Episode 44: Describing in Detail the Myocardial Bridge Provocative Test Procedure with UPMC’s Dr. Jeffrey Fowler.

SPEAKER_01 0:00

So I think it's really important for a patient who's struggling with chest pain and may be told you don't have blockages, and so your chest pain is likely not your heart. Maybe that isn't sufficient enough. That until they maybe interact with a center of excellence that has some specialty in evaluating for other causes of these chest pain, you don't know for sure that it's not cardiac. And there's a lot of patients who would benefit from this testing and some treatment to try to help relieve this chest pain and improve their outcomes as well.

SPEAKER_00 1:04

It's my intention for this content to inform, educate, entertain, and even motivate or inspire you in your personal journey on dealing with a myocardial bridge. Most importantly is to have you leave each episode with hope, knowing you're not alone and that what you're experiencing is real. In this part two of a three-part series in the steps of David Vollmer's journey, we'll meet his interventional cardiologist, Dr. Jeffrey Fowler. I want to be very certain to mention that this is an episode for patients and doctors as well. Dr. Fowler will be discussing the process and the necessity for the provocative test to help alleviate the uncertainty of whether or not the bridge is causing symptoms. This episode has been the missing link to completing an entire journey from diagnosis to proper testing to surgery. And now with Dr. Fowler's generous support, we're going to learn the details of this provocative testing we've been hearing so much about. But first, let me introduce our guest. Dr. Fowler is an interventional cardiologist and is board certified in general cardiovascular disease and interventional cardiology by the American Board of Internal Medicine. His medical degree is from Lake Erie College of Osteopathic Medicine, and he completed his residency at Cleveland Clinic. He is currently program director for the Interventional Structural Cardiology Fellowship Program at University of Pittsburgh Medical Center Heart and Vascular Institute, and Assistant Professor of Medicine at the University of Pittsburgh. He holds other board certifications, professional memberships, has been published, speaks professionally, and is involved in ongoing research projects. It's our privilege to speak with him. Dr. Jeffrey Fowler, welcome to Imperfect Heart.

SPEAKER_01 2:55

Thank you for having me.

SPEAKER_00 2:57

As I've shared with you several times, I can't tell you how excited I am to be able to speak with you. We've covered just about every aspect of the unroofing procedure. We've had multiple doctors. We've even had a thoracic surgeon and explain the step-by-step details of astronomy. But we've been missing that one huge step that determines the severity and the details of the bridge, the symptomatic elements. It's the provocative test. We hear about it, we talk about it. A lot of people have explained it as it was for them. But many people just know the words. They don't really know what takes place or how it's done. So we're really going to benefit a lot of listeners, and I suspect a lot of doctors as well. When we finally get to this first hand understanding, as you're going to explain it of the significance of this testing. But before we get there, could you tell us what exactly is an interventional cardiologist?

SPEAKER_01 3:51

Yeah, sure. You know, so thanks again for having me on this podcast. I do think it's really important to sort of understand the significance of an intramyocardial bridge. To answer your question about interventional cardiology, there are multiple different subspecialties within cardiology. Most people think you just go to a general cardiologist, but within cardiology, we have imaging specialists that focus on particular aspects of the cardiac imaging modalities we use. We have electrical cardiologists that focus on the different rhythm challenges and procedures related to that. And an interventional cardiologist is a cardiologist that had additional training in minimally invasive catheter-based procedures. Most of your audience is probably familiar with a stent that's placed in the coronary artery in the setting of, say, a heart attack or chest pain that somebody may have. That's done by an interventional cardiologist. These minimally invasive procedures are done with catheters placed in either arteries or veins using small wires, small balloons, small stents. We also do diagnostic procedures where we use certain medications and different tools to evaluate the pressure and flow in the coronary arteries, which becomes particularly important in an intramyocardial bridge.

SPEAKER_00 5:03

On the stent, everybody knows you do not stent a bridge for reasons of compression and everything. So I want to make sure it's clear, even though the interventional cardiologist does the stent, it does not mean you're getting a stent if you're working with an interventional cardiologist. It's really all part of the process done properly, in my opinion. They know that the discovery, many of our listeners know that the discovery of the myocardial bridge is uh best done non-evasively through a CT angiogram. And with contrast, of course. Since that's the first step, I'm sure you also review the CT to confirm the nature of the bridge before you suggest moving on to the provocative test. Could you tell us what's important to ask when getting that CT angiogram and just give us an overview of it when somebody's starting their journey on diagnosis?

