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CV Episode

Dr. Hare: [00:00:00] Hello and welcome to the be excited podcast. I’m Dr. Jason Hare, assistant professor of physician assistant studies for the last 10 years, as well as physiology and pathophysiology in the rehab sciences. I have also been a family medicine PA in the inpatient setting for the last 17 years. Today on the podcast, we have the cardiovascular PA episode and our guest finally is Andrew Foster, PAC. Andrew, welcome to the podcast.

Andrew Foster: Thank you so much for having me.

Dr. Hare: I have to start by saying that an in class recitation that you and I delivered. Together in the cardiovascular module in clinical medicine and the success of that recitation that you and I have done over the last three years now was the model in some ways for this podcast.

Knowing the success of our ability to bring the various aspects of PA education and cardiovascular PA education to our students. I think it worked really well. And so I’ve always kind of modeled this podcast on our. interaction during that recitation. [00:01:00] So I have to say a hearty thank you to you for for helping me to provide well, to at least provide the germ for that information

Andrew Foster: It’s such a cool background.

And it’s really an honor and pleasure to be here today to be able to do this with you. We have had some really awesome Q and a sessions. No doubt. And it’s just been a lot of fun giving a chance to help teach and Spread some knowledge to the PA students.

Dr. Hare: Tell us about your, your history then.

So where you went to school and your early work history.

Andrew Foster: Yeah. So I graduated from PCOM, the Philadelphia College of Osteopathic Medicine in 2012. And after that moved back home to New York, my hometown, and did do a year in internal medicine. I got a chance to work with a cardiologist who also continued to practice internal medicine, which is common to see.

 The opportunity, a year later, came to work in general cardiology with Tri County Cardiology here in Pittsburgh. And so I did decide to make that jump [00:02:00] as cardiology was an area I was always interested in. And I’ve been working with the group for the last 10 years now. It’s been… Pretty much exactly 10 years, September of 2013 is when I got here.

And I say general cardiology because predominantly that’s what we see, but we do have interventional cardiologists in our group as well.

Dr. Hare: Is that starting in the general and moving to the more specialized in your career, is that something that you did intentionally or was that something that just developed unintentionally, I guess.

Andrew Foster: Yeah. A bit of both actually, when, I graduated, I really had the mindset working in general medicine, especially when recertification of boards was every six years, it would be beneficial to stay in more of the primary care setting. But as I was at the PA national conference, I was in Washington that year.

[00:03:00] I was talking with others who have moved into specialties and they said if you want to make that jump, especially if you want to move into cardiology, I don’t think you’ll have any trouble. Nor will you have any trouble with recertification of boards and such, since cardiology is such a big part of it.

And it kind of just got the gears turning of, well, I’ve always been interested, and if the opportunity arises, maybe I should take that jump sooner rather than later. And it just happened to be the next year here in Pittsburgh.

Dr. Hare: And I think that’s for a lot of students. They hear that and think to themselves, you know, do I want to put off?

What might be a dream for them, you know, the dream job especially if they get offered that dream job but certainly for the purposes of PANCE and retaining of information longterm, you know, you have multiple passes of information is always going to be the best way to keep things in your mind.

And so going through a generalist time in your career I went the opposite way. I went from orthopedic surgery. back to family medicine in my second year I definitely understand how [00:04:00] that how that can work and well, sometimes work against you if you’re not too careful about it.

So what is it about cardiology that really pulled you in

Andrew Foster: I think I always had this desire to want to learn about the heart because cardiovascular disease runs in my family and I wanted to be able to Since I was moving into medicine, I wanted to be able to be a reference and a help to family members in particular with something that is commonly seen in our family.

There was just something about one of the most vital organs in the body and taking care of it that was attractive to me. It’s something that. When I’m talking to patients and I come in for a consult in the hospital and I introduce who I am, one of the first things they ask me is what’s wrong with my heart, you know, or even in the outpatient setting for longstanding patients, sometimes I’ll walk in and they’ll say, Oh, what are you going to say to me today?

I think [00:05:00] everybody. Gets a little bit nervous when something could be wrong with your heart. And even including other providers, I work very closely with a lot of great internal medicine physicians who really do rely on our group’s help, my help. When they say, I’ve got somebody that I think you really need to see this person because nobody really wants to mess around with such a vital organ.

That is also a humbling feeling that you are in such need and that you can help people. So I think that’s one of the things that has really gravitated me towards cardiology.

Dr. Hare: I can imagine that everyone on some level feels that their own service, the thing that they do for a living is somehow.

thing, you know, that keeps everybody going and moving. But yeah, without the heart, there’s not much that goes on. Certainly. So yeah, I can, I can absolutely understand that. And of course it, as you mentioned before is a huge part of our certification exam and a large part of all [00:06:00] PAs, even surgical PAs have to reference back to cardiology to make sure that their patients, are, healthy enough to, climb a few flights of stairs before you do that surgery and make sure that cardiology is on board

 You had said general cardiology. Now there are other services that are peripheral Presumably you’re kind of at the center of that. Tell me about some of those other peripheral cardiology services.

Andrew Foster: Yeah, that can include something more specialized you’ve got general cardiology and then you do have some more subspecialties. Interventional cardiology is one where you’re involved with coronary artery disease and the implantation of coronary stents, and even some of the interventional cardiologists are.

Board certified in doing peripheral angiograms and even fixing peripheral arterial disease of the legs. You have electrophysiology is a big specialty. Looking specifically at cardiac rhythm disorders. And then, [00:07:00] you know, if you need an A I C D or a pacemaker or some type of a rhythm ablation, then electrophysiology service we’re seeing.

That there’s advanced heart failure, particularly in urban populations, urban cities like Pittsburgh here. You have advanced heart failure, pulmonary hypertension specialist. And then I’m also starting to see more cardio oncology and even obstetric cardiology, where you’re involved with the person’s care.

During pregnancy and postpartum, particularly with preeclampsia, and even if you have maybe a history of congenital heart disease or you’ve developed abnormal heart rhythms during pregnancy, you have some cardiologists that are kind of moving more into those specific fields. So it is becoming quite diverse, which is pretty cool.

Dr. Hare: What kind of conditions do cardiac [00:08:00] oncologists see?

Andrew Foster: Cardiac oncologists are particularly involved with when you are administering specific chemotherapy agents, ones that can be more cardiotoxic, or if a person has a malignant or oncology condition. And their heart already has structural heart disease, then working in collaboration with the oncologist of what do we think their heart can handle?

What do we think would be the best chemo agent here? How can you better optimize the patient from a cardiovascular standpoint to help them through this very trying time that the chemo and potentially, we’ll say, stem cell transplant that they’re going to be going through. So, I think they’re starting, starting to see a bit of a niche there where people are moving into that kind of a specialty

Dr. Hare: So, less primary diagnosis of cardiac cancers and more of a secondary, I wouldn’t even say secondary diagnosis, but certainly in, in a huge support [00:09:00] role for the treatment of any cancer.

Andrew Foster: Exactly. And what kind of got me introduced to this was where I work at with West Penn Hospital it’s a major oncology center and we have been asked and how can you help us and support these patients who have history of coronary artery disease history of CABG valvular heart disease structural from a reduced ejection fraction frequent tachyarrhythmias with atrial fibrillation with what we’re all doing here and trying to treat their cancer How can you also better support their heart and so it’s definitely a growing field.

Dr. Hare: Moving on from that, the idea that the generalists, and we’ll talk about this later on in the episode, but certainly we have a lot.

Of use for cardiology in the generalist fields. And I’ve always appreciated the ability to, get that EKG before we start a medication on someone to check their QT intervals or [00:10:00] something like that. we’re calling because, oh, I’ve got this odd finding I see on this EKG. And can you all take a look at that?

That is , not just helpful for patient care. It’s also really. Calming to see those things and make your own call on those things. Sometimes when you are not closely involved in cardiac care on a day to day basis, that’s really helpful and really a comforting thing, certainly when working with patients and comforting for patients also.

The next thing on our list is must not miss diagnoses. Of course, must not miss diagnoses are conditions that create higher morbidity and or mortality in our patients that cause dysfunction and potentially death in our patients.

If allowed to continue these are often emergent conditions and things that we do not want to come through our clinic. Sit on our exam table and then walk out the door without having been checked, addressed and otherwise dealt with as a practitioner, that’s that’s a crucial part of that. And of course, in [00:11:00] cardiology.

There’s a lot of that. And so our must not miss list is significant here. And of course, number one on the list is the STEMI, the ST elevation myocardial infarction, the classic significant heart attack. So I’m asking you a broad question about something that is , a huge part of your.

job on a day to day basis. Tell me why that makes your must not miss list and why it’s number one.

Andrew Foster: The reason why STEMI makes the top of the list is because, as we say, time is muscle. And what’s happened here is the muscle is infarcted and it’s essentially dying if not revascularized. quickly, and our door to balloon time is 90 minutes.

