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Most people think about their health when something goes wrong.
Next Phase Human is for everyone who wants to start thinking about it before that moment arrives.
Hosted by Dr. Sandhu — a cardiologist with a focus on prevention, longevity, and whole-body wellness — this podcast brings together physicians, researchers, and wellness professionals for honest, evidence-based conversations about the topics that actually move the needle on your long-term health.
Each episode covers the intersection of cardiovascular wellness, modern medicine, lifestyle optimization, and human performance — translated into practical, approachable conversations for professionals, business owners, and anyone serious about living better longer.Topics include heart health, metabolic health, sleep, stress, nutrition, longevity diagnostics, wearable technology, recovery, burnout, and the future of preventative care.
This is not clickbait wellness. This is a forward-thinking physician who believes the best healthcare happens before you need it.
New episodes weekly.
Have you seen energy drinks cause significantly abnormal
rhythms in young people?
Their heart rate variability changes because the heart rate is not changing too
much. So to answer the question is yes.
Welcome to Next Phase Human podcast.
This is a space where we talk about all things related to health,
and health is not defined by set tracks of conventional medicine or
wellness medicine or what you do in your day-to-day life.
I do believe health is a compendium of all these things.
And plenty of times when you're in doctor's offices,
of course, there's a limit to that time, and there are questions that are left
unanswered on different topics. Those topics may be related to health, may be
related to procedures you may or may not need, and may be related to some of
the day-to-day questions, what you can do about prevention.
So this is a space to have all those conversations
with the goal that as we age,
a number does not define our limits, and our genes don't become our
destiny.
Unlocking the next phase of health, this is Next Phase Human.
I'm your host, Rasham Sandhu, and today I have with me is Dr.
Gurjit Singh, a renowned electrophysiologist, former
director of electrophysiology lab at Henry Ford, currently
chief medical officer of California Cardiovascular Institute, and
medical director of AFib and electrophysiology at Dignity
Health Bakersfield and Adventist Health Bakersfield, California.
Welcome, Dr. Singh.
Thank you, Dr. Sandhu, for having me and giving me this opportunity.
Can you tell us
a little bit about yourself, what your background is, and what you
do in day to day?
Absolutely. So I'm a cardiac electrophysiologist.
It's basically a heart rhythm doctor.
I call myself an electrician, so most patients understand that pretty easy.
I did all my training, I did my medical school in India and then came
to Henry Ford Hospital in Detroit, Michigan, where I did my internal medicine
residency for three years. Did a year of heart-failure
transplant training as well. Was not a fellowship, but was
an additional training before I joined the cardiology fellowship at
Henry Ford.
So I switched to cardiac electrophysiology, so did my EP fellowship at
Henry Ford and stayed on as faculty for almost eight years at Henry Ford, where
I led the EP lab, was the director there, trained
cardiology fellows as well as EP fellows and then medical students.
So I had a busy academic practice. I ran the robotic programs,
founded the Society for Magnetic Navigation, called SCRN,
before moving to Bakersfield. And been here for
almost four and a half, five years now with Dr.
Sandhu, and then we run a busy private practice, where I
not only practice cardiac electrophysiology, but all aspects of cardiology and
primary medicine as well. So as you rightly said, we got to
age well.
And today our topic will be atrial fibrillation, but before I'll
answer my claim to fame,
I end up discovering when iPhone 12 got launched, the
iPhone came with inbuilt
magnets inside the phone, which allowed the phone to be
charged on the Qi charger.
Mm-hmm.
And we
as an electrophysiologist, I implant pacemakers, defibrillators, and these
devices have a fail-safe mechanisms inbuilt.
For some reasons, if these devices fail, we can put an
external magnet to change their
capability of what they do.
So our hypothesis was that putting an iPhone magnet or iPhone itself
on a
live defibrillator should not affect those
devices because the magnetic field is small.
But to our surprise, when we tested in a patient with appropriate approvals
and everything, we showed the iPhone 12 actually can turn
off a patient's defibrillator.
What it does is basically makes the defibrillator stop looking at the intrinsic
heart rhythm, and that in turn deactivates a device.
So we published this
patient data in Heart Rhythm Society, and it became an international
sensation because we all knew that magnets are bad for ICDs and
pacemaker, but nobody had actually proven in a real human for the first time.
So from there on, basically, I started getting calls from Apple and
then all the FDAs. So I was on the panel for the FDA,
with all the device companies to figure out what's the best recommendation.
What do we do? We went back and forth.
Should the device companies should change their sensors inside, or does
Apple should take away the magnets?
And the end result was basically the recommendation came in that
patients with pacemakers and defibrillators should stay away from strong
magnetic fields, at least six inches away.
So keep your phones or anything which has magnets six inches away from your device.
So that'll hold true even today for any iPhone or any other phone for that
matter.
Correct.
I tested devices. I took Apple Watches,
headsets, and actually checked the magnetic field and everything.
Even your regular phone, wherever there are cameras, there is a magnet inside.
So we all generate magnetic fields.
But again, the bottom line is keep six inches away from your body.
So that'll be kind of a safety just to kind of explain it to people
that your defibrillator is a device that will shock
you internally if there's an abnormal heart rhythm, essentially
saving your life. So if turning off therapy can be quite problematic.
Correct. That's absolutely correct.
Now, the chances of that happening is very, very low, but there could be one
patient sitting somewhere laying down with a phone in his pocket, especially
males have the tendency to put their phones in the pocket, and you could turn off
your defibrillator, and you may not get the therapy.
Perfect. Well, that's good to know. And let's start today.
We're going to focus primarily on atrial fibrillation
Millions of Americans have it. There are several misconceptions
about it. A lot of people
may know what AFib is or have a basic idea, but there are a lot of
misconceptions and fears, and we'll go through them one by one.
So first of all, for
listeners who are not in medicine,
can you tell us, for a layperson, how would you explain what
atrial fibrillation is?
Yeah. So atrial fibrillation, as the name suggests, atria, and they are
fibrillating. So before we go into the disease, we need to know what the normal
human heart does. So the human heart is basically the size of your fist, sitting in
the middle of the chest. It's like a car engine. It's pumping blood.
It receives blood, it sends the blood to the lungs to get it cleaned.
The clean blood comes back to your heart, and it gets pumped out.
So the heart has four chambers, two top and two bottom.
The top are called the atria. The bottom are called the ventricles.
The atriums, they contract first, push the blood down through
the valves into the bottom chamber, and then the ventricles will squeeze and push
the blood out to the body and to the lungs.
And a normal human heart, if you hold it in your hand, it will not beat on
its own. The heart is a muscle. It needs a signal.
So me and you are born with a pacemaker given by the
higher power. It's called a sinus node, sitting in the right top chamber.
That actually creates your heartbeat, 50 beats a minute, 60 beats a
minute. So think about it as like a car's battery.
It's sending impulses every 60 times a minute.
That electricity travels in the top chamber, makes the top squeeze, the
atrium, and then there is a wire inside the heart called the AV node,
atrioventricular node.
So just to clarify, it's a highly conducting tissue.
It's a highly conductive tissue. The whole heart is a muscle, but then it's also
conducting electricity, and it's the only organ in the whole body which is actually
moving. Rest, everything is stable and stationary.
This is the only moving
organ, which is squeezing and conducting electricity, so a very highly
complex organ. So anyways, the blood goes to the bottom chamber and then
comes out of the body. So that's a normal human heart, and when we
do an electrocardiogram, we can see the heart's electricity.
So the top beats first, then there's a time delay, and the bottom follows.
On an EKG, it's called a P wave and a QRS.
So when me and you right now in normal rhythm, our heart is beating at 60 beats a
minute, so that's normal sinus rhythm. So now we know what normal is.
When people or patients go in atrial fibrillation, the top
chambers stop listening to that pacemaker and start
fibrillating. It starts beating in a very irregular,
chaotic manner. There is no rhyme and reason.
A lot of things we do in electrophysiology have some circuits.