SPEAKER_01 5:58

Yeah, so a coronary CTA is an important non-invasive anatomical assessment of the coronary arteries. So a lot of these patients may not even know they have a myocardial bridge. They present typically with chest pain. And so part of the evaluation of chest pain includes usually starting with non-invasive testing to assess their chest pain. Those can be either anatomical tests like a coronary CTA, where we actually look at the blood vessels and we're looking for things like atherosclerotic or cholesterol plaques, we're looking at the origin and course of the coronary artery, we're looking for abnormalities in the coronary artery like a myocardial bridge. But other patients may get non-invasive testing like stress tests, which look at functional assessment of the coronary arteries. If a patient has a myocardial bridge either diagnosed on a cath originally, or there's some concern for it, and we order a C coronary CTA for that specific reason, what we want to do is we want to make sure that we're fully evaluating that myocardial bridge. So coronary CTA is a special type of CAT scan that does give contrast. It's a gated CT scan, which means that it is timed with the cardiac cycle. Coronary arteries fill in diastole or the resting phase of the heart. And so we want a high-resolution scan that can split off sort of the systolic phase and the diastolic phase of the heart so we can look at when the coronary arteries fill. The whole cardiac cycle is also helpful on a coronary CTA because the imager can look at that whole cardiac cycle and look at both systole when there's often compression with a myocardial bridge, and then diastole and make a comment about the systolic compression that occurs in a coronary CTA. The other aspects of a bridge that we're looking at are the length of the bridge, the depth of muscle that's overlying the artery. So there's a lot of important aspects of a coronary CTA that can help to identify the bridge and important parts of the bridge.

SPEAKER_00 7:58

Oftentimes, too, we know that there could be as many as one in four people with a myocardial bridge. Obviously, not 25% of the population is symptomatic. Somebody presents with chest pain that doesn't seem appropriate for their particular health, lifestyle, etc. Why would a cardiologist not start with this to rule out a bridge immediately?

SPEAKER_01 8:25

Well, as you mentioned, there are a lot of patients that have bridges that are asymptomatic. And when we're evaluating chest pain, a myocardial bridge is not the most common cause of a chest pain syndrome. And so most cardiologists are dealing with patients who have some characteristic of their chest pain that is considered sort of classic for blockages, which may be an exertional chest pain. They may have other risk factors for atherosclerosis like high blood pressure and high cholesterol, and their age plays a role. And so the atherosclerotic plaques or blockages are the most common cause of chest pain. And so most cardiologists do start with either a functional assessment, such as a stress test, to look for the blood flow in the heart arteries as a first step. And then oftentimes, if there's some concern on that, they'll move on to an anatomical assessment with either a coronary CTA or potentially if they're moving directly to a heart catheterization. So while a lot of your audience, you know, is particularly attuned to a myocardial bridge as one of the causes for chest pain. From my practice, that is not the most common cause of chest pain that I see on a day-to-day basis or in most patients.

SPEAKER_00 9:36

And that makes sense. One thing we see often, let's say you go to the hospital where you're presenting with chest pain, you're concerned. Quite often they'll do an angiogram right away. Prior to the CT, why would they do the invasive first versus the CT first?

SPEAKER_01 9:54

Yeah, so it really depends on how the patient presents, what their symptoms are, how convinced you are that there is some abnormality that may need an intervention. If they're having ongoing damage or a heart attack that's going on, moving directly to an invasive study is the appropriate next step. A coronary CTA does have its limitations. We we talked about some of the strengths of what it can identify in the bridge. But as cholesterol plaques calcify in the arteries, that calcification sometimes makes it very difficult to know what's on the outside of the vessel versus what's actually encroaching on the lumen and decreasing blood flow to the heart muscle. We get some some of the calcium just obscures the view of the vessel. So there's a lot of reasons why uh invasive cath may be the first step. And someone, it really depends on their symptoms, their presentation, our concern level, those type of things.

SPEAKER_00 10:46

Yeah, and and that makes sense too. Because if you're in the hospital and you are presenting with a heart attack, you've got elevated troponin levels. I can I can appreciate now then why you might go to that extreme first. So now the patient is fortunate or unfortunate enough to have been diagnosed. We we know you're symptomatic, we know something's going on, you've got your CT. It then progresses to that next step for those hospital systems and cardiologists that are looking to want to understand what's happening a little bit more in detail. So now they're going to say, okay, that's provocative test. And I know even in my case and in many situations from people that we hear, that provocative test is not the first line of thought in many cardiologists' minds simply because their system may not do it, they may not be that familiar with it. And we were at wit's end on our end, cardiologists, the electrophysiologists, everybody that was working on my case said we have no idea. We don't know what to do with you. Yeah. There is one more test because I had severe endothelial dysfunction, and so I had vasospasms. I said, we don't know why that's happening. There's no dysfunctioned arteries, everything looks great. Maybe you just need to get this test, and there's a handful of places that you can get it done. So I was fortunate to be able to be referred to Stanford.

unknown 12:06

Yeah.

SPEAKER_00 12:06

Myocardial bridge never even entered into the equation still, even though somewhere in there we find that they did recognize it. Nobody told me about it.

SPEAKER_01 12:14

Yeah.

SPEAKER_00 12:15

And then, of course, the provocative was a completely different beast once we were done. So you see the CT, the CT demonstrates that there's some something there, that it's a myocardial bridge. Now they're referred to you in the system. What's going to happen next? How do you prepare the patient for what's going on and what you're going to be able to identify through this provocative test?

SPEAKER_01 12:37

Yeah. I mean, if I take a step back even, you know, in that scenario, it is not uncommon once a myocardial bridge is identified, say on a coronary CTA, and you have some amount of symptoms associated with it, to do an empiric trial of medications. And some of that's a risk-benefit, you know, sort of analysis. When we talk about doing a provocative test, we're talking about moving on to an invasive procedure with manipulation of certain medications to change the dynamics in the heart to make a diagnosis. However, there's some amount of risk with that as well. And so a lot of patients respond very well to an empiric treatment of medications that can help to reduce their symptoms. I think it's becomes when we're really unsure what's going on and they're either not responding to an empiric treatment of medication, or in the case we're thinking we're going to talk about a little later today, there are some patients who are very adamantly against taking medications without having an established diagnosis that we move on to an invasive test that can help to establish a diagnosis. And so when that's the case, we move on then to the heart catheterization. And when we do this heart catheterization, most of the times at this point we know that atherosclerosis is not the driving concern here. We've seen on the coronary CTA, they have no coronary calcium. There is no atherosclerotic burden. And we're really looking to identify the other causes of chest pain that are often overlooked or sometimes not even assessed for because, as you mentioned, certain systems don't have the ability to do that, or or maybe even some of the understanding of how to get that accomplished. So when I bring someone in for that type of provocative testing or physiologic testing, I usually prepare them by first describing what's going to happen. So I bring them into the cath lab the day of the procedure, and we talk about what's going to happen during their heart catheterization. So I will enter the artery either in their wrist and the radial artery or in their groin and the femoral artery. And we talk about we bring them into the cath lab, we we sterilize and place sterile dressings down in them. I give them some light sedation to help to relieve some pain and anxiety, but they're still going to be, for the most part, awake. We want them breathing on their own. We want to be able to talk to them if we need to. We'll provide numbing medication over the site that we're going to be entering, and we enter that artery, like I said, either in the wrist or the groin. We then put catheters up into the arteries and we take pictures with contrast dye of the arteries. After we take those initial set of pictures, then we start to work through an algorithm where we assess the different causes of chest pain. So one of those causes you mentioned may be endothelial dysfunction or vasospasm. We will do a full assessment of the microvasculature of the heart and understand if there's any dysfunction there. And then if there is a concern for a bridge, and we'll go on and do physiologic testing and perhaps even intravascular imaging of the bridge as well.

SPEAKER_00 15:36

You mentioned we're awake, which I recall vividly. And for anybody that's thinking this is a painful procedure, you really don't feel much. You have us pretty well sedated and comfortable, but I will suggest it is a bizarre procedure when we are actually talking to you as you're in our hearts doing things and we recognize things happening. And yeah, then the next part of that is you use a chemical that's from what I understand, not so easy to get hold of, acetylcholine. But it's a chemical that's found naturally in our system, it controls muscle contraction. Right. And by inserting that into the artery itself, how it responds is what dictates the severity of dysfunction, correct?

SPEAKER_01 16:22

Yeah, so for vasoreactivity or looking for vasospasm in an artery, we'll start with the acetylcholine provocative test. This is specifically looking for endothelial dysfunction and vasospasm. And you're right, that while this is a naturally occurring substance in the body, getting it in a pharmaceutical form that we can then deliver into the coronary is a little bit challenging. It actually is a formulation derived from eye drops, acetylcholine eye drops that the pharmacy helps to create a stock solution of that's been diluted down that we can use to inject into the coronary artery. And acetylcholine works on the inner lining or the endothelium of the artery. And in a normal endothelium, there's a chemical process that occurs that when in response to acetylcholine that releases nitric oxide, which dilates the artery. However, in a dysfunctional artery, we often see we don't have that nitric oxide response. Instead, we have a smooth muscle contraction response, which also occurs with acetylcholine, and we get a vasospastic response. And so if somebody has a normal intact endothelium with no propensity towards vasospasm, the escalating doses of acetylcholine that I introduced in the coronary artery will cause no change to the caliber of the coronary artery. But if there is either endothelial dysfunction or significant vasospasm with even some of the lower doses of acetylcholine release, we immediately see that artery clamped down and the blood flow reduced to the heart muscle. And often that's associated with symptoms, chest pain. I see EKG changes on the monitor that I'm monitoring with. So it's it often can be quite dramatic.

SPEAKER_00 17:59

I can attest to the drama of that because as it was being injected, under sedation and pain relief, it got to the point where I was like, that's the symptom. And that is it's really severe. And I recognize it right now. And immediately the anecdote was inserted, which I'll let you explain as well for somebody who's fearing this testing. Well, boy, if the thing starts to clamp down, what do you do to fix it once you've stuck the stuff in there?

SPEAKER_01 18:25

Yeah, luckily we do have the ability to reverse the acetylcholine with nitroglycerin. So we then inject a good dose of nitroglycerin into the artery, which will then vasodilate the artery and relieve the symptoms and the changes that we see. And so while we're doing this, there's very close monitoring of the heart rhythm on the EKG, their chest pain symptoms, the hemodynamics, meaning their blood pressure, as well as the angiogram that's looking at the response that the artery is having. And we have the ability very quickly to reverse any spasm that may be occurring. So once the diagnosis is made, we don't just let the patient sit there with the spasm and the pain. We immediately reverse it, dilate the artery, symptoms resolve, and we now have a diagnosis or at least part of a diagnosis there.

SPEAKER_00 19:09

Yeah, and that's the beauty of being communicative when you're on the table. It's like, uh yeah, this is hurting. This is the pain, this is what a sensation is, and you've been able to create it and then and then negate it.

SPEAKER_01 19:19

And some of that, those concerns get addressed ahead of time too. When I when I do a procedure like this, I try to go step by step with the patient before the procedure, but what medications I'm going to be using, what the responses that we may anticipate with these medications, and how we'll handle those to try to just way some of that anxiety as well. That these are controlled settings. We're we're doing this in a very stepwise fashion, and we have the ability to you know to take care of what happens in there.

SPEAKER_00 19:46

And to emphasize the use of the chemical, the proper use of the chemical, the understanding, the skill set on how to relieve the symptom, all of this is this is a trained skill. This isn't something somebody's going to come into and start just attempting to do on their own in a system that thinks they can do a provocative test. It's it's it's quite a sophisticated procedure. Yeah. And in a myocardial bridge situation, you may or may not have an endothelial dysfunction. So you may find people who you do this test and everything works fine, even though they are having a symptomatic bridge, correct?

SPEAKER_01 20:21

Right. So vasospasm or endothelial dysfunction does run hand in hand with bridges that we often see them together. But when we are assessing for the physiologic significance of a coronary bridge, what we're really looking to see is how impactful is the systolic compression of that muscle in the artery, especially as you elevate your heart rate into what it would be in an exertion. And so that's yet another part of the test. So we may start with the acetylcholine provocative test to assess the endothelium to see if there's also spasm as part of the problem that's going on. But then we also will move on in a bridge and do special physiologic testing with yet another medication called debutamine. So debutamine is an inotropic medication that works on the betareceptors of the heart to speed up the heart rate and increase the force of contraction. And by giving escalating doses of debutamine, I can drive a patient's heart rate up into a range that they would see when they're saying exercising. And in fact, in order to get a diagnostic test, my goal is to reach 85% of their peak predicted maximal heart rate. And so if I can hit that heart rate goal and they don't have a drop in their blood flow, then that bridge is really not physiologically significant for them. But if at any point prior to hitting that 85% goal, we see a significant drop in the blood flow from that bridge, then we know that systolic compression, the decrease in the diastolic filling time or the relaxation filling time of the vessel is causing a decrease in blood flow to the heart artery. That's a significant bridge.

SPEAKER_00 22:01

And I'll share again in that process and the procedure as the devitamine is being entered. It's almost as if the interventional cardiologist is speaking to you as if you are the recipient of a gas pedal. And okay, we're going to accelerate your heart. You're going to feel this is going to feel a little bit awkward. It's one of the most bizarre sensations to be laying still and have your heart racing as if you were running up a hill. And just feel the sensation of the movement upward in terms of the heart rate to the point where you know it breaches its its desired beats per minute. And then you start to back it off again just as if you were stepping on the brakes. Right. Again, for the for the people who are listening and about to undergo a provocative test, it's all intentional, it's understood, and you're in great hands. It's just going to feel very, very strange as you go through the process.

SPEAKER_01 22:54

Yeah, it's it's a bizarre feeling to feel like you're exercising while you're laying flat on your back on the table.

SPEAKER_00 23:00

There's some people who would like that and think, hey, can I lose weight by I'm lending you? Can I find a way to do this? Yeah. Why do you think there's only a handful of healthcare systems that do this provocative testing? Or do you see now more and more acceptance of learning and using the testing?

SPEAKER_01 23:17

Yeah, I mean, I would say there's definitely more and more acceptance and learning and a growth in the field here of assessing for different types of chest pain other than atherosclerotic plaques. So in that, I know your your audience is probably familiar with the term ANOCA or anginoa without obstructive corneal artery disease. And there are there is definitely a growth in this field. However, it is still, for the most part, organized into what I would call centers of excellence. So these tests are highly specialized tests. They require some specific equipment and software and the pressure wires or flow wires we're using to assess the blood flow in the heart arteries. It also takes time and specialized medications and specialized observation of the patient, ability to reverse what's going on. And so, as you can imagine, you want those expertise to be centralized in areas that do these frequently, that see these patients on a regular basis and are comfortable with these things. So while there is definitely growth in this field, and I think that there will continue to be growth in this field and it will become a little bit more ubiquitous. There are still, you know, centers of excellence that will likely carry the bulk of the volume and be driving the this field.

SPEAKER_00 24:29

And I also want to applaud you. You mentioned Inoka, and I know during the process of David Vollmer's testing, you actually reached out or or had communicated with Dr. Shaw, who is doing the the Yale study, who has been one of our guests. And I just think this the collaboration and the understanding of trying to get some best practices for these procedures for all of us who have the condition, we just can't do enough of that. And if I'm not mistaken, you actually communicate with Dr. Tremel of Stanford as well, correct?

SPEAKER_01 25:00

Yeah, I haven't I haven't actually spoken with her directly, but we have reached out to her, and she will be coming to Pittsburgh to UPMC to be giving one of our cardiology grand rounds. And I have a dinner meeting with her the night before. So I'm I am looking forward to to picking her brain even more directly during that meeting. But Dr. Shaw and I, you know, are close and we we communicate through phone call and text, and he certainly is one of the leaders in this field, along with Dr. Tremel as well. But they have helped to grow the knowledge in this field, both in some of the research they're doing, some of the protocols they're developing. And so, as we are developing our own practice, it's not uncommon for me to reach out to Dr. Shaw or Dr. Trummel or some of the others in this field and say, hey, I got a really interesting case. Here's how I was going to tackle it. How would you tackle it? In in David's case, which you know we're going to talk about a little bit, I was actually going to do some of the bridge testing first and then finish with the provocative testing. And Dr. Shaw made a comment that he likes to do the acetylcholine provocative testing first before the wire is introduced, because the wire itself can cause some vasoconstriction. I thought that was a wonderful recommendation. And so I think right before we started the procedure, I may have mentioned to David that I was going to change the order up a little bit from my discussion with him in the pre-octave period. And I don't think he was thrilled by that, but I think he understood the rationale for it as well and trusted us to move forward with it.

SPEAKER_00 26:29

And by now, I'm hoping most people have heard David's episode of his journey. He is quite the research-oriented individual with a very strong opinion on how he wants it to get done. And he was one of those characters that would have said, no, I don't want the medication, just skip the medication part of it. I'm happy, I'm I'm authorizing you to go ahead and do the provocative test on me and let's figure out what's going on. I actually think that's a a good point to discuss the procedure in his case. Yeah. He's given us the permission to use his report as an example. And would you now walk us through what it looked like going through David's provocative testing?

SPEAKER_01 27:07

Yeah. So as you mentioned, David came to us with a myocardial bridge that was seen on a coronary CTA. Now, this was done at a different institution. I don't have those images for you, but at the point that he was referred to us, we were at the stage where we were recommending proceeding forward with an invasive coronary angiogram, the heart catheterization with all of the provocative and physiologic testing. So I'm going to share the screen. And so what you're going to see here is this is David's angiogram, which he has graciously allowed us to show. And so we can see at the top of the screen, if we can see my cursor, this is the catheter that's been inserted into his radial artery coming down his aorta and cannulating his left main coronary artery. And the radioopaque or black lines you see here are the contrast dye going into his arteries and lighting up the lumen of his arteries. You can see his arteries are large, there are no blockages inside the arteries, they look normal for the most part. We, because this is a 3D structure and X-ray is a 2D modality, we take these pictures in multiple different views. And so if you focus on this panel here, we're looking at the contrast die going into his LAD or left anterior descending artery. And I hope if you focus on this segment of the artery where it sort of straightens out a little bit, as you watch the contrast dye go in and you watch the heart beating, you can appreciate maybe the caliber of the artery becomes compressed when the heart actually squeezes. And we call that dynamic systolic compression. So with each systole or each squeeze of the heart, the muscle overlying the LAD is squeezing some of the contrast dye and therefore some of the blood out of that artery and compressing that artery. Now, as we discussed, the arteries fill predominantly during diastole or during the relaxation phase. And so oftentimes there's no symptoms at rest because even though there is some amount of compression with each systole or each contraction, because it fills during diastole, the blood flow to the rest of the heart muscle or the myocardium is still preserved at rest. When you exert yourself and you increase your force of contraction in the heart rate, and then you decrease the amount of diastole or filling time that the coronary arteries have, we can then see a drop-off in the blood flow to the distal vessel. And that's what marks a hemodynamically significant myocardial bridge. So as you mentioned, there are a lot of patients who have a bridge that are not hemodynamically significant and are unlikely the cause of their chest pain. But if we can prove that at elevated heart rates and force of contraction, this blood flow is decreased to the heart muscle, then that is the most likely cause of their chest pain in a bridge. So I hope you can make out that squeezing, that is his bridge, and it's confirmed where it was seen on the CTA as well. So the next phase of the test, as I mentioned, is we went to the acetylcholine provocative testing. So on the far left here, this is the baseline angiogram for reference that we just looked at. And we're going to keep our eye on the LAD vessel, so the major artery running down the front of the heart here. And you can see here I first gave him a test dose of just 10 micrograms of acetylcholine just to see how he would tolerate it. And he tolerated it well without any concerns. And so then I went on to the provocative dose, which is 100 micrograms of acetylcholine. And you may be able to appreciate there is a slight decrease in the diameter or the caliber of the artery, especially just after the bridge, sort of in this segment by the branch, this diagonal branch. And that does indicate that he does have a little bit of endothelial dysfunction associated with this bridge. But a diagnosis of vasospasm would require that this artery constricted down to less than 90% of what it was in its original, original caliber. So we have just a little bit of constriction here, which is some evidence of some endothelial dysfunction, but not overt vasospasm.

SPEAKER_00 31:15

And if I could ask just a quick question there on the endothelial dysfunction, there is some assumption that the compression, the beating that that artery takes is sometimes what causes it to dysfunction. It's been getting beat up for so long. It doesn't open up as much as it should, even in the resting phase of the heartbeat. So it doesn't fill as well as it should. And on top of the endothelial dysfunction with the compression for the vasospasms, you you have a compounding effect of cascading pain in some cases or ischemia, correct?

SPEAKER_01 31:54

Yeah, absolutely. That's absolutely correct. And that's why it's important to sort of assess this part of the test as well, you know, with the endothelial dysfunction, the vasospasm with the with the bridge.

SPEAKER_00 32:04

You know, in a severely endothelial dysfunctional situation, would you just see that whole image disappear?

SPEAKER_01 32:12

Yeah, almost the artery itself would almost completely disappear, almost like it's on a shoestring or it's almost the caliber goes to almost nothing. Like I said, it has to be greater than 90% uh constricted. So you get a very robust constriction of this vessel.

SPEAKER_00 32:27

Okay.

SPEAKER_01 32:28

And so as we mentioned earlier, we then reverse the acetylcholine agent, and you can see now his arteries are back to the sort of their normal caliber they were before the acetylcholine went in. So that's an important part of the provocative test. So then we'll move on to the next phase of the test. So this is the debutamine challenge that we talked about. So we insert a special pressure wire with a pressure sensor as a surrogate for flow down the artery, and we measure at baseline the flow at the catheter and at the pressure sensor here in the middle of the artery past his myocardial bridge. And at baseline, he has normal flow through this myocardial bridge. We then start giving him escalating doses of debutamine. And what we're trying to do is get a decrease in the ratio of blood flow or the pressure ratios from before the bridge and after the bridge less than 0.76. So this number up here shows the decrease in blood flow from before the bridge and after the bridge at escalating doses of debutamine. And when we hit 130 beats per minute, which is well under his 85% of peak maximal heart rate, his bridge became hemodynamically significant at 0.69. So I didn't need to drive him up to 140 or 150 beats per minute, which would be you know sort of that that 85% mark, because even at 130 beats per minute, which as you can imagine, someone as active as David is, he hits that heart rate target probably fairly quickly with his exertion. We can see a drop in the blood flow across that bridge.

SPEAKER_00 34:04

Therefore, you're symptomatic. That's where you start to feel.

SPEAKER_01 34:08

So at this point, we can say he David definitely has a drop in blood flow across that bridge at a heart rate of 130. And so, given his exertional symptoms and the lack of all of the other causes of his chest pain, that this is the cause for. And so before I can before we you know say the bridge is the only cause of it, I do we do go on and we do further testing, which I'll show you here. We tested his microvasculature as well. So that same pressure wire has a temperature sensor as well. And so what we do is we take small aliquots of cold saline, three three milliliters of cold saline, and I inject the cold saline down the coronary artery, and I measure the mean transit time of the cold saline down the artery at rest, and then I give him a vasodilator medication, yet another medication. This one is called adenosine, and adenosine will dilate all of the microvasculature and all the arteries of the heart. And so I can then look at the mean transit time of that cold saline when the arteries are fully dilated. All right, and so that should increase the mean transit time because we're getting increased flow through the arteries, and that difference of the rest flow compared to the fully hyperemic or fully dilated flow is called your coronary flow reserve. It's your ability, your heart's ability to increase the coronary flow reserve by dilating the arteries in response to an increased need, such as exerting yourself. There are patients who have coronary microvascular dysfunction where their microvasculature cannot dilate appropriately in response to a demand like an exertion, and therefore they get chest pain from microvascular dysfunction. So the coronary flow reserve, which you can see listed over here, to be normal, should be greater than two. And so that's a flow ratio that increases greater than essentially double of what it is at rest. His is robustly normal at 3.2. If his coronary flow reserve were less than two, then on top of his bridge, we would also diagnose that he has some dysfunction of his microvasculture and the ability for his microvasculature to appropriately dilate in response to an increased demand in exertion. Because that wire also can assess pressure, looking at the ratio of the flow based on the transit times and the pressure, we can also calculate his resistance in the artery. So this is the IMR or the index of microvascular resistance. This should be less than 25 in a normal scenario. So he has normal coronary flow reserve with normal resistance. And so this confirms that his microvasculature is normal. He does not have coronary microvascular dysfunction. So now at the end of his testing, we have really identified very important aspects of his chest pain. Number one, we know he has no atherosclerotic plaques or cholesterol plaques that are causing a decrease in blood flow in the heart artery. We tested with a provocative test in acetylcholine for vasospasm. And while he does have some mild endothelial dysfunction associated with his bridge, he does not have Frank vasospasm. The microvasculature is robustly normal in his coronary flow reserve and his microvascular resistance. And with the debutamine challenge of his bridge, we do indeed see a decrease in blood flow at a heart rate of 130 beats per minute that's consistent with ischemia or decreased blood flow with the debutamine across that bridge. And so these are all confirmatory that he has really no other cause for his chest pain than this positive intramyocardial bridge. And so then I went one step further and we did intravascular imaging of his myocardial bridge. So what we're looking at here, this is a movie here of intravascular ultrasound. So this is an ultrasound catheter that's placed inside of the artery over the wire. And so this is the inside of the artery, and you can see the sort of the layers of the artery around the catheter that the ultrasound is using sound waves to identify. And I hope you can appreciate. If I give you this still image, you can see this sort of crescent moon muscle band that's overlying the artery. This is at the location of his bridge, and this is what is now causing that artery to compress with each heartbeat. Another example of it. Yes, absolutely.

SPEAKER_00 39:20

Wow.

SPEAKER_01 39:21

Yep. So that's really I'm I'm gonna stop sharing now. That's those are the pictures I have for you. That's really uh the totality of his testing, where we went from looking at the diagnostic coronary angiogram, um, doing vasoactive testing with acetylcholine for spasm. We assessed the microvasculture, we assessed the physiology of the bridge and the blood flow, and even did intravascular imaging of the bridge. With all of that information, we can then package that together and send that to his surgeon, Dr. Bonatti, and we can sit down together and evaluate this testing and talk with David about what the next steps for treatment would be for him.

SPEAKER_00 39:57

Well, and two things. It certainly gives you the confidence, you as the interventional cardiologist, the patient, the surgeon, that what you're about to do in terms of the unroofing procedure is more likely than not to be relief of some of the symptoms. Again, no guarantees we all understand. The other part of that I wanted to ask you, because a lot of these are not even acronyms, but they're the identifications. We see IFFR and FFR and DFFR. Is there significance to those or relevance to what you just showed us?

SPEAKER_01 40:32

Yeah, so those modalities are you know very similar to what we're doing. And in fact, some of that you saw when we're assessing an atherosclerotic plaque in, say, the main artery, we use these same type of pressure wires looking at the flow before and after a blockage, similar to how we would in a myocardial bridge. We can use certain hyperemic or vasodilating agents to look at the flow across them as well. We also can look at just the diastolic phase of the of the cardiac cycle to look at the flow across it. And so that's where we get the different indices that we're looking at. Some are what we call non-hyperemic or without a vasodilating agent, looking at just the diastolic phase. Some are a full hyperemic, meaning a vasodilator agent was given, and we're looking at the flow across that blockage in that sense. It's the same sort of technology. The difference then is we're now using certain medications to manipulate the artery and look for provocative testing with the vasospasm using the debutamine to speed up the heart rate and look at what those physiologic flows are at different heart rates or different levels of exertion. And then even this intravascular ultrasound that I talked about, the imaging, we often will use this tool when we've placed a stent to assess how our stent has expanded. Is it opposed to the vessel? Is it large enough? What the size of the vessel is to grow the stent to the appropriate size? And so all these tools are used in other cases as well, but you know, have specific indications in working up this type of chest pain as well.

SPEAKER_00 42:03

And and I think for the novice to be bantering around a lot of those terms is is maybe a little over all of our heads. We just need to know are we hemodynamically significant in the outcome?

SPEAKER_01 42:18

To be honest with you, a lot of the different alphabet soup of IFR, RFR, DFR, these are also somewhat developed as each company who provides these wires and makes these wires come up with their own sort of proprietary algorithms and how to assess pressure and flow, identify them with a different terminology. They're sort of proprietary software that helps to determine what the flow is. So that's where a lot of these different terms IFR, DFR, RFR come from. But in essence, they're really all testing a very similar thing. They're testing the flow from a proximal portion of the artery, either at the guide catheter, and then past the blockage at the transducer of the wire, and then where they're looking at that flow and whether they're using a hyperemic agent like adenosine or using just a portion of the cardiac cycle with diastole. That's sort of how we get so all these different variations on the same theme. So, yeah, we could spend a lot of time going through each one of those and how each company sort of developed their specific pressure wire and what they're looking at, but they're all testing a very similar concept.

SPEAKER_00 43:27

My head already hurts from the explanation. I'm trying to absorb all of it as I'm sure many people will, and we'll be watching this episode frequently just to make sure we have a good understanding. And in many cases, this is an opportunity for the patient to take this to their own cardiologist and ask the questions, if nothing else, to get the dialogue started. And it's going to be so helpful because it gives them a tool now to actually help them along the way for people who aren't familiar with myocardial bridges, of which many are not. Taking a break from the weight of what we just went through. And I I can't thank you enough. The the description was it was just absolutely beautiful to understand what happens. You live and work in an extremely stressful environment. And I know as patients like to interview and speak with the people who are going to be working on their bodies, we wonder what do you do for fun? How do you relax? What's the a little bit of the personal side of Dr. Fowler look like?

SPEAKER_01 44:30

Yeah, of course, you know, certainly the job can be stressful whenever you're dealing with patients' health and and doing these procedures. I like to relax uh with my family. I'm married and have three kids, 16, 14, and 12. They're very active in in different sporting events specifically. And so we spend a lot of time at baseball fields and softball fields and hockey rinks and you know doing fun things with them. I also you know like to exercise. I'm a I'm a big runner and do some biking as well and some resistance training. And so those are you know the best ways for me to unwind is getting active, being with family, friends, loved ones, trying to keep perspective on what's going on and try to untangle some of the stress sometimes.

SPEAKER_00 45:16

Sure. Well, and good for you. Having having three almost teenagers now, I can attest, having have four adult children, you'll have your hands full for a period of time in there that'll just keep you very, very busy in a variety of different ways that you never even thought could keep you busy. Yeah. So and and it's great to hear that you're actually taking care of yourself as well because it's so important, you know, given the uh you know the stress that you're under. Yeah. How about any last words to leave with our audience before we wrap? I know your procedures now in the hospital at UPMC are are changing to where you're taking on different cases, you're looking at things a little bit differently. And we are thrilled that we now have another resource in Pennsylvania to go to, trying to establish somebody in every state where we can say, here's you know a quality institution. Yeah. Tell us what's happening there.

SPEAKER_01 46:10

Yeah. So, you know, like I mentioned, the most common cause of chest pain is still atherosclerosis. And so oftentimes patients get to cardiologists and get testing, even invasive testing, looking specifically for atherosclerosis. And that often is the cause of their chest pain. But there is a whole nother group of patients who do not have any atherosclerosis, but still have very real cardiac chest pain. And a lot of these patients after they go through a cath that shows no blockages, are told, oh, your chest pain is non-cardiac. It's not associated with your heart. And that may not necessarily be true. And so what we're developing here has been developed at many other large institutions as well. We're looking at chest pain syndromes that occur for reasons other than atherosclerotic plaques. And so we've talked about those today that could include vasospasm or microvascular dysfunction or intramyocardial bridges. And so we have developed a whole team that includes not only our some of our non-invasive cardiologists that see the patients oftentimes initially in the office, or our cardiac imagers who specialize in reading these coronary CTAs, or interventionalists like myself who can do advanced testing in the CATH lab, to even our cardiac surgeons who can offer unique treatment modalities for these patients. And so I think it's really important for a patient who's struggling with chest pain and may be told you don't have blockages, and so your chest pain is likely not your heart, that maybe that isn't sufficient enough. That until they maybe interact with a center of excellence that has some specialty in evaluating for other causes of these chest pain, you don't know for sure that it's not cardiac. And there's a lot of patients who would benefit from this testing and some treatment to try to help relieve this chest pain and improve their outcomes as well. And so that's what we're doing at UPMC. We're not the only ones, and certainly we weren't the first ones. Like I'd mentioned, we we talk a lot with a lot of the other institutions that are uh part of this group. There's actually a network called the microvascular network that you can look up online where you can look at other institutions that are doing a lot of these, you know, sort of protocols or algorithms and testing for other cardiac chest pain that's not from atherosclerosis.

SPEAKER_00 48:24

The microvascular network is I will put those in the show notes as well for anybody that's that's interested. And Dr. Fowler, what if somebody's interested in reaching out to you? What would be the next steps, the best way to go about connecting?

SPEAKER_01 48:37

Yeah, so you can certainly reach out to us at our Heart and Vascular Institute. So our outpatient cardiology office, you can call our appointment line, which is 412-647-6000. If you specifically ask for either myself or one of the cardiologists who specialize in these chest pain syndromes without maybe atherosclerosis, that helps to kind of guide you to the right direction. You also are welcome to reach out to me directly. I'm happy to share my email, which I think you can put in the show notes as well. Yes, I will. And I'll do my best to you know try to field some questions if that would be helpful.

SPEAKER_00 49:14

Be ready for some questions because I'm sure they'll be coming. The process and the procedure and the acceptance, the way that you've not only explained it but demonstrated it, is something we've been working so hard to get more and more doctors willing to do. And you are exemplary in the way that you're doing this. And it thrills me to know and to know that there's some progress being made. And I'm sure for people who are listening, going, somebody is actually saying that this could be my heart. It's not stress, I'm not overwhelmed, I don't need rest or valium or some sort of a relaxant, muscle relaxant, is is so refreshing. And I think the listeners are going to really appreciate and say, well, where's the one in my area? Where's the one in the UK? Where's the one in you know, up in the Pacific Northwest? What's happening there?

SPEAKER_01 50:09

Yeah.

SPEAKER_00 50:09

I I I could go on for another hour asking questions because we hear so many of them. As I'm sure you're going to recognize too, as more and more people now interact with you, with you know, their situations, but we don't want to get in the weeds and confuse everybody. It's it's it's such an interesting conversation. Um you've now given us that missing episode that I've wanted to get for over a year now, with somebody who could really walk us through and explain it. And again, thanks to David for allowing us to use this. I know thanks to David as well for pushing because I know he was on you guys right away. You and Dr. Bonatti. And this is part two of a three-part series that started with David. Now you and we followed up with Dr. Bonatti, the actual cardiac surgeon that did the unroofing procedure for David. So thank you so much for what you're doing and your team and setting it up at the system at UPMC. The leadership there has a brilliant foresight for something that's that's coming down the coming down the pike as we continue to learn more about these myocardial bridges. And again, thank you for the excellent and and beautiful demonstration of all these things we hear about but haven't seen. So, from the bottom of my imperfect heart, I appreciate you. Thank you for all you're doing, and thank you for your time today.

SPEAKER_01 51:28

Yeah, thank you for having me on. I think you're in for a real treat for your next phase of this with Dr. Bonatti. He's he's got some really neat things to show you. And I just appreciate the opportunity to come on, and I thank you also to David as well for being so willing to share this with the world. So thank you for having me. Thank you again, Dr. Fowler.

SPEAKER_00 51:48

Thank you for listening to Imperfect Heart. It's my hope that this information helped in some way to improve your situation or will help you better understand this condition. More importantly, that it gives you hope through stories that there is help and you most certainly are not alone. If you've been diagnosed with a myocardial bridge, please be sure to join the private Facebook group, Myocardial Bridge Support Group. For more information about our program or to reach me directly, visit the website, myimperfectheart.com. If you like what you heard today, please give a positive review, thumbs up, high five, whatever your app likes. And be sure to share with everyone important to you so they understand what it is you're dealing with. Please subscribe as well. Welcome each day with gratitude and positivity. The views and opinions expressed in this program are solely those of the host and the guest and are not intended to provide, nor are they a suitable substitute for professional care by a doctor, therapist, mental health professional, or other qualified medical professional. Imperfect Heart is a production of Hear Me Now Studio.