So from the moment that EKG is obtained, showing the ST, elevation myocardial infarction, and the STEMI alert pager team, however your system is set up, once they’re activated, [00:12:00] you have the stopwatch going you’ve got 90 minutes to revascularize. That’s door to balloon, and then obviously you need to Fix and revascularize the culprit vessel.

Otherwise, if you leave these alone, if you don’t call it or you delay it, then you can have irreversible damage of the myocardium. And in some people, that can lead to death. In some people, that can leave them severely disabled with an extremely low ejection fraction, when potentially this can be. Fixed and

reversed.

Dr. Hare: So the pump gets less efficient. Those surviving a STEMI have the potential to have a less efficient pump. And significant amounts of dysfunction as a result of that. And of course mortality obviously with a heart attack classically we would call that a heart attack is impactful for our patients.

we talk about the STEMI the flip side of that is the N STEMI. So the non ST elevation, can you [00:13:00] speak a little bit to the, to the pathophysiologic changes that occur, differentiating those two?

Andrew Foster: Yeah. With a non STEMI, you’re not seeing the ST elevation that you classically see on EKG.

So what’s happening here is there is. Significant occlusion of the vessel, but it’s still probably some limited blood flow and enough to provide oxygen and nutrients to the myocardium where it is. hurting, but it’s not enough to actually cause muscle death with a non STEMI. So it is a heart attack. It is significant, but it’s not that emergent heart attack where you have completely infarcted muscle that is not receiving any oxygen, not receiving any blood flow, and therefore this is dying muscle.

Dr. Hare: And of course, those

vessels that you’re speaking of are the blood vessels that are supplying blood to the muscle, the myocardium of the heart and, and various [00:14:00] branches making their way all the way around anterior, lateral, posterior, and the septum of the heart.

 A significant network of blood vessels supplying that. And, , any obstruction in those is going to be Problematic for the heart depending on how much. And of course we talked about in our recitation today how a 90 percent occlusion is often where we start to see symptoms in an individual up to and including the point where they have a rupture of that plaque and then, then we get a sudden complete obstruction of that and that can cause some significant pain.

Andrew Foster: Yeah,

exactly. More specifically to these vessels, we say that the epicardial vessels, and you’ve got the right coronary artery wrapping around the Right side, taking the inferior territory, you’ve got the LAD, classically called the widowmaker, wrapping down the center of the heart and usually covering the most amount of territory.

And then the left circumflex, which more of the lateral side, left side of the heart. You have the [00:15:00] left main that gives you the circumflex and the right coronary artery. It’s more owned vessel. And it just goes to show with one of the things you just said was you can go a long time with a pretty significant blockage in one of the epicardial vessels before you have symptoms.

 it can suddenly rupture and when it does suddenly rupture, that’s usually when these ST elevation myocardial infarctions happen as the body is trying everything it can to repair that tear in the vessel that was caused by the ruptured plaque.

Dr. Hare: Along those lines, one of the things that we talk about with students is the recognition and understanding that no matter who walks into our clinic with a symptom, with some sort of pain or any sign or symptom of anything, we want to take that seriously and deal with that consistently amongst all patients.

One of the issues that we’ve seen and it’s come to light certainly more in recent years is the difference between those who are identified female at birth and the way that they present with their cardiac [00:16:00] symptoms versus those assigned male at birth who historically have been.

 Taken more seriously than those who are assigned female at birth. It’s obviously something we want to get away from any group that we are presented with those kinds of symptoms we want to do everything we can to help them.

Have you seen a significant difference in the way those assigned female birth present? Versus assigned male at birth

Andrew Foster: I

 have and we a lot of times say that they present with atypical symptoms Patients who are assigned male at birth You will read about the classic symptoms of chest pressure Tightness some elephant feelings on your chest with radiation to the jaw neck down the left shoulder is whether your classic angina and even unstable angina symptoms with associated diaphoresis, nausea, vomiting.

But those more classic symptoms are not always seen in a patient who [00:17:00] is assigned female at birth, where they may be experiencing sharp chest pain, no radiation. They may not have the classic diaphoresis, nausea, vomiting, or it may be just nausea and vomiting. And you’ll also see sometimes atypical presentations with diabetics as well.

So there has been this, I would say, recognition when you have somebody who is assigned female at birth. To realize, okay, since they are having chest pain, even though it may be a typical presentation, you should not just think, okay, well, just because they’re assigned female at birth, they’re not going to have coronary artery disease.

You have to keep that in your differential. If you don’t think about it, you’ll miss it.

Dr. Hare: Nausea and vomiting symptoms.

You don’t want to just say, okay, well, this is not an acute abdomen and send them home without some backup to that, some, some [00:18:00] cardiac investigation the next one on your list is complete heart block. And of course, complete heart block does sound intense. Tell us about

that.

Andrew Foster: Yeah. With complete heart block, we have. Complete dissociation between the top chambers of the heart and the bottom chambers. Our natural pacemaker, the SA node, is firing and doing what it’s supposed to do, but there’s been a loss of and conduction from the atria to the ventricle through the AV node.

So the heart’s pretty cool and it has different backup mechanisms to make sure it keeps going. And so your ventricles will typically contract on their own at a ventricular escape of around 20 to 40 beats per minute. But the ventricular contraction is at its own rate, completely separate to the atrial rate.

And that complete dissociation, the complete heart block, is usually not well tolerated by a [00:19:00] person. Most of these people are older, and they physiologically cannot handle a heart rate of 20 to 40 beats per minute.

Dr. Hare: Not perfusing, in other words. Not perfusing. Okay.

Andrew Foster: The only way to really help them is to put a pacemaker in.

And so if you’re not recognizing this on EKG, if you’re not recognizing not only the symptoms, which could be a presenting symptom is syncope, then dismissing this, this person could decompensate very quickly. They could have more syncopal episodes. You’re not going to help them until that pacemaker and a better heart rate is restored.

Dr. Hare: We have time set aside for cases as we always do on be excited. And so the next two on our must not miss list, we’re going to delay a moment, but I do want to make note of them. Number three on the list is congestive heart failure and number four on the list is coronary artery disease which has a significant preventative component to it to, to prevent significant damage.

[00:20:00] So we will talk through some cases here in just a bit. The next number five on the list, tachyarrhythmias. And so are we thinking atrial or ventricular at this

point?

Andrew Foster: I would say both. I, when I think of tachyarrhythmias, I mostly see a lot more atrial. And whether it’s atrial fibrillation, atrial flutter, SVT, particularly AVNRT, AV nodal reentry tachycardia.

And most of these are not going to cause death. But they’re frequently seen and they’re seen so frequently, something like atrial fibrillation you don’t necessarily want to miss because you could be then missing putting the appropriate person on anticoagulation and then if they have a stroke while in AFib.

And you didn’t anticoagulate them appropriately, then you didn’t prevent something, a cardiovascular event like a stroke that was easily prevented.

Dr. Hare: That idea that you have a. Knowledge of understanding that that individual was in a [00:21:00] fib. You knew, for instance, that they had a fib for 24 hours prior to our intervention somehow.

In other words, they were in the hospital for the most part, right? That’s going to be our most common way of identifying a fib. Some folks, I recall you saying, identify in themselves a fib and can catch that. Maybe their Apple watch catches it. Maybe they. have that sensation of palpitations that they recognize, and then we use that to decide whether or not they may have been in AFib long enough to really form a significant clot inside the heart.

And that’s where does the clot form and where, where is the danger of that going?

Andrew Foster: Most clots with atrial fibrillation are formed in the left atrial appendage. And Though a clot can form anywhere in the heart, it’s most likely to form there. part of that with atrial fibrillation and you no longer have atrial contraction, you have this fibrillation, you’re not seeing the velocity then through the left atrial appendage [00:22:00] move as vigorously as when there’s contraction of the atria.

And so, Blood in the left atrial appendage then starts to swirl and over time, long enough, can actually form a clot. These clots can be very tiny. They can be much larger. But if it does leave the left atrial appendage and move its way to the ventricle, It then has a likelihood of being shot out of the heart, and one of the more common places it’s going to go is right up the carotid to the brain and cause an ischemic stroke.

We want to know if they have a left atrial appendage clot, particularly prior to cardioverting, because we don’t want cause significant contraction with electric cardioversion that could dislodge that clot. So knowing if that’s there and if it is, you’re not allowed to cardiovert them until that clot is dissolved.

Dr. Hare: Dissolved.

is that a clot buster

Andrew Foster: so how we do that is just anticoagulation. There is different anticoagulants that can be [00:23:00] used, but typically you would wait. anywhere from four, six weeks, as long as they’re not missing any doses of their anticoagulant, that is about the time that the body needs to break this clot down on its own.

So we’re not actually giving any clot busting medication, we’re just anticoagulating, preventing further clots from forming, and letting the body take care of this on its

own.

Dr. Hare: That’s really interesting. if someone comes in who’s already being treated for AFib and is on an anticoagulant of some sort, Do, does that impact your decision making when they come in for that second or third episode of AFib?

Andrew Foster: Absolutely. If they’re a reliable person and we know, and they are certain they’re not missing any doses of their anticoagulant and then sometimes we will move to cardioversion a lot sooner. Knowing that there’s a lower likelihood that there is a clot there. Some of us will still prefer to do a transesophageal echocardiogram first to just make sure and say, [00:24:00] I’m certain there is no clot, I’ll go ahead and cardiovert them.

There are others who will say, I believe you, you’ve been anticoagulated long enough, it’s very low likely you have a clot and I’ll just do the cardioversion and skip the transesophageal echo.

Dr. Hare: In the interest of creating structure around some of the terminology that we’re using the TEE or the transesophageal echocardiogram is the partner, I suppose, of the TTE, which is the transthoracic echocardiogram, obviously going transthoracically, going across the ribcage externally with ultrasound in that echocardiogram is less invasive.

So tell me As far as moving to a TEE, how is that decision made to go to TEE then?

Andrew Foster: When it comes to atrial fibrillation in particular, you’re not really going to be able to visualize the appendages without a transesophageal echocardiogram. A transthoracic is very good at seeing many parts of the heart, but you’re going to be missing that, [00:25:00] the appendages in particular.

There are certainly a lot of other… potential reasons for moving from a transthoracic to a transesophageal. One of the things that we talk about here is evaluation for endocarditis. Sometimes it’s a better look at valvular heart disease and looking to see if it’s mitral or aortic Though you can get a lot of information from the transthoracic and sometimes that’s all the information you need.

To get sometimes a better, more detailed picture, a transesophageal is always going to give you that because you’re Ultrasounding the heart from closer. What I mean by that is the esophagus sits right next to the heart. So the closer you are to the heart when you are ultrasounding and the shorter the distance of the ultrasound waves have to travel, the more detailed the images will always be.

Dr. Hare: Folks who are in line for a TEE will often say, oh that sounds… So why can’t you just look from the outside? But I think that’s a great way to explain to a patient. This is directly [00:26:00] next to, inside that esophagus, the heart. We can get a much better visualization of the areas that we’re concerned about.

I think that’s something that a lot of patients I think would feel comfort in knowing that they have to undergo that particular procedure. Any other tachy arrhythmias that, that come to mind in that significant must not miss category?

Andrew Foster: I would think any of the ventricular, particularly ventricular tachycardia, though a lot of times a sustained ventricular tachycardia, that person’s presentation is that you may be coming upon them after a cardiac.

Resuscitation code has been called, right? I mean, somebody who is in sustained VT is likely already lost consciousness, and somebody might have started CPR and activated the emergency response system that we all learn about in ACLS. But if you’re seeing, in the hospital on telemetry, if you’re seeing frequent runs of non sustained VT.

if it hasn’t been looked at, it should be looked at. Why is that happening? Is it as simple as the [00:27:00] potassium or magnesium levels are off? Is it that this person has an unknown reduced ejection fraction that makes them susceptible to this? So I think that these more non sustained episodes.

sometimes are a warning sign of, hey, this needs to be looked at where then when that sustained episode happens, you’re now trying, you’re in the emergency setting of really trying to save this person’s life.

Dr. Hare: We use these electrolytes to signal conduction through the heart.

Which are the The electrolytes that you would you place high on the list of things that you go after when you’re looking at a lab work set on a patient coming in with potential cardiac abnormality of any

sort.

Andrew Foster: Potassium. Potassium. And potassium and magnesium are very closely related, right? If you have too low of a magnesium level, and you have also associated with it very low potassium, you’re going to need to correct the magnesium level before the potassium starts [00:28:00] to rise and be replaced as well.

And in some cases you have just isolated hyper or hypokalemia. But potassium is a major substrate to arrhythmias, and it’s something that we really harp on in the hospital When they’re being diuresed when they have diarrhea and they’re losing potassium through their stool We really harp on make sure this person never becomes hypokalemic in the hospital they shouldn’t and It’s something that can be replaced.

It’s typically done orally and You can really limit or help yourself with these tachyarrhythmias if you can keep the electrolytes normal. Certainly calcium and phosphorus and sodium play a role, but potassium is a big one.

Dr. Hare: My students in my physiology and pathophysiology courses sometimes get a little bit frustrated because there are more kidney…

Discussions, then there are cardiac discussions and I [00:29:00] always point out to them that each one of those lectures, including both the volume lecture regarding kidneys and the electrolyte how do we handle particulates in the bloodstream all have significant conversations revolving around cardiac function and Blood volumes for instance, and the amount of electrolyte in the system that has been cleared by or is being held on to by the kidneys.

 Those kidneys and that volume and those electrolytes are directly impacting the cardiac function at any given moment, including blood pressure.

And arrhythmias and, function within the heart when it comes to electrical activity, that is really crucial. It’s also why our renal module in clinical medicine in, this program is prior to the cardiac module, So that we can cover those basics before we get to the heart the fluid and the electrolyte that is being supplied to it by those kidneys.

Andrew Foster: The term Cardiorenal Syndrome is there for a reason, because they are so closely related, whether it’s the kidneys that are failing first, and that affects the [00:30:00] heart, or the heart is failing, and then that affects the kidneys.

The two are very interconnected.

Dr. Hare: And so, on the perfusion level Do you watch kidney function in patients before they’re discharged from the hospital after a cardiac event of some

sort?

Andrew Foster: Absolutely. Whether we’ve done a heart catheterization, we’ve exposed this person to contrast and we are looking at the potential for contrast nephropathy.

Whether it’s diuresis, whether it’s our medications such as our ACE inhibitors, our angiotensin receptor blockers, our corticoid antagonists like spironolactone. Our receptor blockers I want to say Entresto as well. I mean, all of these, have an effect on the kidney and as well as your overall fluid status.

 Too volume overloaded, you can have congestion within the kidneys that prevents the kidneys from functioning correctly. And you can see the creatinine start to rise because of that, which is then improved with appropriate diuresis. Versus, oh, I’ve diuresed them too much and [00:31:00] them, and now my creatinine is rising again because of that.

But it’s all so closely interconnected, so we are always watching. What our electrolytes, particularly our potassium, because a lot of our medications, we’re always watching what is the effect with the kidneys, you just have to.

Dr. Hare: What sort of volume do you like to see in the urine output in a patient like that?

 Is there line you draw for discharge liters per

day?

Andrew Foster: When they’re in the acute volume overloaded state. then usually a goal of two to three liter output in 24 hours is good. Sometimes if you’re not diuresing them appropriately, you’re just lengthening their hospital stay, potentially even stressing their kidneys, and stressing their other organs, mostly the kidneys.

if you diurese somebody too fast, well that can sometimes have its own complications. Loss of electrolyte. Electrolytes definitely. I think sometimes uric acid can be affected. I would say at least in the initial hospitalization, as you are working to get fluid off of them, a goal of two to three [00:32:00] liters and knowing what is their dry weight, we really do rely on a person.

And we teach them extensively when they’re coming in with a new diagnosis of congestive heart failure, which I know we’ll talk about, is what do you think your dry weight is? And sometimes we have to explain what that means. But we have to sometimes teach a person, this is what your dry weight is.

Remember that. And when you go home, if you start to deviate from it. Quickly that’s water retention and we want to know what is the difference between where you are now and what your dry weight is. So we know good idea of how much fluid we need to take off of you.

Dr. Hare: Of course, long term you would be looking at, adipose tissue and muscle tissue combined on a long term average.

This would be a relatively short term add of fluid or loss in that

individual.

Andrew Foster: Absolutely. I tell people when they go home. If you see a weight gain of three pounds in 24 hours, five pounds in three days, that’s water. Yeah. It’s impossible for that to be adipose tissue or muscle, [00:33:00] whether it’s muscle loss or muscle gain, that is always water.

And that’s too quick of weight gain. You need to start responding and treating that. The patient needs to be responsible for that. We need to be able to give them the correct instructions, but that’s the importance of get up in the morning. Ideally, you haven’t ate yet. You go to the bathroom, and then you step on the scale, and that’s your dry weight for the day.

Dr. Hare: cardiac palpitations This is to me one of those interesting things that some patients can sense, others cannot. I would think most patients would find this to be a stressful sensation to be able to feel this

I can imagine that it would be a stressful moment to be able to feel something that feels irregular inside your chest and certainly wanting to get that worked up so what, what are our common causes of cardiac palpitations and being able to sense that beat inside your chest?

Andrew Foster: That’s a good question.

I’ll say that it’s on the list more so for a common morbidity instead of mortality. It’s just a very, very common. Complaint that a person comes to [00:34:00] the office with maybe a new sensation of I don’t know what this is, but it’s around my heart. And so I’m nervous and want to know what is it? And is there anything to be done about it?

A lot of times Dr Google has played a part. Sometimes it’s Talking with other family members or friends and what is their experience and do you think it’s this and so it leads to Some workup. What is the cause of it? Most commonly it’s a premature beat Now I’m not gonna say that’s for everybody but a lot of us have these whether atrial contraction or a premature ventricular contraction That we, a lot of times don’t feel we are so busy throughout our day.

We don’t feel them until maybe we’re in more of a quiet environment, such as going to sleep at night, laying on one particular side, left versus right quiet environment, just kind of resting. And then you feel that. And then you start to really feel for them and become more hypervigilant. But all it is, is with that, [00:35:00] premature beat that’s happening outside of our normal rhythm at that time.

Our normal rhythm beat, let’s say it’s 70 beats per minute. All of a sudden you have this premature beat, that sudden sensation. Some people are more likely to feel that than others. It doesn’t necessarily mean that there’s anything wrong. But it could be that you’re having a frequent amount and such a high amount that we need to investigate that.

It could mean that you’re actually having brief runs of a tachyarrhythmia, such as an SVT. It also could be a sensation that you’re feeling, but after wearing a Holter monitor, we find that there’s not really anything there. So it is a sensation, but it’s not necessarily your heart. it’s a common thing that we look at and we evaluate, particularly with a Holter monitor, where we can watch we can record the rhythm for a length of time, ideally two weeks, to get a better idea of what’s happening.

And is it a concerning abnormal heart rhythm? Or [00:36:00] is this something that’s very benign? And let me talk you through this process and more reassure you.

 I see a lot of PVCs, honestly. But I also see a lot of PACs in some people. Some people have more of a propensity to a PVC than a PAC. Don’t know exactly why. So that’s

on the ventricular side as opposed to the

premature atrial side. Pretty evenly split. Okay. I would say. And that’s just based off of looking at multiple. heart monitors without actually keeping statistical data. I would say on average, when I look, I see a lot more of PVCs, but ultimately pretty close mix between premature atrial contractions and premature ventricular contractions.

Dr. Hare: And is this an area whereas everyone else is sending their patients to cardiology, is this a moment when cardiology is now looking at other potential sources for those palpitations? For instance. an endocrine source with the thyroid or urine catecholamines with some sympathetic overdrive you know, those kind of things.

This is [00:37:00] where you’re looking at other, potential sources of this drive that’s causing the palpitation.

Andrew Foster: Absolutely. We typically will get lab work. And part of the reason for that is what is your electrolytes doing? Common one being potassium. If you haven’t had a recent TSH, or you have a known history of a thyroid condition, we’ll consider repeating the TSH easy blood test to be done, just to make sure that maybe you’re not over medicated, under medicated, versus is this a new thyroid condition for you?

These are usually quick, reversible things, so you want to be able to catch them, and not overlook them. And then a lot of it is also, let’s just start to kind of understand what your day to day process is like. What are you eating? How much sleep are you getting or not getting? How much caffeine are you consuming?

How much alcohol are you consuming? How little exercise are you doing? And other potential triggers, such as, do you find for patients [00:38:00] who are female by birth, Do you find that this happens around menstruation? Is this happening right now? Mostly during a pregnancy. So, you know, personal story is I’m a new father.

I’m very proud of that. Congratulations. Thank you. And my wife during the third trimester had a ton of palpitations. And we were walking to the car. And I said, hold on, let me just check your pulse and her pulse was so irregular. I thought she was in atrial fibrillation. I was certain. and we got home, pulled out her stethoscope that she had and I’m listening to her heart and I said, your heart is just flipping all over the place.

she’s overall fine. I said, let’s just, let’s just see if we can get you an EKG tomorrow at work. We did. Plenty of PVCs seen there. And then we did have her wear a Holter monitor. We had her wear a Holter monitor for at least a week. And that’s what it came back as. You’re not having AFib. It’s [00:39:00] just premature ventricular contractions.

You’re having quite a bit, but that’s all it is. And it’s related to your pregnancy. She had a good, solid week, week and a half of how bad this was, which felt like an eternity to her, but as quickly as they came on, they went away. And I honestly just attest that to my son. He just changed position and wherever he was or whatever was happening at that time, it calmed down.

 We do tell. pregnant patients that once they start to have palpitations, which is a common finding, they get worse during each trimester until delivery, essentially.

Dr. Hare: So as is often the case, the cure for things during pregnancy is often delivery. TSH is one of those labs electrolytes, CBC. We order those a lot. TSH is for so many different differential diagnoses just in that list, you know, there’s so many different things that the thyroid. Gland really impacts significantly [00:40:00] everything from fatigue and psychiatric issues to hair loss and cardiac issues and anxiety, it is really wrapped up in a lot.

 The last thing on this list now is valvular heart disease, and I suppose at this point we could transition over to talking through a case if, if you’re willing to do that.

 This case valvular heart disease, so we’re talking about the valves between the chambers of the heart allowing blood in an appropriate fashion and then sealing to prevent blood from backflowing into that, the previous chamber. So, valvular disease can take on a variety of sources, has a variety of causes What kind of a case do you have in mind for this

one?

Andrew Foster: I’d say most commonly is aortic stenosis. stenosis is typically progressive degenerative, meaning it’s a lot of times caused by calcium buildup on the leaflets that gets worse slowly as we age. And so

 Your patient population is typically older than 70 years old, [00:41:00] it may be, particularly in a primary care setting, you’ve recognized that this person has a murmur, and year over year over year of continuing to follow them, you have slowly listened to this murmur get worse, more severe. Maybe that is, you’re noticing less and less of hearing the S2.

So you hear S1, but you don’t hear S2 or eventually it does go away completely. And you know that this valve is just becoming more and more severe as well as what is the person’s symptoms starting off probably asymptomatic. That’s the most common. And they just have a murmur to eventually, I’m short of breath with exertion.

And then that dyspnea on exertion just eventually progresses to more short of breath at rest. And then have they started to actually have left sided heart failure symptoms, which the last thing we want is to see that their ejection fraction has declined because of the severity of the aortic stenosis.

We want to obviously fix the valve before that point, but that is the natural progression.

Dr. Hare: are you one of [00:42:00] those guys in cardiology who has mastered making the heart sounds to demonstrate for their patients?

Andrew Foster: I just go with lub, dub,

lub dub, lub,

dub. But as my, my work colleagues laugh at me because I always say, Oh, really severe aortic stenosis just sounds like one. And you just hear one sound and they go, how does that go again? And I just keep repeating it and they go, you sound so ridiculous.

Dr. Hare: that particular sound is kind of a crescendo of overcoming the resistance into the aorta.

Correct.

Andrew Foster: The leaflets will have typically a high amount of calcium buildup that then restrict their mobility. And so normally when the leaflets and it’s typically the three leaflets when they open. then you should have this large orifice to allow blood to move from the left ventricle into the aorta.

But the more those leaflets are thickened due to calcium buildup, not only are they restricted in [00:43:00] how much they can open but that orifice ultimately becomes more narrow. And so it’s very similar to, I think, putting your thumb over the hose, where… water should just pour out of the hose with some force, but not an incredible amount of force.

But then you start to narrow the opening and you see how it tries to really shoot out with more force. And that’s because there’s an increase in gradient. And that’s essentially what you’re seeing on Echo is this change in gradient. And over time, the left ventricle has to compensate for that. Narrow opening by typically left ventricular hypertrophy, but as it wears out, then you’ll get a decline in the ejection fraction.

Dr. Hare: It is interesting to me that then heart failure is often the result of that. And we’ll talk about heart failure in just a moment, but that, that needing to overcome resistance by the heart and the ventricles especially is really the source of a lot of dysfunction in older individuals.

Andrew Foster: Absolutely. [00:44:00] So I think of one patient in particular who had a history of coronary artery disease. He was 90 years old. He was well functioning really enjoyed his square dancing one day a week. That was part of his social get together. And He had presented to his doctor was saying, I am becoming more short of breath and I’m having trouble square dancing.

I’m taking a lot of breaks. And of course they were referred to us and we had already known them. But the question was, do we think this shortness of breath with exertion is all related to their coronary artery disease or do we think it’s related to the valve? the aortic stenosis that they had. And so this person had already received two stents in the past.

We repeated the echocardiogram, it had been about a year, and typically when the aortic valve is getting to that Critical junction that, you know, this is severe. You may be doing [00:45:00] echoes even every six months and really assessing this person’s symptoms. So you’re bringing them back to the office quite frequently, three, six months.

We had repeated the echocardiogram and we saw that, yeah, technically you meet the criteria of severe aortic stenosis. You’re 90 years old. You’re not really a great open heart surgery candidate. And so, we did take him to the cath lab for a left heart catheterization. His previous stents were open. There was no new concerning obstructive coronary artery disease.

And the decision was, you have severe aortic stenosis. You’re starting to have symptoms from that. And luckily, your ejection fraction is not any weaker, or not weak. It’s not a new finding. But let’s go ahead and see about if you’re a candidate to have your valve replaced. And at that point, based on his age, it was felt he would do better with a transcatheter valve replacement than an open sternotomy.

And there’s a whole team that, it’s called the TAVR team, that looks [00:46:00] into these cases. Sometimes they need a specific CT to make sure that their femoral artery is large enough to be able to allow the collapsed valve to make its way up to aortic valve position. You need to know what their kidneys are doing.

You need to know what their ejection fraction is. You need to know all of their comorbidities and decide, especially the valve area, can they put a valve inside of a valve there? All done with catheters. He was a candidate. He got his valve replaced. It was not a same day. I think it was go home the next day procedure, but he did very well with it.

And, you know, he’s still square dancing. So, you know, and we’re talking two, three years later. Doing just fine. That’s great. So that’s a more of a success story with mm-hmm. TAVR related to aortic stenosis with the type of patient population that you’re seeing

Dr. Hare: and the TAVR team. I find, I find that an interesting concept is that a, a multidisciplinary team then that’s making that

call.

Andrew Foster: It is the [00:47:00] team is comprised of interventional cardiology as well as cardiothoracic surgery because you wanna make sure you have the right valve. You want to make sure you’re putting in the right place. It is being done in a cath lab with an interventional cardiologist and a surgeon there.

So I do believe it is a multidisciplinary team making sure we’re picking the right patient. Patients. Interesting.

Dr. Hare: All right, so let’s move on to and going in reverse order here The second case on the list is congestive heart failure And of course, we’ve already talked about multiple scenarios in which congestive heart failure is at risk One of the things that I find interesting about the term heart failure is that it sounds so very Final.

It almost sounds more final than a heart attack. the heart is failing. It’s failed. What does that mean? And what does that imply for the patient

with their function?

Andrew Foster: So you can see why when I walk into a room to introduce myself, especially as a [00:48:00] new consult, first thing they’re asking is what’s wrong with my heart?

Because if I say, well, we’re consulted to see you because of. congestive heart failure, obviously you’re going to get looked at excuse me, what, what do you mean? Heart failure? The name is so concerning and it scares a lot of people who, what do you mean my heart is failing? But I take a step back and say, your heart is a pump and.

You’re in a fluid overloaded state that the heart has not been able to accommodate and this overloaded state is in a very general sense how I define congestive heart failure. Congestive being the fluid overload, the heart failure being that the pump has not been able to accommodate this shift in change in volume.

There’s two main types of heart failure, heart failure with a reduced ejection fraction where the ejection fraction is lower than 50 percent and heart failure with preserved ejection fraction where the EF is [00:49:00] preserved 55 to 75%. The main difference between the two is one is more of a clear pump failure.

A weakened ejection fraction versus the other one is a noncompliant left ventricle and that it is very stiff. And so it’s not able to accommodate the normal amount of diastolic volume as it should, but both lead to a fluid overloaded state. I think one of the important things about heart failure is that it typically is an end point.

We’ve talked about. Valvular heart disease and how it can lead to heart failure, how potentially tachyarrhythmias that go untreated and remain persistent can lead to heart failure, heart attacks, coronary artery disease. So many things can lead to the endpoint of a fluid overloaded state, which is what congestive heart failure is.

So that’s why I think it should not be missed, but it also, even in the United States. Your five year survival is 50%. So it’s a chronic progressive condition that [00:50:00] has significant mortality data associated with it.

Dr. Hare: And so CHF, in medicine we talk about HF, but a lot of folks associate that C at the beginning, the congestive part of that.

Why congestive? It brings you back to, having a cold and having a, having sinus congestion, , or upper respiratory infection. Tell me why congestion. What, what does that imply about this particular set of conditions?

Andrew Foster: That implies that the person is above their dry weight.

They’re retaining fluid.

They’re retaining fluid to where it could be they’re having fluid overload in the lungs pulmonary edema. It could be that they’re retaining fluid, particularly in the venous system where you’re seeing edema in the legs, edema in the abdomen. In severe cases, ascites you’re watching the jugular vein distend because of excess volume.

So the congestive state is this fluid overloaded state where you’re no longer euvolemic. You’re not dehydrated, you’re not euvolemic, [00:51:00] you’re fluid overloaded.

Dr. Hare: And that’s causing fluid to back up. And I always associate it with that, , the sinus thing. So things are getting congested inside your head.

You’re not, you know, things aren’t flowing out of your head the way that they should. In this case, this is fluid that’s backing up behind the potential source of pathology in the heart. Correct. it’s a very interesting state in that.

Some folks can have issues with this that are not readily visible on physical exam. So you have to have a significant amount of excess fluid before you really start to see that on the physical exam. Is that correct?

Andrew Foster: Yes. The earliest findings I’ll see are more left sided heart failure.

And by that I mean the person is noticing that they’re short of breath. When they lay down at night, orthopnea, they may be experiencing proxismal nocturnal dyspnea, starting to have more shortness of breath when they exert themselves. And then maybe you’re hearing crackles or you’re seeing on chest x ray evidence of pulmonary edema.

They [00:52:00] don’t necessarily have to have any right sided symptoms. They don’t necessarily have to have lower extremity edema at this point or JVD or any type of abdominal edema. But they still have heart failure symptoms and typical evidence of heart failure, particularly on the left side.

Dr. Hare: I tell students a lot about this, especially in the undergraduate classes, that the left side of the heart, left sided.

Heart failure, you think of the heart pumping blood to the periphery from the left side of that heart, but it’s not really the periphery that has the problem here. It’s the lung side, everything backing up, everything behind it. So that’s to me, congestion, you know, maybe traffic is better metaphor here where things are backing up behind the problem.

In this case, if the left ventricle is having an issue. Getting blood out to the periphery, it may be that it’s backing up to the lungs behind it or vice versa. And as a result, I find it interesting that the most common causes of heart failure on one side of the heart are often heart failure on the other

side of the heart.

Andrew Foster: Right. [00:53:00] So I say the most common cause of right sided heart failure is left sided heart failure. And part of that is just how the circulation, the circuit of the heart is. It’s a big closed loop. Big closed loop. It’s a big plumbing system, right? So you’ve got the whole right side trying to get blood, venous blood to the lungs to get oxygenated, return it to the right side and then get that oxygenated blood from your brain down to your toes.

And if the left ventricle isn’t able to accommodate a change in volume status, because The ejection fraction is weak, lower, or it’s a diastolic issue, or it’s a combination of the both, which is equally possible. And it was, the old term was combined heart failure, which was supposed to encompass systolic and diastolic.

Now we just say HFREF and HFPEF, or heart failure with reduced ejection fraction, heart failure with preserved ejection fraction. But… Either one of those dynamics leads to, an increase in pressure. That increase in pressure has got to go somewhere in the path of least resistance is into the [00:54:00] lungs because the lungs are such a low pressure system.

You know, a pulmonary pressure is supposed to be. And I’m going to, don’t quote me, but like 20 over 10 millimeters of mercury compared to a systemic pressure of, of one 30 over 80 or one 20 over 70, where is that pressure going to go? It’s going to go to the lungs and then everything just starts from

there.

Dr. Hare: Backing up to way to the beginning of our discussion about the kidneys, hypoperfusion, not enough perfusion of the kidneys. In the sense that the left ventricle is not able to provide enough of that perfusion to the kidneys. Now we’re looking at an inability to get rid of that extra volume. And now we’ve got a cycle that is leading to more failure.

Andrew Foster: Yeah, your kidneys are big Brita systems Somebody told me one time that your kidneys are like fish and they just love water. And so they, your kidneys love blood and they love a lot of perfusion and love things moving through it. And if all of a sudden the cardiac output has declined and your kidneys recognize that and they say, well, with a decline in cardiac output, I have less perfusion.

I’m going to [00:55:00] do things to you. get perfusion to increase because I want to keep it at this level, that’s what triggers your whole angiotensin aldosterone system, which the end result is to increase cardiac output by increasing preload, increasing afterload and increasing water retention and that.

This all leads to Ultimately, a fluid overloaded state,

Dr. Hare: Even if all of those systems are working well, it’s still going to put an increased burden on the heart in that moment with increased pressures and volumes to deal with somebody who is already in a pathologic state or having difficulty with.

That volume is going to get even worse in that situation. Right. It is a fascinating and it’s one of those terminologies that I always feel that is one that should be changed somehow with patients.

Andrew Foster: I’m going to a hundred percent agree with you. It’s some conditions get their name changed more frequent than others.

Why somebody has left congestive heart failure or heart failure has just left it, it needs to be changed because , it’s scary and it [00:56:00] sometimes gives the wrong perception, honestly.

Dr. Hare: As if something has, is non reversible in a way that they cannot be significantly addressed. That’s a hard pill to swallow for some folks, so the last one on the cases list here is coronary artery disease this would seem to me to be the bread and butter, or at least the thing that most people associate with the cardiovascular service in any given setting.

Tell me about a case with coronary

artery disease.

Andrew Foster: It is definitely our bread and butter is CAD. I think of one guy, one patient who came to mine, and this just happened last year where in his 50s, and he ended up in the cath lab due to a right coronary artery inferior wall STEMI.

And it was my discussion with him afterwards that I said, wow, this really probably could have been prevented. The STEMI was activated. The RCA was fixed. And remember that’s happening in such a fast time. So sometimes our ability to really sit down and talk with the patient is afterwards.

And because you’ve got a door to balloon time that you’re meeting for the emergency. So, and that’s what we were [00:57:00] doing. I was essentially doing the consult after the event. And I’m sitting there talking with him and he brought up his lipid panel and I said, your LDL in particular has been consistently over 160 for quite a long time.

And he said, yeah, and I’ve been actually concerned about it. I’ve brought it up to my primary care provider and said, I am concerned about it. Risk calculator really didn’t put him at that greater than 7. 5%. He didn’t have any other real comorbidities that said you really need a statin such as diabetes.

He never had a cardiovascular event before or for example, a stroke or mini stroke. but it was the fact that his lipids were. Not familial hypercholesterolemia, where they’re just insanely high, but consistently elevated. It was probably a genetic thing. And when they’re just above, the LDL was above 160 for how long?

And he’s saying, I’m actually concerned. And then the end result is an RCA STEMI. well, [00:58:00] maybe if. Over five years ago, this guy was actually put on a statin. may be, I mean, you don’t know, but maybe this would have never happened or maybe it would have been delayed even further. part of why statins are so important is because not only do they lower our cholesterol, particularly our bad cholesterol, but they help reduce inflammation.

And a STEMI is a plaque rupture, which is typically from inflammation. So that’s why I just kind of harp on that. And maybe if this guy had been put on a statin in the past, that inflammation would have been reduced enough that this plaque rupture might have not happened. And so luckily he had a good result.

But. when somebody is like, Hey, I’m concerned about this. And you say, well, based on this or based on this, yeah, maybe just diet and exercise. Sometimes that’s just not enough.

Dr. Hare: When I do my lecture on atherosclerosis and metabolic syndrome, I talk about, bile acid sequestrants and niacin treatments and all of these other categories.

And I always point out to my students, you know, the one that’s always [00:59:00] going to be at the top of this list are the statins and the, the ACC, AHE, AHA recommendations for treatment for hyperlipidemia are based on statins. It’s basically the on off switch for statins. And do you need statin or do you not need a statin?

They get used a lot these days. Maybe they don’t get used quite enough for a lot of patients and I’ve had this discussion on this podcast before about statins in that a lot of folks, hear about the potential myalgia issue and the potential side effect of statins that is myalgias and think, that, that sounds like influenza.

That sounds like always having COVID and , I’m causing it in myself. This viral prodromal muscle ache. And. I think that a lot of folks just shy away from it because of that. Not practitioners necessarily, but certainly some patients. They’ll hear from someone else in their life that they have experienced that side effect and not realizing that, yeah, we can, we can move between.

statins. We can move between classes if we need to. We can also titrate up and down. We don’t have to [01:00:00] try one medication, see if it has the side effect. You’re miserable for a while and then we either decide to keep it or not. You know, we can make changes to make that better. I think a lot of folks shy away from that as a result or or have that initial response of myalgias and then never go back to it, never allow themselves to be put back on a statin.

And I think that’s really a

shame.

Andrew Foster: In clinical practice, I get a lot of resistance from patients about being on a statin. They’ve all heard all different stories. I have plenty of patients who are doing just fine with their statin. And we tend to use the high intensity statin, atorvastatin, or risuvastatin.

Because of the patient population we have of already established coronary artery disease, congestive heart failure, and such. And really, the best statin to try, the best types of statins are the high intensity statins to try to really lower their LDL below 70. But I do tell people, give me a chance with, if we’re going to be working with the high intensity statin, let’s [01:01:00] try a lower dose.

You’re right. The recommendations are that you’re at this dose, but let’s try here and let’s just Start low and go slow You know with these high intensity statins, they tend to have a longer half life. So Maybe instead of trying this every day Can you try it every other day for me and just see how you do and let’s just see if we can get your body adjusted to this If you want to try it faster, if you want to escalate the dose faster because you’re feeling good, great.

And a lot of pushback I also get is, well, my cholesterol is good. My cholesterol is within the normal range. And I say, yes, but you still have coronary artery disease. You still have a stent or you still have had. coronary artery bypass surgery. And now the statin is not only to help preserve patency of your revascularization, but to most importantly, decrease inflammation, which all of that inflammation within the epicardial vessels is one of the things that led to this problem.

and so Taking it away from this is just purely a cholesterol [01:02:00] lowering agent and how this also works with your vascular system sometimes helps. Oh, I didn’t realize it was for that. luckily in the cardiology world, we’ve started to have additional lipid lowering agents Repatha, for example.

We’ve brought back Zetia. to use in conjunction with a statin or if the person has had a heart attack and they really can’t tolerate the max, the high intensity statin at the dose, High enough to lower their LDL below 70 or they just can’t tolerate statins in general to prevent that secondary event that’s where you do have something like Repatha, which is a injectable and it’s one injection every two weeks it is a different pathway than how a statin is utilized and effectively lowers the LDL so we do have that available and injectables, as you’ve mentioned on one of your other podcasts, injectables aren’t taboo anymore. You know, injectables are widely used in various type of conditions.

 Patients overall, a lot of them are quite [01:03:00] prone to using injectable medications.

Dr. Hare: Semaglutide may have helped with that a little bit. Seeing the some of the positive benefits of, of a drug like that, that is injectable and seeing how that can impact positively lives probably adds to some willingness in the, culture , to use those kinds of medications.

I’m curious, have you ever seen? The evidence of statin use up close, in other words, maybe a stress test pre and post statin use or maybe an angiogram that has really demonstrated a significant benefit that you’ve been able to, to really

see.

Andrew Foster: Yes. And I would say most of the time that evidence is seen with a repeat left heart catheterization.

Some of it could be due to the technology of the stent, but some of these stents are remaining patent for quite a long time, really long time, over 10 years and known non obstructive disease. Most importantly, non obstructive disease that hasn’t gotten worse. It is completely stayed stable.

It stayed at that 40%. It hasn’t progressed to 70 or more. And it’s due to the fact that the [01:04:00] person is taking their statin the way that they’re supposed to. Or somebody who’s had a heart attack before, who has remained on a statin, who has never had a heart attack ever again. A likely occurrence, actually.

A likely occurrence. Yeah. I, I do say that’s a testament to the statins.

Dr. Hare: you don’t see necessarily a reversal of plaque formation, but you do see a… Slowing to halting of that

Andrew Foster: most of the time, I see a halting instead of a actual reversal. I know that there is some documentation that there is a possibility of reversal, but I see mostly just a halting.

Dr. Hare: It’s still an amazing finding. It’s great. would imagine that therapeutic lifestyle changes TLCs, I should say, are still, even in a population that has a major cardiac issue, still a problem, still difficult to get a durable therapeutic lifestyle change out of a patient for that longer period of time, for that 10 years that you described.

How often do you see that really taking effect, that therapeutic lifestyle change?

Andrew Foster: I see with that, it plays a role, [01:05:00] but it’s usually not sustainable. What I mean by that is, people get excited to exercise and be healthy, and then they fall off the bandwagon. And so, we definitely encourage Daily exercise.

And I tell everybody, if you can, please just go on a walk and try to do that every day, if possible, try to do it, particularly after a meal, because there’s some definite glycemic benefits to aerobic exercise after eating, give your pancreas a rest a little bit, right?

Anybody who gets a stent, automatically gets signed up for cardiac rehab. They don’t have to go, but we recommend it because of that cardiovascular exercise is so important. almost like a silver sneakers thing, right? You get them enrolled, and you get them moving, and you do it with supervision, and all of a sudden, people start to notice the progress.

I’m doing this two or three times a week. But somebody is kind of putting my feet to the fire and I’m starting to see progress and I feel good and now I want to keep it going. So yes, eventually their cardiac rehab [01:06:00] session ends, but they feel good where I don’t want to go back to how I was feeling. I want to keep it like, keep it like this.

I want to keep this momentum going. So I do think that helps. Obviously. When it comes to lipids, management, atherosclerotic disease, diet and exercise are still at the forefront. It’s extremely important. It’s important to maintain appropriate weight. It’s important that we’re not eating as much sugar as we’re eating and exercising.

But I find that sometimes that is just not sustainable for a person based on their lifestyle

Dr. Hare: and familial kind of Influences you know, the genetic influence of hyperlipidemia is often a significant one and those are the folks who probably are an automatic statin in those situations.

Andrew Foster: Maybe it’s because of my, some of my inexperience, but I just found my first Familial hypercholesterolemia this year.

You’re inexperienced? I’m serious, I… I’m not buying that. I, I don’t know if I just wasn’t looking right and looking hard enough, or I just, I don’t know. But this, this, this particular person, I [01:07:00] couldn’t believe. The lipid numbers I was seeing, I’m talking total cholesterol in the 600s. I’m talking LDL. In the 300s, I was just, and then the first question I got was, okay, what cardiovascular event have they had?

And I said, none. They haven’t had a heart attack. They haven’t had a stroke. This person. I was reviewing their chart for an outpatient follow up. I was reviewing their chart and I was planning on just seeing them for high blood pressure. As I was reviewing their chart, I couldn’t believe the numbers I was seeing.

And I said, Oh my gosh, I’ve actually seen them in the past twice. And why didn’t I say anything about this? And it’s because we were just focused on a different topic. You only have so much time with a patient in the office. so I started looking at why is this person not on a statin at the very least.

I went through, they had spent some time with. Our health system and the other health system. So I’m trying to look at records of both and I see at one point they had developed transaminitis and that’s the reason why their statin had come off, but it had never been [01:08:00] restarted or tried. And so I’m having this discussion with her and she said, well, I’ve been on a statin before, but it got taken off in the hospital.

If it got taken off, it got taken off for a reason and it doesn’t need to come back. And I said, well, hold on, in this case. I do think we need to reintroduce this and I think we need to do even more testing. I think we actually need to check a lipoprotein a, and we need to see if that’s elevated if you want, I could try to set you up for a genetic test, cheek swab, to look for evidence of familial hypercholesterolemia. And what we ended up doing was repeating her lipids, got essentially the same numbers. She was willing to try back on a statin. I put her on the highest dose of Crestor, Resuvastatin. I then followed up with LFTs and a few weeks.

liver function is fine. No signs of inflammation or transaminitis. I checked a lipoprotein a and that was significantly elevated. That number strikes out 222. I won’t forget that. [01:09:00] And that just is a saying that not only does that help support the diagnosis, but that this person is definitely at increased risk of a cardiovascular event.

So I went to one of the cardiologist in the group who is a board certified lipidologist, lipid certified specialist, and I showed him the numbers, showed him the case and everything, and he said, this is familial, guaranteed. And not only should you have them statin, and put them on Repatha. And just drive that number, drive that LDL as low as you possibly can.

I’m currently in the process of prior authorization debate with her insurance company about the Repatha. She can take the Crestor. She can take the Zettia. Numbers have come down, but LDL is still nowhere near 70. She luckily has not had an event, but that was my First, like striking, this is familial and the numbers are so dramatically different than hypercholesterolemia that we’re used to seeing in [01:10:00] clinical practice.

Dr. Hare: I’m going to call you out, I guess, in your own defense because I’m guessing that a lot of the time that’s probably developed long before that gets to you. Yeah, in primary care or family medicine or internal medicine doing those kind of labs early in that process Long before they get to you.

Of course LDL is the number one factor in all of these concerns all these discussions in adding plaque to the to the coronary arteries and all the arteries in the body that are impacted by arterial blood flow, which is to say this is, this is a significant risk factor and a significant issue.

Andrew Foster: I

told her, you have a child. She is an adult as well, but I said, they need to be on a statin right now. They have this, there’s no doubt they can go get. Their lipids checked with their doctor, they can come here, however, but please have that discussion with them. If you want me to have that discussion, I’m happy to do that.

The only thing I haven’t done yet is the genetic testing, but the evidence that this is familial is so strong that unless the insurance company says we [01:11:00] really want to see that, I just don’t think it’s necessary. I am a big proponent of not over testing when you don’t have to

 I’m a big proponent of not doing unnecessary testing. And I think that if there’s enough evidence here to say you don’t need to, it’s not really necessary to genetically test and I’m not going to.

Dr. Hare: I personally have

caught one in my career, this individual’s, her lab work. was impacted and some, some of it was marked as unreadable because of triglyceride levels.

And so, you know, if you can’t read a CBC because of triglyceride levels, then, okay, yes, we, we certainly need to do something. In the same way that you have had one of those in your career, I’ve had one of those in my career as well. And we were able to, I don’t get to see the long term in my patient population, but we were certainly able to get things started get the initial lab work and then send to primary care for that

follow up.

Andrew Foster: You talking about the triglycerides just now makes me also think about this same, the patient I’m just talking about and how with familial hypercholesterolemia. For people listening, a lot of times the triglycerides are perfectly [01:12:00] normal. So total cholesterol is off, is off the charts. LDL is off the charts, but her triglycerides were well below one 50.

And when you do look at the literature, I spent some time on UpToDate, common reference source that I use. I was on UpToDate looking at that. And that’s one of the things that they do describe mm-hmm. , how the triglycerides are normal. Mm-hmm. . And when I looked at her previous lipid panels, they were always normal.

Where. For example, with a diabetic, their triglycerides can be very hard to control, especially until you get their hemoglobin A1C under control. So you can see the reverse picture. Just to bring that up.

Dr. Hare: Triglycerides, of course, being most impacted by the diet a little bit more variable relative to diet

but cholesterol certainly being more of a, a longer term and more well, more difficult to move number that LDL cholesterol, anything else about coronary artery

disease?

Andrew Foster: I would say it starts with primary prevention. Prevention. Don’t smoke. If you can help a person [01:13:00] not smoke, quit. If you can really aggressively and it’s, it’s having a lot of education with a patient. Sometimes the reason why that person is in our office is just to get another perspective on what

the primary care provider has been saying and they just want them to hear another set of have some second opinion of essentially saying the same thing. This is why we really need to aggressively control your diabetes is why we have to really aggressively control your hypertension, control your weight, try to get you to stop smoking all of these things because something like coronary artery disease most of the time can be prevented.

Which is, as we know, CAD is still a leading cause of death in the United States, right? primary prevention, primary prevention.

Dr. Hare: One of the things I talk about in our very early preventive medicine module, in the spring of the first semester that our PA students are with us, is Keep an eye on, as this year goes on, all of the things for which cigarette smoking is a risk factor.

And you’re [01:14:00] going to find that it’s more than half of our acute conditions, and a lot of chronic ones as well, have risk factor increases with cigarette smoking for a variety of reasons. some of the more satisfying moments in my career have been both in PA school and in my family medicine career have been around finally helping someone to stop smoking because that’s a, it is a very difficult thing for any patient to go through, but very worth the while to make it happen.

 Let’s talk about, the potential referrals from, other areas of medicine. The possibilities are endless it seems, but, chest pain is obvious and kind of an obvious one that we talked about knowing that there are also atypical presentations for a lot of these things.

Andrew Foster: Whether it’s a referral. From the emergency department, whether it’s a patient who was referred to us in the outpatient setting and they’re coming in as a new patient to the office. A person who has been admitted to the hospital and has been in the hospital for a few days and has developed chest pain.

I [01:15:00] mean, chest pain is just such a common reason to say, Hey, cardiology. Can you take a look at it? Maybe because there is the true concern that there’s something actually. Related to the heart going on, maybe it’s to gather some reassurance. I mean, as much as maybe people refer or ask for us in consultation for some guidance and reassurance.

We do the same as well in cardiology. When we ask a different specialty for help, it’s some guidance and reassurance. a lot of chest pain is actually not cardiac related. That is true. Yeah, but. At the same time, you don’t want to miss something. So hey, if you, that’s what we’re there for.

Dr. Hare: And then the abnormal EKG kind of plays along with that as well.

Even on a screening EKG, you see an odd finding and uh, going to the folks who do this on a daily basis all day long, every day in some cases is a really helpful and comforting thing.

Andrew Foster: Yeah. an abnormal EKG can be as. Vague as a nonspecific T wave change.

It can be a new arrhythmia. It can be, [01:16:00] something significant, QT prolongation. There’s so many different things that can happen with an EKG. Sometimes lead placement can really affect the outcome. But either way, an abnormal EKG, particularly in a pre op workup, and that goes to one of my other things pre op, is a lot of times the person is getting an EKG prior to a surgery, there is this odd finding.

It doesn’t necessarily say anything specific, so we say it’s a non specific finding, but You know what, we’re gonna have you see cardiology because maybe you have other risk factors. So the question is, the reason why we’re sending them to you from a pre op standpoint is, do you think this EKG alone is good enough?

Or do you think that they need something else, such as an echo, a stress test, or the ultimate being a heart catheterization prior to their surgery? And that all depends on risk factors, their story, and what type of surgery they’re having. , uncontrolled hypertension is when you’ve really run into a [01:17:00] resistant, maybe you’ve actually found a secondary cause, which is about 5% of cases.

Mm-hmm. , but that type of patient should be referred to cardiology and particularly a general cardiology who feels comfortable with using some not so typical medications to treat blood pressure.

 In some cases I think of medicines like minoxidil or clonidine where there can be significant side effects, number one, and two, it’s just not, your usual go to first line agents in particular, but maybe needed for your uncontrolled resistant hypertension.

Dr. Hare: I always think of. Centrally acting medications and hormonally acting medications as being two of the ones that would fall into that category of, boy, these are significant adds to someone’s medication list.

Andrew Foster: Absolutely. you think of minoxidil with the potential of pericardial effusion as a side effect.

Maybe you need to get an updated echocardiogram afterwards just to make sure you don’t have a significant. effusion after starting this medication.[01:18:00] that’s just an example.

Dr. Hare: What do you And what does your service think of medications and speaking of minoxidil?

Medications that have multiple uses in an individual patient, for instance, someone who is, let’s say, trying to, on minoxidil for hair regrowth, and then suddenly we’re thinking of this as maybe a blood pressure change medication as well. How does your service see that kind of overlap between, same medication, two different conditions?

Andrew Foster: We definitely see it. We definitely see it. If it has the ability to, the phrase kill two birds with one stone, , let’s do it. when it comes to , diabetes and coronary artery disease, right?

Yeah. Yeah. So, well, let’s just take Jardiance for example. Can we help your diet? we’re not in the world of treating diabetes, but you have congestive heart failure with a reduced ejection fraction, coronary artery disease, and you’re not on an SGLT2 inhibitor and there’s no contraindication.

Maybe we should get you on that. It can help your hemoglobin A1C further, [01:19:00] plus it’s helping your heart. So, love that situation . That’s probably my best example right off the top of my head.

Dr. Hare: I have come across a couple of situations where patients, you know, especially coming into our hospital, we see individuals with a long list of medications.

And one of the concerns, I think, that we have seen amongst our medical hospitals services is that if they have that medication on… With two different indications, somebody might take that medication off, not realizing that there is in fact a secondary effect, a secondary diagnosis that that’s treating and then losing that without really having a sense of it is often a concern in my setting.

And of course we’ve got, central actors, anxiolytics, benzodiazepines, a lot of different medications have cardiac impact. we talked about the endocrine side of things too, they also have psych impact. And so trying to keep those two things separated sometimes , is a priority with our patients.

Andrew Foster: That line of thinking is also why I’m also a little bit hesitant to make medication [01:20:00] changes without speaking with the primary care provider first, because I say your PCP is the nucleus of your health care and everything, as you’ve mentioned before, comes back to them.

I think you used a quarterback reference and it’s a great reference, but I don’t want to step on their toes because there is the I’m, I’m in cardiology. I do have some blinders on and I am looking at a few things in particular where they’re looking at the whole field and I certainly don’t want to potentially step on their toes by making some changes.

So simple discussion if available. And a lot of times we can get a hold of people don’t even have to pick up the phone anymore a lot of times to get a hold of somebody and send a message and just talk about it and say, what do you think about this? Is this cool? And vice versa. They’ll sometimes ask me, Hey, I’m seeing this person.

What do you think about this medication? SGLT2 inhibitors? I’m bringing those up because they’re kind of a hot topic. I see that they’ve had congestive heart failure. I see that they have diabetes from primary care perspective. I’m thinking [01:21:00] about adding this on. Do you have any, Um, objections to it?

No, go for it. Let’s, let’s do it.

But I want to just kind of read off this list here. Like, you know, dyspnea on exertion. We talked about chest pain, dyspnea on exertion. You know, maybe this person has already seen pulmonology. Maybe they’ve already had PFT testing or something.

And you know, let’s just make sure that the heart is not or is part of the cause here and How that can be treated, fixed, helped. Abnormal EKGs, we’ve talked about pre op, uncontrolled hypertension, obviously heart failure, and any type of new arrhythmia. A lot of people who end up with atrial fibrillation in the PCP office, they’re in rapid AFib, so they’re going right to the hospital, but then we’re intercepting them at the hospital.

Right, right. Occasional where person got diagnosed with atrial fibrillation, but they were rate controlled. It’s possible. There’s reasons that that can happen. And then they’re just being referred to us as, Hey, this is a new, a fib. PCP already went ahead and put them on an anticoagulant [01:22:00] Elequis or Xarelto.

And I at least got them on anticoagulation, but now I’m handing it over to you as to what else do you want to do with this person?

Dr. Hare: In my primary care setting, my family medicine setting, I should say, in the hospital somebody comes in, they may not have been taking care of themselves, we see that a lot in our populations come in, have not been taking care of themselves, have not seen someone for some time.

One of my favorite things about working in family medicine. in a psych hospital is that I’ve got all of those, services on a phone call, I can curbside somebody and say, Hey, I’m going to send this patient to you when they are discharged.

What do you want me to do to set them up before they walk out the door? Especially for a patient who has difficulty with follow up. That really makes a huge difference in their ability to actually follow through with that treatment

 There is a palpable relief at times. When I find a cardiology note somebody’s chart or an endocrine note in somebody’s chart that this has been identified and worked up previously, we’ve got something in place. At least follow up is in place, whether or not there’s a medication on the list or not is, then the next question.

 I’ve heard you say many times, somebody comes in with a [01:23:00] good story. You add that into your descriptor of somebody who’s got, who’s got a cardiac issue. So what’s your definition of a good story then?

Andrew Foster: Good story. I’m referring to chest pain. I a lot of times say chest discomfort.

And a good story is somebody who has The typical risk factors who’s coming in with typical angina symptoms. So somebody who has hypertension, high cholesterol, maybe a history of tobacco abuse, particularly smoking or actively smoking, and may or may not have diabetes, likely has a family history, for example, of coronary artery disease doesn’t necessarily have to be premature.

Could be coronary disease that’s resulted in a heart attack or just a finding. a story of, I was out playing golf. And I’m an avid golfer. I golf three times a week, maybe more. I play this one course in particular. I was walking up this hill and man, I know it was a hot day, but I was sweating more than usual.

I got this pressure in [01:24:00] my chest that I’ve never had before and it didn’t go away right away. I stopped. I didn’t, I skipped that hole. I just kind of got some shade and this lasted for 15, 20 minutes before it went away. That’s a good story. I was shoveling snow here in Pittsburgh. I’m shoveling snow and I really got a lot of chest heaviness.

Halfway through clearing my driveway, that’s not usual for me, or as easy as a push lawnmower on a flat surface, I actually had to stop because of the chest discomfort and it was a tightness or is squeezing. It’s just right here. And when people are describing it to you, it’s almost as if they don’t realize it’s their heart.

But then when you say, I think you’re having what we call angina, and you go about explaining that, that’s, yeah, that’s what I think. I think it’s my heart and you know, a good story is likely going to lead to a heart catheterization, sometimes over a [01:25:00] stress test. And the reason for that is because if you do a stress test, which is not the gold standard end all be all test.

There are false positives and false negatives that can be associated with a stress test. Even though we have various types of stress tests we can do, if the test comes back ultimately negative, or a low probability, and the person still has symptoms and you send them home, I feel like… Garbage sending that person home.

So I really want to know definitively what’s going on. And with a good story, sometimes that’s all you need is a good history, good physical, good EKG, maybe a troponin, and send this person to the cath lab and definitively know. But that’s a good story.

Dr. Hare: So a good story is a bad story, or at least one that you can dig into, I guess, as a cardiology practitioner.

Andrew Foster: Yeah. It just screams all the alarm bells. That this is either that this is unstable angina or this is the beginnings of a heart attack and we should invasively work this up with a heart [01:26:00] catheterization.

Dr. Hare: So along those lines, along the good story lines, what is your piece of advice for students, especially going into clinical year or getting a new job

Andrew Foster: going into clinical year, don’t be afraid to ask questions.

I think sometimes, and I did this myself and my clinical year is that’s an opportunity to really learn and just kind of continue to advance the knowledge that you have. Maybe see some examples of things that you were learning in, in the didactic classroom. But don’t be timid to ask questions. There is no such thing as a bad question.

You’re there to learn. You should ask questions. And sometimes you’ll find that you’re stumping the expert. And that’s a good thing. Because then you can dig into it together and so ask questions, but also be proactive. Don’t be the person who sits in the corner and waits to be asked, do you want to do this?

Obviously, when a student is with me on a rotation for an elective, it’s Sometimes harder to say, [01:27:00] can I do this? Where in the ER you might say frequently, can I do this? Can I do this? Can I help with this, when you’re on a rotation with me, for example, try to go see every single patient you possibly can learn about this person as much as you I tell people practice as much of the physical exam as you want to, because this is your opportunity to do it.

And I may not practice percussion and egophony as much anymore, but if you want to practice, practice. Yeah. We’ll practice with you. Yeah. Be proactive. If you’re proactive, it always looks better and you’ll get more out of the rotation than sitting in the corner waiting for permission. As far as looking for a new job, I would say don’t just jump at the first job that’s available.

Because there is a chance you may end up getting into something that you’re just not happy with. So really think about what you want to do, what you’re interested in. I know you’re just graduated. You’re excited and you want to get working. You want to make some money, get it. But just because the first thing becomes available, if it’s not really what you want to do.

Don’t just jump [01:28:00] at anything.

Dr. Hare: sometimes hard when you’re hungry, I suppose. That’s right. Hopefully it’s all good experience, but I totally agree with that.

Thank you for all of that. Anything else you wanted to add

Andrew Foster: I just have so much fun talking with you. Oh, it was a great time. I appreciated it too. We always have a great time talking about medicine and cases and things. It’s really a privilege and an honor to be here to be able to do this with you because we have talked about it a lot and I’m glad we finally got to make it

Dr. Hare: Well, the honor is all mine and certainly anyone who listens to the podcast.Podcast. Many thanks to our esteemed guest, Andrew Foster, cardiology, PAC, that’s it for now. Be sure to check out the podcast website at beexcitedhq. com for more episodes, show notes, and full transcripts of every show. Email us at contactbeexcited, one word, at gmail. com with questions, comments, or future show suggestions. And of course, follow us on Facebook and Instagram at beexcitedpodcast for news, new episode notifications, [01:29:00] and maybe a picture or two. Thanks for listening and remain excited.