We can define the wavefront and things like that.
During atrial fibrillation, the top chambers are basically squeezing in a very
haphazard manner. So the top chamber loses
their squeezing capacity, and the rhythm becomes irregular.
So the definition of an atrial fibrillation, you have to have a
30-second documentation of an irregularly
irregular rhythm on an electrocardiogram or a variable or any
kind of recording of the heartbeat.
So that is what the definition of atrial fibrillation is.
So a lot of these
thought process will come, okay, is every irregular rhythm
atrial fibrillation? Because people get alerts on their variables all the time.
So would they worry every time they see an irregular
flag on a variable? Is it AFib always, or could there be other things that it
could be pointing out?
Correct. Just somebody has an irregular rhythm doesn't mean they have AFib.
Again, you have to look at the data.
If you're doing a one-minute EKG, you have to show it to somebody.
See, all these variables or all these
devices, they have what we call a PPG, a
photoplethysmography.
Mm-hmm.
So what these variables, like an Apple Watch or a Garmin or all
these sensors, they
send a
light signal towards your wrist or towards your palm, and then the
light intensity changes based on your blood flow.
Mm-hmm.
So what these devices are doing, they are actually measuring from one
beat to the second beat. That's all they know.
But they don't know where is the beat coming from.
If you have an extra heartbeat called a premature atrial contraction,
called a PAC, or a premature ventricular contraction, called a
PVC, that can fool these devices. So again, as I said above,
loss of a normal P wave on an electrocardiogram or a
variable, and if we show it for 30 seconds consistently,
then we call the rhythm as atrial fibrillation.
But again, to answer your question, if your watch or your variable
tells you that there is some irregularity, it's better to get it checked.
And generally, the thought process always has been heart disease is a
disease of older people. Could young people have AFib, too?
Yeah, that notion is changing. Atrial fibrillation,
when I was in training, this is what my mentor taught me, that it's the
wrinkle of the heart. But I can tell you,
our average patient now who are coming to our clinics in atrial fibrillation, I'm
talking about 30s and 40 years of age.
Mm-hmm.
The whole health, and that's why we're doing these podcasts, our people
are not aging the way they're supposed to age. So it's all connected.
So the disease is manifesting early.
Plus, also now because we have all these variables, we are detecting more of these
rhythms. Before, we didn't have the technology.
So there are the two explanations for early detection of these rhythm problems.
So
could there be,
do you feel AFib, or do you not have to?
You could still have AFib and not know about it?
Absolutely. So almost half the patients who I see on a daily
basis feel AFib, and half do not. Especially if you're a female.
Mm-hmm.
They don't feel their AFib, and on the worse, if you're diabetic.
As we all know, diabetic patients have changing in their autonomic nervous
system. They have nerve injury or neuropathy, so they don't feel their symptoms.
So the common symptoms of atrial fibrillation are mostly a fast
pulse, an irregular pulse, some unease in the body People
can get short of breath, they can get tired.
Fatigue is a very common symptom for atrial fibrillation.
If you are underlying heart disease, you have low blood pressure, you can get
almost passing out symptoms. But the most common symptom my patients
tell me is that something is not right in my body.
That's the most common symptom I see from atrial fibrillation.
So if they feel they're just not feeling right, regardless of age, could be
a younger person, could be an older person, this could be one of the things.
Correct.
It may not be the thing, it could be one of the things you look for.
Absolutely. If you don't have an alternative explanation, it could be
atrial fibrillation.
Got it. So I presume, how long have you been practicing
now in this space?
Practicing electrophysiology since 2014.
So you must have seen thousands of AFib patients and treated.
That's what the bread and butter for all the electrophysiologists in this country
is.
So tell me a couple stories which really stick
out,
shocking stories.
What did you find most shocking when you treated a patient like AFib?
What sticks out in memory?
So, obviously, we treat a lot of AFib patients.
And I'll tell you one more thing, no two AFibs are same in terms of their
presentations and in what they have inside.
So a lot of patients say, "Oh, this patient had an ablation done, this had this
done, and they did this." So I'll tell everybody, please do not compare your
atrial fibrillation to other patients.
So again, atrial fibrillation causes a lot of problem.
It creates the blood to clot in the heart.
So I've seen patients who their first presentation is a massive stroke in a young
person. So again, that is a shocking story.
If somebody would have detected AFib early on a patient, something could have been
done. A lot of AFib. AFib increases the risk of heart failure five
times. It increases the risk of stroke five times.
It actually changes your mortality.
Patients who have atrial fibrillation, they are on a different trajectory
altogether. AFib brings chronic kidney disease, worsened
kidney impairment. The worst now, or the new data coming out, atrial fibrillation
is linked to dementia, and there is some data showing that early treatment of
atrial fibrillation with ablation does help or prevent some dementia.
I'll tell you a recent story. A patient came to me, atrial fibrillation diagnosed
almost 15 years ago.
And I can tell you, most people agree that the longer you stay in AFib,
now we're talking about two different kinds of AFib.
The AFib, one is called paroxysmal AFib, when the AFib episode comes and
goes, goes away on its own, or we do something.
That's called paroxysmal atrial fibrillation.
If you stay in the rhythm continuously for more than seven days,
we call it persistent AFib. And these definitions
help us figuring out the underlying pathophysiology or what is
happening inside the heart at the molecular level or at the structural level.
So the shocking story, this patient for 15 years of AFib has heart
failure.
Everybody abandoned his rhythm, and they said he came to me with symptoms of
fatigue, tiredness. His heart pumping was somewhat weak, and we
discussed that it's too late now. He's a relatively young person.
And usually at that stage, if we feel that somebody's having symptoms from
AFib, we usually give them a strategy called an AV node ablation, pace
and ablate. Patient said no. He said, "Can you do something about it?" Long story
short, I started treating his AFib.
We did procedures, and we also have the capability now of doing what we call
an epicardial ablation. So when I do my procedures, I go from inside the
heart. I work with some surgeons who can go-
Can you explain it for the listeners what AFib
ablation is before we-
Correct. Ablation is a therapy where we go inside the heart,
not by opening the chest. We go through the groin to the femoral veins, and we go
inside the heart with tiny tubes called catheters.
Those catheters help us map the atria electricity,
and based on what the scientific literature has shown,
pulmonary vein, so all the blood coming back from your lungs, you have
a right lung and a left lung. Both of these lungs have these tubes called pulmonary
veins. These tubes are draining blood into your left upper chamber.
Right before they enter the heart, the lining of these tubes is where
90% of the AFibs actually get triggered, so that's called pulmonary vein
trigger. Back in 1999, Michel Haissaguerre from
Bordeaux, he's the one who actually discovered.
They took patients with atrial fibrillation, they put catheters, mapping catheters,
and they waited for AFib to start, and they figured out 90% of the AFib
started in one of those four tubes.
So the ablation in layman explanation is we are going to go inside your heart,
and I'm going to isolate, create electrical scar in your heart around
the openings of those four tubes. You can do by burning, called the radiofrequency.
You can do by freezing, called cryo energy.
And these days, the new kid in the block is called electroporation or pulse field
ablation. So once we isolate those four tubes, the
AFib can start in those pulmonary veins, but it will not enter your
main heart, and you will remain in normal rhythm. So that's what an ablation is.
So what we do is called endocardial. We're going from inside the heart.
On that patient we talked about, we did also what we call an epicardial.
Heart is a thick structure. The atrial tissue, the wall is at least four to six
millimeter, depending on which way you look at it, and then you can also burn
from the outside. So believe me or not, and that patient has been six months after
treatment. He's in normal rhythm after 15 years of AFib.
Heart failure's improved. His life has changed.
So again, I
see those shocking stories pretty much every other day in the clinic where
we have done something for AFib.
And is it correct to say,
in the past, so you defined atrial fibrillation as paroxysmal, which is the early
pathway, and then you defined it as persistent, which is
well established, has been there for a long time.
Right.
And those are harder to treat. So is it a fair statement several years ago that was
really not considered treatable, that you will just manage it?
You're not going to try to get the person out of it?
Absolutely. So there were a couple of trials which were done
in olden times. We call now them olden times, and the famous one is called the
AFIRM trial, where basically they took patients with AFib, persistent and
paroxysmal, mostly paroxysmal
Half the group was treated with the regular medications, control the rate, keep the
blood thinners on, and see what happens. The other one had ablation done.
And that time, the trial with those technologies showed it doesn't
matter you do rate control versus rhythm control.
You keep them in AFib or you don't keep them AFib, patient have the same outcomes.
Things have changed. 20 years later now with the new technology, with the
aggressiveness, and with more early diagnosis, I believe the
trajectory after an AFib ablation for most patients is changing
in a positive way.
And then there is something called long-standing persistent.
When somebody's in AFib for more than one year, we call them a long-standing.
And the reason we define these things is, again, AFib is not just one
particular disease. A lot of things I do as an electrophysiologist, people are born
with extra wires called WPW, AVNRTs.
We go in the heart, actually find the little tiny wire, and burn it.
Those are curable rhythms. AFib is a final representation
of many different things happening to your heart, and the final disease shows up
as an AFib on an EKG. But behind the AFib, we're talking about the triggers we
talked about.
So trigger is one thing, but the second component of the atrial fibrillation world
is the substrate. What is happening at the structural level in the
atrium? What is causing fibrosis?
The more scarring, we call it scar.
When I go inside the heart, when I make a 3D map, I can see which part of the heart
has scarring and not. So the more scarring,
you have a bad substrate, the longer you're going to stay in AFib or you become
persistent AFib. The third thing we talk about is the ionic level.
At the cellular level, what is changing?
And the fourth is your genetic predisposition, and the fifth is your age.
So all these things actually combine together to bring out paroxysmal versus
persistent atrial fibrillation.
So when you talked about substrate,
just to clarify, we are talking about modifiable risk factors
that people can fix in their day-to-day life. What would those be?
So again, as everything in medicine, there is something we talk about risk factors
or the comorbidities for a patient.
So there are modifiable risk factors, just like for atrial fibrillation, and a
non-modifiable. So what are non-modifiable risk factors?
Number one is your age. You cannot change your age.
You're going to grow old, right? Number two is your genetics.
We know that non-Hispanic whites have the highest incidence of AFib.
Then comes the Hispanics. Actually, having a African
American descent or
Black Americans have lower AFib. And there is data that because the
atrias are smaller, they actually have less AFib compared to whites,
and then obviously Asians. So there is some genetic predisposition.
European whites have the highest risk of gene, and there are so many,
we call this single nucleotide polymorphism. Now, there is a big studies going on.
So there are some genes which predict that you are going to have a higher risk of
atrial fibrillation. So again, those are non-modifiable. We cannot change them.
What is modifiable is your standard, your hypertension, your diabetes,
obstructive sleep apnea, smoking, weight,
obesity, exercise. All those are what we call the modifiable risk
factors. All these things work, and diabetes.
All these things work together in one form or fashion to create
the right milieu or the substrate to bring out the AFib.
And then,
as I said, the AFib, usually there's a trigger for AFib, and then there is
something to maintain the AFib. So there are two separate things in different
patients, or there could be two same thing in the same patients.
A lot of patients start the AFib as what we call paroxysmal.
AFib starts, goes away. There are some patients from day one,
they become what we call persistent AFib.
The moment they go in AFib, they stay in AFib.
So again, there is something going different from those patients.
Okay. So just to clarify, all these modifiable risk factors or
non-modifiable affect the top chambers in a way that creates
scarring in an erratic fashion to create irritability and spread
it to suppress your normal rhythm and create irregular rhythm.
Absolutely.
Correct.
And then on top of all this, what actually runs the
main thing behind all this is actually your
neurosystem, the autonomic nervous system, and the brain.
Remember, mind over the heart always, right?
So the brain is doing something to your heart as well.
So it's the balance of your sympathetic and your parasympathetic.
As we all know, humans have two different nervous system, the
fight-flight-
Mm-hmm
... which is your stress, which is your adrenergic or the sympathetic nervous
system. And then the other one is called the vagus nerve, the 10th nerve, which
keeps things calm down. So this balance, whatever changes
this balance can bring out AFib or promote AFib.
And we know at a cellular level, like if you take a single
cell and put two probes in it, and you actually look at the electricity, we
know that too much vagal tone, too much cholinergic, they
actually changes the electrophysiology of those tubes we talked about.
That can trigger AFib. Too much sympathetic tone, we all know that,
high adrenaline levels. Caffeine or too much exercise or things which
increases the-
Energy drinks
... energy drinks, or stress. Whatever increases your adrenaline,
it irritates you through the beta receptors.
It's going to bring out, irritates the heart, and can bring out atrial fibrillation
at the top or bad rhythm from the bottom chamber.
So again, these two things, the balance.
The moment that balance changes, we are predisposed to these arrhythmias.
Just for curiosity, have you seen energy drinks cause
significantly abnormal rhythms in young people?
I see a lot of young peoples coming with these energy drinks or the vaping
or drinking too much of coffee. Anything which increases,
just common sense, it is going to bring out some kind of arrhythmias.
Usually, the resting heart rate is high.
Their heart rate variability changes because the heart rate is not changing too
much. So to answer the question is yes.
Okay. Perfect. So we're going to go through, there is
a lot of talk about, so there is disease and there is
cures that people talk about, whether that be medical or non-medical, and some of
those are
good recommendations and suggestions, and some of those are just urban legend.
So we're going to try to myth bust a little bit here.
Absolutely.
So short answers, let's go through them.
So coffee, can it cause AFib?
So again, a lot of the answers I'm going to give you, in the world of
electrophysiology, is cardiology.
There is a positive and negative, and all the studies keep fighting with each
other. But there is data, somebody did actually trial complete
coffee abstinence versus a cup of coffee, and they look for AFib
development. And the data shows that coffee in moderation
does not increase the risk of AFib.
So I don't stop my patients who have AFib to completely restrict.
Yes, if somebody's drinking four cups or 10 cups a day, that is a problem.
But a cup or two of a regular caffeinated coffee, there is data
that it does not increase the risk of atrial fibrillation.
For our listeners, just to clarify the dose in the study, like one cup, two
cups?
One cup. There's a trial called the Decaf Trial, 200 patients.
Again, not a big study, but it's a randomized controlled trial, so absolute no
coffee versus one coffee, and they showed no major change in atrial
fibrillation risk.
So for your patients who have either AFib or who have
had ablation, what do you tell them typically?
Can they drink a cup or two of coffee a day?
I tell them, what's the point of me doing a procedure or something if I
cannot make your life easy or don't let you enjoy your life?
If you enjoy a cup or two of coffee a day, I'd let them allow, and actually,
that's what the data show, that anything below three cups a day, it's okay.
Okay. And energy drinks, would that be okay for such people?
Stay away from those, because God knows what is there in those energy drinks.
First of all, they're high in sugar content, and then who knows what the molecules
are. So since these things are not FDA regulated, I tend to usually
tell my patients to try to stay away.
Even the reputable ones, the caffeine content may be just too high-
Correct
... for some people.
Absolutely. So it all depends on the caffeine-
Yes
... and what the source.
Got it. And
magnesium is making big waves these days.
How does that affect your AFib? Can it help?
Can it hurt, or does it do anything much?
So we all know that
magnesium does help improve our sleep.
All these
molecules, the magnesium, potassium, sodium, they have to
be in a certain level, and heart depends on these
elements to stay in a normal rhythm.
Magnesium per se, when the studies were done, especially in the ICU
settings or dedicated magnesium supplements, did not show any
change, worse or good, in atrial fibrillation.
Got it. And let's go to
something that's ubiquitous in our lives, and people talk about it,
stress. How does that correlate to AFib risk?
So again, and I mentioned first, right, the parasympathetic and sympathetic.
So anything which was going to overdrive our sympathetic system, and obviously the
stress, right? So stress, work-related stress, depression,
anxiety, all of these,
people have studied in population-based studies, ARIC study, the MESA study.
People who have these
over the normal depression, anxiety, increase your risk of AFib by anywhere from
10% to 30%. In severely depressed patients, almost 30%
have atrial fibrillation risk.
And the bottom line is, right, whatever increasing your sympathetic tone, you're
increasing inflammation. Inflammation causes changes in your
cellular structure, more fibrosis. So all these things are connected.
So like we talked about in the premise for the
podcast, Next Wave Is Human, mental health is not separate from your physical
health.
Any imbalance in your mental health, whether that be depression or
anxiety, will upset the balance in your body.
So just for our listeners to clarify, sympathetic system is a system that is fight
or flight, that helps us
rev up the body's systems, and parasympathetic system is the rest and
digest system, which calms the system down-
Correct
... in the simplest terms.
Right.
So
we talked a little bit about this. Someone comes to your office, they feel
palpitations.
Is that mostly AFib, or is that mostly something else?
So palpitations means the patient feel that
they're feeling extra heartbeats or something is running fast.
That's the definition of palpitations, right? But then you have to look into that.
So which means we have to do some kind of monitoring to figure out what
is their palpitation. Sometime what they feel is just your regular
natural resting heart rate is high, and whatever they're doing is, and that's going
faster, and they can call that a palpitation.
So it's very important for us to actually do these, what we call diagnostic
testing, which talks about start off in the clinic as a 12-lead
electrocardiogram, where we hook them up those EKGs.
If that gives you an answer right there, and then you're done.
Otherwise, we put them in monitor called Holter monitors, event monitors from
14 days to 30 days. There is something called a loop recorder monitor.
People who complain of palpitations, and all other regular tests keeps coming
normal, we implant a device. And then obviously now is the age of wearables,
the Apple Watch, the Fitbits, and the Garmin.
And then there's another called the Kardia App.
You can buy this thing, and you put your fingers on it, basically doing a
single-lead EKG. So you need to have some kind of
information collected from your body in terms of electrocardiogram to give
us the diagnosis, what is causing the palpitations.
How good is Apple Watch for AFib detection?
So the Apple Heart study almost had 400,000 patients, and
these patients never had AFib. So these are patients who
have not been diagnosed. And I think 2,000 of these patients
were found to have an abnormal rhythm detected by the Apple Watch.
This is the first study. And then those patients did the
formal testing with the 12-lead electrocardiogram or monitors.
The sensitivity, specificity, or the chances of how good this
Apple Watch was all almost above 90%.
So the Apple Watch actually is pretty good, and to the point that now,
you won't believe this, obviously it's designed or is approved to detect atrial
fibrillation. But I have a few patients who I've seen, they're having
palpitations. They put their watch on, they did a 30-second
EKG, and you believe it or not, I have discovered patients with what we call
ventricular tachycardia, one of the most deadly rhythm.
So I have happened to have a few patients who are actually giving us
diagnosis. But again, remember, you have to wear it.
You have to do the EKG,
and then data in, garbage in, garbage out.
If you don't put it right, if the watch is not well tied, you're going to
create artifact. The biggest thing from all these variables is how to
differentiate the noise from the real data.
So just to clarify, ventricular tachycardia is a very serious rhythm,
but you can live with AFib for a long time, but ventricular tachycardia, usually
it's an emergency.
Correct.
Correct.
Yeah. That's a total-- Anything which is happening to the bottom chambers is taken
more seriously, even AFib is serious, but AFib doesn't have the imminent-
Mm-hmm
... what we call cardiac arrest or risk of death. People do die from AFib.
It increases your mortality by
twice. But what happens with AFib is either you end up developing a stroke, then
you have disability, pneumonia, and so and so forth, or you develop heart failure.
And if you don't manage the heart failure, eventually the pump will fail, and
you'll die from it.
So just to kind of go into why does AFib cause stroke?
So in the beginning, remember I said the top has to beat in a synchronous
fashion. The two top chambers beat together, the bottom follows, at 50, 60 beats
a minute, and the heart has to squeeze and push the blood down.
So me and you, all humans are born with a tiny chamber, just like you have an
appendix in your gut, and we don't know why that is.
Same way you have an appendix in your heart.
It's called left atrial appendage.
It's a tiny finger-like projection, where in a normal rhythm, the blood
goes into that chamber, it squeezes and pushes the blood out.
When somebody goes in AFib, that chamber or the left atrial appendage,
it loses its contractile function. It starts fibrillating.
The blood starts pooling inside the appendage.
And
there are other things going on, but that blood will clot.
If the clot breaks, the left atrium is going to send to the left
ventricle and through the aorta. It can go anywhere.
It can go to your tip of your toe, to your kidneys.
Usually, more or less, it goes straight up your carotid artery and goes in your
brain and then gets lost into one of the arteries.
And whichever part of the brain doesn't have a blood supply, you call it a
stroke. So AFib is the most common reasons for
disabling strokes.
So
to prevent it, these patients have to be on blood thinners, correct?
Correct. That's the best we have. As I said, atrial fibrillation causes
stasis. It makes the blood start becoming thick
and start pooling. So obviously, the only thing we have to prevent that is to
prevent the AFib and then to keep the blood thin by using drugs called
anticoagulants.
So we'll tackle more into this management part in a little bit, but I just want
to touch up on the drinking. So alcohol is associated with
irregular heartbeats or atrial fibrillation.
So how big a deal is that? Can just one night of drinking
cause AFib?
So alcohol is an important topic.
37 million Americans drink alcohol.
That's the data statistics, right?
Mm-hmm.
With the alcohol, there is a dose. Everything has a dose and response
curve, or if you can draw. So alcohol actually has a
linear dose response. As you start increasing the dose of alcohol, the
risk of AFib goes up, and other things, too.
And so for alcohol, just like radiation, there is no
clear safety threshold. Any amount of alcohol is bad, right?
So there's a pooled analysis cohort of
100,000 patients. They looked at those patients, how much were they
drinking. One drink per day, which is 12 grams of ethanol.
Just one drink increases the risk of atrial fibrillation by
16%.
Wow.
So again, there is no safe zone. The more you drink with
beer or cider-based alcohol, the
dose response is absolutely clear.
You increase the number of beers, the AFib risk is going to go up.
With red wine and a white wine, the dose response is what we call a J
curve. So a little bit of a certain extent, it
protects you, but the moment you cross the limit, the risk of AFib goes up.
So again, to my patients who drink alcohol or who come with
AFib, we usually tell them, "Please do not drink." And alcohol, a binge
alcohol drinking. Let's say you don't drink on a daily basis, and on a weekend you
end up drinking four or five drinks in a short period of time.
Alcohol, again, is going to make you diabetic, right?
So you're losing
fluid, you're increasing your catecholamines, you're increasing, again, the
sympathetic and the parasympathetic comes in.
And poor sleep, your heart rate variability goes down.
And guess what? You're going to develop atrial fibrillation because that is
triggering those pulmonary veins to bring out AFib.
So
even one night of heavy drinking can put the right person
in AFib. Is that correct?
Absolutely. And you don't have to be diabetic, you don't have to be obese.
Certain
drink or
too much alcohol in a short period of time is usually a trigger, very well-known
trigger for atrial fibrillation.
So there's a term ascribed to it, holiday heart.
Correct.
That's a real thing?
That's a real thing because you give rest, and you're not promoting the surges
of sympathetic tone.
So holiday heart mean if you're on your holidays, you drink a lot, you can have
AFib?
Correct.
Potentially. Again, as I said, even one drink increases the risk by
16%.
So we talked about risk factors earlier, and we talked about
sleep, weight, alcohol, exercise, stress.
If you had to rank them, like, okay,
I come to your office and I'm like, "You know what?
I have stress in my life. I do like to drink every so often, a
drink or two.
My day starts with coffee."
So what are the things, okay, give me top three that I must not do if I am at risk
or if I've had AFib. Like you'll tell me, "Don't ever do these,"
and the rest may be a little bit you can manage.
That's a good question, but remember, it's patient specific, so when you come to my
clinic, I have to assess all your modifiable and non-modifiable risk factors.
But let's say you're a little bit overweight, so we know obesity,
again, has a dose response. So
let's talk about obesity first. Obesity or overweight, anything
above 25 kilogram per meter squared is defined as overweight.
Anything above 30 kilogram per meter squared is the definition of obesity,
and above 40 is severe obesity. And in the obesity trials, so the people who have
done trials, and then the American College of Cardiology recommends
losing 10%. If you're overweight or obese,
losing more than 10% has shown 30% reduction in atrial fibrillation.
So it reduces your risk directly-
Directly
... correlating to weight loss.
And again, obesity is again linked to so many things.
Remember, everything is connected, right?
You lose weight, you're going to have improvement in blood pressure, you sleep
better, you changes your sleep apnea risk profile.
Again, obesity's adipose tissue is linked to inflammation.
And then, obesity also has a direct link with the heart.
Your heart actually is protected. It sits in a tiny...
It's covered by a balloon-like cover called pericardium.
And inside there is adipose tissue.
So people who are obese or truncal obesity have a higher
epicardial, on the surface of the top chamber, higher the adipose
tissue.
The fat deposition.
The fat deposition actually promotes inflammation, and that brings out atrial
fibrillation as well. So there is some direct link from obesity to your heart.
So when I look at the patient, let's say if he's...
Again, we all live in a stressful environment, so again, the mental health needs to
be managed first, right? Coffee, we already talked about.
But
the two things I would recommend is your alcohol intake, and number two is your
sleep apnea, actually. People with AFib, almost half the patients, or
more than actually 60% of the patients with AFib, have undiagnosed sleep apnea.
The number is actually up to 75%. And it's bi-directional. It's both ways.
People who have sleep apnea have AFib, and people who have AFib have actually sleep
apnea.
So one pulls the other and then they keep feeding off each other.
So when patients come to me the first time for any young, old, for atrial
fibrillation, what I'm doing simultaneously, I'm making them go do
a sleep study in a home base or whatever you do.
Go talk to a sleep doctor and start working.
As we all sleep on, especially people who sleep on their back, the tongue is
supposed to fall backwards, so we all obstruct.
So that's called obstructive sleep apnea.
So that is one of the most underdiagnosed modifiable risk factors for
atrial fibrillation.
Interesting. And
exercise,
and obviously exercise will cause weight loss, and we'll get into it, but one of
the big topics that's been doing the rounds is, of course, the semaglutides,
the Ozempic, the Wegovy, the Zepbound, and they help you
lose weight.
Is there any data that if you use these drugs for the
right patients, do they have less AFib? Is there any studies on that?
There is data now. Semaglutides, these are the, I
call the wonder drugs now. They're changing everything, right?
They're designed for weight loss, but we know that they reduce inflammation.
They have cardio protective, semaglutide, liraglutide have cardio protective
risks. And then there are studies, and there is like a
meta-analysis where we combine all the studies together, of 26 studies.
They show using GLP-1 agonist, semaglutide, reduces the risk of atrial
fibrillation by 17%. So there is data getting collected.
Again, remember, this is all new. But yes, if patients are
having other cardiovascular, patients with heart failure, these drugs are helping.
Invariably, it does correlate into helping with the atrial fibrillation, too.
So say someone comes to you, he's moderately overweight,
and you tell him, "Lose 30 pounds." Can it fix his
AFib?
It can, but the problem is how we're going to do that.
Because now once you're obese, you are in a vicious cycle, right?
These are big patients. I want them to go exercise.
Their knees are already hurting. So again,
the theme in atrial fibrillation used to be,
I think we were putting Band-Aids, right?
You're giving drugs, you're doing ablations.
But now the new goal, even by societies from the heart rhythm from ACC, is
AFib prevention is the new, actually, the theme that we need to prevent, nip it in
the bud. So again, it's a challenge.
Unfortunately, patients in persistent AFib, they're in AFib 24/7. They're obese.
Once they exercise, they get short of breath. So you have to start somewhere.
So in some patients, unfortunately, we have to go aggressive up front,
treat the atrial fibrillation with catheter ablation by taking the chances of
the obesity. But if I can maintain sinus rhythm for at least six months in
these patients with ablation or whatever, at least I can make
them exercise, and do all those things. So it's a continuous cycle.
So exercise is interesting. Of course, exercise is good
for body.
Now, what is the relationship of exercise with AFib?
I read some data that endurance athletes are also
likely to get AFib. What's that? Is there any truth to that?
Like if you're a marathon runner as they are a long-distance cyclist, which a lot
of your patients can be,
they are living a healthy life. Are they increasing their risk for AFib?
It's very interesting. You will think these are thin, slim people, patients coming
bicycling.
These are not your prototypical AFib patients.
These are not. And these are the patients who are very well read.
They are good in their supplements, and you name it.
They're doing everything right, in other words.
They're doing everything right, but believe me, I see a lot of athletes, especially
avid cyclists. We have this nice bike path here.
Mm-hmm.
A lot of cyclists are developing atrial fibrillation.
And why is that?
And that's interesting. So exercise, remember I talked about alcohol.
Alcohol has a direct dose response. The more you drink, the more AFib.
Exercise has what we call a J or a U-shaped curve.
So if you exercise less than a certain amount, you have more disease, more
AFib, more obesity. And there is a perfect inflection
point. So if you start exercising more than, the number
is 55 Mets
per week. MET is like the metabolic equivalent, right?
So more than 10 hours of vigorous exercise
in a week increases the risk of AFib and other heart rhythm problems.
So in endurance athletes. And the reason for that is many, many reasons.
So one of the things is when somebody's athletic, remember, when they are doing
their activity, the heart is pumping, it's racing fast.
To compensate, first thing the heart does is, two things it does, the
chambers will dilate
Number two, they develop sinus bradycardia.
It means their resting heart rate is always in 40s, so that's a compensation.
Most of these athletes actually develop their AFib during their sleep.
They never develop their AFib during exercise, actually.
And that is called the vagal-mediated AFib.
Because, again, it comes back to the sympathetic, parasympathetic, athletes have
a very high resting vagal tone, and during sleep, that vagus
nerve is going to promote those pulmonary veins.
It's called the cholinergic mediated. It triggers the AFib.
So most athletes actually develop their atrial fibrillation during their sleep,
which is even worse. They don't even know that they have AFib.
So that's one reason. Number two is what we call the remodeling of the whole heart.
Their ventricles thicken. The atriums.
There is data now that people who are endurance athletes, marathon
runners, their atriums are dilated.
And unfortunately, there is data shown that that dilatation never
reverses. It stays on. Even if you stop, it stays on for years and
years. And the bigger the upper chambers, the dilation, the
more the risk of all these arrhythmias. And there is data, actually.
They took rats, again, I'm not comparing humans to rats.
They have these healthy rats, and they ran them, like
vigorous exercise training for 16 weeks, and then they cut the heart, and they
look under microscope. 60% of those rats, compared to the controls who
did not, have fibrosis, which would be scarring, which you can see through an
MRI or under the microscope. So that's the link between too much
exercise. So the recommendation is to cut down.
So,
200, 240 minutes or something like that, or two to three hours.
If you're doing 10 hours vigorous in a week, cut it down to two to three
hours.
So vigorous means,
how do you define vigorous? My exercise tolerance could be very different
than yours. In terms of heart rate, okay, if I want to tell my
patient, "At this heart rate for this many hours," because that's how people
want to quantify.
Right. And again, it becomes different.
Guidelines recommend, they give us a total timeframe.
Okay, do these amount of minutes or, as a 240 minutes.
Mm-hmm.
Again, is there a limit for a particular patient?
Okay, you're starting at 40 and you go up to 200.
I think that's something-
So exercise which is making you breathless and tired-
Then you should not
... in the simplest terms-
You should not, correct
... for a prolonged period.
For a prolonged period, yeah.
Is that simplistic?
For my cyclist patients who are averaging 100 miles a week,
I usually tell them, again, there is no exact limit, but I say, "At least cut it
down by 25%."
Mm-hmm.
"Bring it down to 75 and see what happens."
Mm-hmm.
And now there is data, actually, for the athletes, and it's very difficult to tell
them to not do what they want to like to do, so catheter
ablation is becoming a first line for actually athletes.
Because think about it. Their resting heart rate is slow, which means I have no
medication, no heart rhythm medication, we call antiarrhythmics, beta
blockers to give it to them. They're already too slow. They tend to get dehydrated.
So I don't have much options from a medication standpoint to give to these
patients. So ablation usually helps.
And a good part of these ablations are we're targeting those pulmonary veins, so
the resting heart rate does goes up a little bit post-ablation, but a lot of data
coming out of early ablation for athletic patients.
And they are at risk for stroke equally, too, if they have AFib.
That exactly right. Stroke risk in atrial fibrillation is defined by
your, there's a risk score we call the CHADS VASC risk score, which
is C stands for congestive heart failure, H is for hypertension,
A is for age. Age above 75 gives you two points.
Other ones, everybody else is giving you one point.
D is diabetes, S is stroke or any myocardial
infarction history of peripheral artery disease.
All these risk factors, we do a point-based system.
So if you're a male and this CHADS VASC score is above two
and above, the risk of having a stroke is basically two out of 100
chances. If your score is three, three out of 100 chances.
For a female, you have to have a CHADS VASC score of three and
above. So that's the risk scoring used throughout the world in all
patients,
male or females, athlete or non-athletes, to determine the
need for blood thinners called the anticoagulants.
So let's dive into the day-to-day stuff, okay?
Say one of your friends develops AFib now, okay,
comes to you.
As a patient,
what are some of the questions that I should be asking my
doctor if I am found to have AFib? Where would I start?
So first of all, again,
the first thing we assess is are you symptomatic or not? If you have symptoms.
And then the other things you're going to ask me, most patients ask me, "Okay,
should I get the ablation early on, and what are my treatment options?" Again, we
talked about prevention is the goal.
We want to prevent further episodes, which modify, we talked about the risk
factors. But the question is, should we
offer these patients an early ablation, more aggressive ablation?
So even before we go to that, it's new onset,
there is a procedure called shocking the heart to get people out
of-
Correct
... AFib. Would that be an option for a lot of people to start with?
Right. Because the first episode, and let's say you are staying in AFib, right?
So which means you're developing early persistent atrial fibrillation.
Most patients, we end up doing what we call a cardioversion.
Before even we do that, again, my goal is to figure out why did you get into that
AFib. Again, stress, did you not sleep well, too much alcohol, sleep
apnea, obesity, uncontrolled diabetes, history of myocardial
infarction. So we assess for all those, but then in terms of
treatment-wise, step one, usually if you are in a hospital, we end up
doing a procedure called the TE cardioversion.
We make sure there's no clot in your heart, and then we
manually reset your heart by putting paddles on
your chest, and we do a procedure called cardioversion.
That will get you back in normal rhythm.
The problem is, it's very hard to predict which patient is going to have a
recurrence. We know that the older you are, the poor diabetic, the
obese you are And if you already have a heart failure, the risk of
developing atrial fibrillation goes up.
So the other thing we talk about in atrial fibrillation is, what is your pumping
chambers doing? Atrial fibrillation can cause heart failure.
And now there is lot of data and impetus
towards what we call arrhythmia-mediated cardiomyopathy.
We all know that atrial fibrillation causes stroke, but because your
heart is not in a regular beat, think about your bottom chamber.
Your bottom chamber is sometimes slow, sometimes fast, so this irregularity
actually can itself promote what we call LV dysfunction or left
ventricular dysfunction, or called heart failure.
So-
So the heart becomes weak.
The heart becomes weak, and if you don't treat those AFib, they will
behave just like any other heart failure patients.
So if you treat them, the heart function can improve, it can get stronger?
Mostly. Mostly if it's purely based on tachyarrhythmia or the fast heart
rhythm-related heart failure. The moment you restore the rhythm normal by
cardioversion, by shocking, or by ablation, or by medications, those
heart failure usually reverses completely.
So let's go step by step. So
I came to you, AFib is diagnosed.
Mm-hmm.
Or even if I go a step before, I had palpitations.
You did a monitor, now I have AFib.
Mm-hmm.
Now,
you offered me cardioversion with transesophageal
echocardiogram, which is essentially putting a probe down my mouth under sedation-
Right
... taking a look at the heart-
Mm-hmm
... make sure there is no clot, and then shocking the heart.
Correct.
The rhythm is restored. What would you do next with that patient?
So usually in those patients, the fact that
I had to go in and cardiovert you, which means you're already developing the
persistent, that your heart wants to stay in AFib.
So those patients should be, especially if you're in a relatively younger age,
and
that definition is changing, but we want to be aggressive.
So usually the step first is we can give you a medication called an
antiarrhythmic to prevent the next episode.
And there are several medicines like that.
There are several medications, and they all work on ion channels, sodium channel
blockers, we call class I agents. There is potassium channel blockers,
there is a beta blockers. So all these drugs are designed so that whatever
triggers your AFib, it doesn't let you go in AFib. Okay?
So those are the heart rhythm medications.
Plus, simultaneously, we're also managing your stroke profile, your risk profile
with blood thinners. But then after heart rhythm medications, usually the next
step is what we call the catheter ablation.
So
the question is when to do these procedures, right?
If you only had one episode of AFib and you're a younger person, and then I'm
able to tell you to modify your risk factors, usually we can wait and watch
and keep doing monitoring, by self-monitoring or by event monitoring and things
like that. That's usually the right way to go.
The other thing in AFib
field is called the atrial fibrillation burden.
All the trials of AFib to this date, if you look at any randomized trials or
whatever we do, the definition of success is
30 seconds or more of AFib after an intervention, which, in my
opinion, is absolutely wrong.
30 second
So let's say you do an ablation. I'm doing a trial where I'm going to do half the
patients are going to go on a drug, and the second one is going to do ablation.
So how do we define success in the AFib world is
after an ablation or after a procedure, are you developing episodes
of AFib? And the definition to date has been any 30 seconds
of atrial fibrillation documented by any monitor-
Is a failure
... is a failure, which my opinion is absolutely wrong. The field is changing.
Now the goal of all these interventions is actually reduction of
AFib burden. If you had AFib 50% of
time before an ablation or an intervention, and now you're down to 1%,
in theory, that should make sense that-
Right
... that is there. So that's where the field is going towards.
If you come to me for the first time, my first job is to assess how much AFib
you're having.
If you are paroxysmal, means you come and go, how many episodes you're having in a
month. If you're having, let's say, three to six episodes in a month, it's pretty
clear that we should do more for those patients.
If you're going to have one or two in a year, you can argue
whether you can just manage them medically or procedure's
usually not recommended for those patients.
So now that we've gone through the blood thinner part you mentioned,
so blood thinners obviously scare people. There is risks to it.
It used to be warfarin, which again, people know it as rat poison-
Mm-hmm
... and people talk about it also. Now there are-
Right
... newer drugs like apixaban or rivaroxaban,
and we use them. But people are still scared of blood thinners.
Now, if I'm a patient and you tell me to take a blood thinner daily,
I'm worried about bleeding. If I have an accident or a cut, I can bleed a lot
more. What are my options? Do I have any other options to that?
Correct. You're right. So based on the risk factors we talked about, the
CHA2DS2-VASc score, if you're risk two and above for a male and above three for a
female, you have to be on a blood thinner lifelong.
That's the guidelines as of today.
Trials are ongoing where patients who can self-monitor their
AFib, when they know they're going in AFib, they can start a blood thinner.
But again, that's future.
But unfortunately-
And that's with Apple Watch?
That's where the Apple Watch or the wearables are coming, but again, those trials
are underway. But as of now, as we speak today in 2026, if you have
AFib and you have these risk scores, whether or not you had an ablation or
not, you're supposed to take the blood thinner lifelong. And we all know that.
We all scared about blood thinners.
You talk about reasons, you can cut yourself and things like.
So there are alternatives we call the left atrial appendage management.
We talked about 90% of the strokes
during atrial fibrillation come from the left atrial appendage.
So just to recap, that's a small out-pouching in the top chambers-
Top chamber
... which does not have a lot of other useful function as far as we know.
As far we know. So the surgeons can cut it during a heart surgery,
you can put a clip on from the outside, or we, as an interventional
electrophysiologist or the structural heart specialist, we can actually
Percutaneously go from the groin, go inside the heart, we can actually
plug those chambers. And there are two devices out there which are approved.
One is called the Watchman device, and the other one is called an Amplatzer device.
So these are like filters, so to speak.
You put them inside those appendages, and then the body's going to form a
layer of cardiac tissue to completely occlude those chambers,
so that when you go in AFib, the blood doesn't go into this appendage, and you
won't form a clot, and you won't get a stroke.
So again, for the right patient at the right time, these devices are
available.
So if my doctor suggests to me, "Okay,
you don't want to take blood thinner, we can do Watchman or Amplatzer
for you. Let's start there." Is there any particular questions that I should be
asking? Is one device better than the other? Is there any data to that?
Or is there any particular question I should be asking as
a patient from my perspective, being responsible
about these devices?
So again, to get these devices even approved, remember, these
are
big procedures. So to be a candidate for left atrial
appendage devices, you have to have a CHADS-VASc score of three and above.
So let's say you are a 45-year-old coming to me for AFib, and you don't have
high blood pressure, no diabetes, no stroke, nothing.
You do not qualify for this device, just to be very clear and honest.
But you won't qualify for blood thinner in that case also.
You also won't qualify for blood thinner, depending outside the ablation timeframe.
Remember, anytime we touch your heart or we do an ablation or a cardioversion,
those four to six weeks after electric shock on an ablation,
you are supposed to take a blood thinner.
So we're talking about these long-term blood thinners.
Mm-hmm.
Right. There is no
head-to-head comparison between the Watchman device and an Amplatzer device.
The endpoint is whoever does the procedure, the goal of the left atrial appendage
management should be complete occlusion of your chamber.
How you do it, that is up to who does it.
But we talked about in the past, we're doing these devices, and there was an
acceptable leak around the device at the time of implant under three millimeter.
Now, the data has shown that you don't want any leak after 45
days or after the device is completely healed.
Okay. So now we got past the device.
You decide the patient needs an ablation.
Can you tell our patients what the procedure,
or for general people to know what the procedure entails?
How big of a deal it is?
So again, catheter ablation is a first-line therapy now.
And in the beginning, I remember I said, ablation means to ablate or to
change or modify a heart tissue. In the catheter
ablation for AFib, we are going inside your left upper chamber,
and we're isolating those four pulmonary veins, those tubes where the-
So you go from the groin with-
We go from the groin. So the procedure, again, entails, right now, the procedure
can take anywhere from one to two hours, depending on what technology you use.
But the procedure is still done under general anesthesia
or some form of deep sedation. The access is
through your groin. We are going through your femoral vein, so the tubes
which are draining the blood, taking blood back from your leg into your
heart. So we're going to, under X-ray or under 3D mapping, we
pass these tiny wires, electrical wires, and these tubes called catheters.
And then the procedure, the most important part of this procedure, is what we call
transseptal access. To go from your right upper chamber to the
left upper chamber, we have to make a tiny hole in the heart.
It's called a transseptal access, where the needle, we cross to
the left side. And then we take all our equipment into the left upper chamber.
We create a 3D map of your heart to see how big the heart is and
define what the areas of scarring are.
And then, once we know where to go and burn or
freeze or electroparade, we take this catheter, and we can
deliver energy. So the bottom line is to deliver energy to that part of the heart
where the AFib triggers or starts.
How you do it, again, that depends on the operator.
But these days, pulse field ablation is becoming pretty
much to go the energy source. And the reason for that
is it's faster, the tools are much more simpler,
and the energy is supposed to be cardioselective.
When we used to use radiofrequency energy for ablation-
The heat energy. Mm-hmm
... heat energy. We use radiofrequency that generates the heat.
Not only you are ablating the heart tissue, you're burning the heart tissue, but
think about it, the heart is sitting around many other things.
There are arteries, there are nerves, there are other tissues in the heart.
The left atrium sits in front of your food pipe.
So the Achilles' heel of catheter ablation for atrial fibrillation
was actually damaging the esophagus, which can be
catastrophic. And
we don't know the exact number, but there are chances of development of what we
call atrioesophageal fistula. That's the worst
case scenario from an ablation procedure.
So you essentially create a hole between the food pipe and the heart.
Food pipe and the heart-
That's a problem
... which is pretty much catastrophic, and the mortality is above 90%.
Fortunately, touch wood, has never happened.
Again, that's where the field has moved away from radiofrequency to
pulse field. Pulse field ablation is cardioselective.
It spares the esophagus to the most part.
And that's why the procedure's becoming faster and much more safer now.
And once we do the procedure, we take all the catheters out, and then
we have groin management. And most patients are going home within three hours after
the procedure.
So same-day discharge.
Same-day discharge on pretty much 90% of the patients.
Unless you have a severe heart failure or you're really old or frail, then we
usually keep them in the hospital. And the recovery is fast.
Within three to four days, we tell you not to drive, not to put too much pressure
on your groin, and you're back to your normal lifestyle.
But that's what ablation entails.
What are some of the other risks for the procedure?
So again, the common risks usually are from the groin access.
We are accessing your veins. Even though we are using, these days we call the
ultrasound, we know exactly where to put the needle in.
But hematoma formation, blood clotting,
or injuring the artery is one of the risk factors.
During the procedure, the biggest risk is what we call thrombus
formation or a clot formation on these devices we are putting in your heart.
So when we do your procedure, your blood is absolutely thin.
We use a drug called heparin, so you're fully heparinized for the duration of
the procedure so that you don't form a blood clot and don't cause a stroke.
So stroke is a risk from the procedure.
The other risk is we are moving, heart is a beating structure, right?
So we are pushing these catheters inside your heart.
These catheters can make a hole. The upper chambers are very thin-walled structure
compared to the bottom chambers. So we can cause what we call bleeding
into the outside of the heart, which can cause pericardial tamponade,
which can be life-threatening and can cause much problems.
So those are the main risk from the procedures are vascular complications,
stroke during the procedure, or cardiac tamponade.
Are these high percentage complications or uncommon?
These are uncommon. The numbers in high volume centers, if you're doing a lot of
procedures and you're using all your
checks and balances, the risk is less than 2 to 3% for most of these
complications.
And you said you go home the same day for most patients.
Correct.
Any particular downsides after the ablation?
That's a great question. So again, it all depends on at what stage of the AFib
you're ablating, right? So when we are doing ablations for paroxysmal AFib
or when your AFib is coming and going, usually those ablations
we are ablating the pulmonary veins. We call pulmonary vein triggers.
So the ablation is very focused, and we're not creating too much scar
tissue. The longer you're in AFib, what we call long-standing persistent atrial
fibrillation, the atria, the top chambers are very enlarged.
Again, the data has never shown. There are a lot of trials, other than ablating the
pulmonary vein tissues, no other strategy has ever shown to
improve
the recurrence of atrial fibrillation.
But invariably, we end up ablating more tissue based on the
3D map we have. So the more scar you have, those scar areas
can harbor AFib. It can promote AFib.
So we end up ablating the back of the heart, called the posterior wall isolation.
We're ablating a lot of flutters. These patients tend to go into many different
fast heart circuits. So the more you ablate, you're creating more scar
tissue. And whatever is ablated is not going to beat.
So if you ablate, keep on ablating, ablating, ablating, if the whole atrium
is pretty much scarred and ablated, those
atrias do not contract. So you can develop what we call atrial
myopathy. They call it stiff heart syndrome.
The people can develop heart failure symptoms.
They tend to retain more fluid in their lungs, so they start developing heart
failure symptoms.
But on the flip side, if you stay in AFib, you will still scar the
atria.
Correct.
And you can still develop it.
Correct. The famous
statement
by one of the giants in the EP field is the goat model
of AFib. So they discovered they put goats into AFib, induced
AFib, and the longer these goats, this is like 30, 40 years
ago, they stayed in AFib, they tend to have more AFib.
So there's a term called AFib begets AFib.
So whatever starts the AFib, but once you go in AFib and you stay in, the
fact that your heart is in irregular rhythm starts
changing your own cells at a cellular level.
So you're right. AFib creates scar.
Atrial fibrillation can cause the
chambers can get bigger,
promotes more scarring. So it's all connected.
So let's go a step further. Someone who's had AFib for a long time or is
too old, is there such a thing as too sick or
too old for AFib ablation? Do you offer it to everyone or?
Again, this is per patient. When they come to my clinic, we have to
assess those risk factors, right? Is this patient able to lay flat?
Is the patient able to tolerate the sedation?
Remember, for me to do the procedure, I don't want you to move.
We have to create a map of your heart.
So most patients require deep sedation or anesthesia.
And if your heart pumping is weak, so people who have severe heart failure, usually
those patients will succumb to the anesthesia than the procedure itself.
So you have to be in a good shape, a decent shape for me to put you on the table
to do the procedure. In terms of age, frailty
index comes into if you are a thin, old, small
female, we know that those patients are at a higher risk of what
we call cardiac tamponade. So the risk of perforation becomes an issue.
Age is not becoming a bigger
impediment to the procedures. I have done ablations on patients who are 85, but
they're good, functional 85, have a good lifestyle.
They want to do more.
So yes, the ablation is being available to more older population.
Can pacemakers prevent AFib?
Pacemakers by itself do not prevent AFib, but there is a
treatment strategy we use when everything fails or patients who are very frail,
or especially in extremes of ages, there is a procedure we do what we call AV
node ablation. Remember I talked about the wire which connects the top to the
bottom? So in those patients, we abandon rhythm control
strategy. Means they will stay in AFib forever, but
we will make their bottom chambers, they don't race, they don't
go slow, they don't go fast. How you achieve is by ablating
or burning the AV node. But because you're burning the main wire which
connects the top to the bottom, the bottom chambers cannot beat on its own.
So to do that, you have to implant what we call a permanent pacemaker,
which is a wire. We have to make an incision and put this device called the
pacemaker. So it's called an AV node ablation pace and ablation strategy.
Usually, actually, is one of the most effective,
one of the strategies which has shown to improve the most quality of life
in these elderly patients post-ablation. Because their heart's never going to race.
They never get hospitalized for a racing heart.
Their heart failure improves, actually.
And there is something about making the ventricles or the bottom
chamber beat at a regular rate. That itself actually has been
shown to prevent fibrosis and improve heart failure.
So you mentioned a little while ago, I just wanted to touch up on this, that
treating AFib or ablation can reduce the risk of
dementia. Is that correct?
That's correct. Data is coming in.
The AFib itself,
remember it's all inflammation. We have no idea what is changing.
There's autonomic tone, the sympathetic tone, everything is changing.
This vascular stasis, atrial fibrillation causes stasis of the blood.
People are developing most likely microthrombi.
You don't have to have a full stroke, but you have silent strokes.
And any time a piece of a brain tissue has a stroke or doesn't
work, that area's gone, and that can become dementia.
So there is data coming on. Patients who have early an ablation done
actually we're changing the trajectory of developing downstream dementia.
Because remember, they're all connected.
These are the patients who have already the higher age risk. They have diabetes.
They have sleep apnea. All these things are promoting
the neurological changes.
Great. So AFib ablation, in your mind,
is it fair to say it's a first-line strategy for most patients now?
It is becoming first line for most patients now, absolutely.
Back in the day, we have to show that patient failed.
You have to fail one anti-arrhythmic drug before you even qualify for an
ablation. But now, based on the guidelines, it's a class one indications for
most paroxysmal atrial fibrillation, early persistent atrial fibrillation, patients
who have heart failure. There is a trial called
CASTLE-AF
shown that patients with advanced heart failure, actually, who end up getting
atrial fibrillation ablation, their changes actually, they improved heart failure.
In fact, time to transplant and time to ventricular assist devices.
So there is now randomized data coming, showing that ablation, even a sicker
population, is actually helping.
Very interesting. So let's look into the future a little bit.
Say we are able to look 15 years from now,
and you're looking back on this, "Can't believe we used to do this." What would
that be?
Two things which come to my mind is, as remember I mentioned
prevention.
Mm-hmm.
So can, like you sitting in front of me right now, and if I have something on you,
I put something on you and predict 10 years from now you're going to develop
AFib. If we know we can do that,
then we should start working on prevention.
So lot of artificial intelligence.
So AI is able to look at your EKG and actually
predict your downstream risk of developing myocardial infarction, heart
attacks, and AFib. There's a Mayo Clinic study, couple of other machine
language,
big data EKGs, millions of EKGs. They have
signatures, like they look at the patients who had AFib and who don't have AFib.
What are those EKG signatures? So apparently, there is AI-based-
Algorithms
... algorithms coming out pretty soon, which will actually predict your risk of
developing AFib.
So that's one, AI based. Number two, the AFib ablation
world is changing, like the therapy one is changing.
But for me, if I have to predict, I think what the field needs to
move is patient-specific atrial
fibrillation treatment.
What that means is, right now we are ablating tissue.
We are just basically burning or electro creating a substrate, preventing
triggers. But AFib is a complex,
nobody's targeting all the things at the same time,
right? Whereas the proteomics, the genomics, your genes, all those things
needs to come together. So the ablation, as I do a lot of persistent
AFib, so patients come to me who are been in AFib for years and years and
years. Is there a way, without me going inside
the heart, can I predict from outside how much ablation I need to do?
Where should I do an ablation? Or what areas, what nervous system
we need to modify? So I think that's where the field is.
I predict in 10, 15 years, we will have those tools that
this patient needs this ablation at this point in time and this location.
Is there a world in which we don't even create a scar with burning or pulse field?
That's a very interesting question, and I think that point goes back
to modulation of your nervous system.
There is something with your nervous system, because something triggers your AFib.
Right now, me and you are in normal rhythm, right? Think about it.
Your own sinus node is connected to the billions of your top
chamber, right? So one area in your heart is what we call
the orchestra. He's the master-
Mm-hmm. The conductor
... the conductor, right? So whatever changes that balance of the
conductor from the rest of the tissue, that promotes arrhythmias.
If we can figure out a way how that conductor maintains its coherence
with the rest of the upper chambers, we may have a chance of
prevention or preventing arrhythmias without burning anything.
So
my 45-year-old friend, who
is a business executive,
a little bit overweight, not crazy, does exercise two or three times a week.
Mm-hmm.
On the weekend, couple drinks.
Comes and asks me, "Hey, my mom had AFib,
so I have family history of AFib. What can
I do to prevent my risk of AFib?"
And that's a great question, right?
This 45 year is enjoying life, because if I stop having him drink his
alcohol, he's going to come to me, "Look, what's the point of living?" Right?
So
I think
we talked about all those risk factors.
So at least
if the guy is thinking to prevent AFib, I think that's the winning starting point
to begin with. At least he start thinking about his own health.
Mm-hmm.
That's the biggest thing we all need to do in all our patients.
Most patients who are coming to us have no clue what their underlying disease
processes is. So that 45-year-old at least is thinking about it. That's number one.
Number two, overweight. