human every support meaning balloon pumps and paella even ECMO to allow for mapping. There's no strict cut off for that. A lot of it depends on understanding how sick the individual patient is. Um But every patient is different. Um And so experience plays a big role in understanding which patients need that extra support form a safety standpoint because in the long run their goal is to get these patients through these procedures safely. Here's one more example of an interesting case where a number of decisions had to be made. There were somewhat atypical an older patient for our patient population thought to be needing hospice by referring doctors. His family insisted to be transferred to our institution had been incessant, slow tolerated VT for months, suggestion fraction had dropped substantially. He came in in two B. T. N. D. T. To the cath lab had been in Bt so long that he developed left appendage clots and so we went retrograde for activation instead transept and you see the catholic coming through his bio prosthetic aortic developed here. We found mid diastolic potentials on the anterior wall and terminated the VT with the initial abrasions in this area. Here on the anterior wall had an extensive scar on the mid typical part of his ventricle. We consolidated the ablation in the region of the termination. We did not try to re induce the V. T. To the clots and the risk of needing to shock the patient in the risk of stroke related to those clots and the patient did fantastic. His he was without Bt for many years in just a fraction improved and he did it very well. In some patients with VF we can do ablation typically that's for patients that have a triggered PVC, a consistent PVC that can be reproduced. That then leads to VF because BF itself can't typically be mapped. But if you can find the triggering PVC, you can often control of VF by targeting that PVC in rare instances were also considering more of a de bulking of the Perkin Gee system. This is very early data looking at the fact that the Perkins, the system in some patients is hyperactive and reentry within this system can lead to VF and so oftentimes in small numbers. Again this early data, potentially we can control the arrhythmias by de bulking the distal Birkin gee system. It often involves patients that have some scarring in the area at the base of the popular muscles where the break in the system lives. Hybrid surgical ablation is something that we do a lot of work in for patients that need that have had previous cardiac surgery. They often will need ablation using surgical techniques where the surgeon will open up access with the economy or subsidize avoid window. In this case the patient had a double mechanical valve. The access is shown here, the beating heart. That's the l the impacts that you're seeing there. We can make activation maps and see diastolic potentials in the operating room. In this case, the VT was mapped and you can start to see the circuit here. Here's the VT and we use cryo ablation and you'll see VT terminate as you go along here on the first cry a lesion. This is the cryo pro and that we often use freezes to the surface of the my accordion. And it's very effective informing leach notes. We can do these procedures on pump Western economy, but we prefer not to. It's only rare instances that we do that when no other options are available. We are looking at understanding lesion technology and how we can best deliver deep lesions for these patients while protecting the coronary arteries. One last note sP R. T. Or radiation for VT is an area of interest for a number of centers looking at external beam treatment finding ways to make VT treatment noninvasive still in the early stages but a number of promising reports in this area. We still have a lot to learn, however, about how to optimize these lesions sets and how to deliver effective non invasive lesions over the next few years will get a lot more data in that area. In conclusion, VT ablation works. Comprehensive planning, however, is essential for the best outcomes. Ablation should be considered earlier in the treatment of patients before the african storm or long term side effects from anti arrhythmic drugs. Again, thank you to the organizers for having me and thank you to my team at UCLA.
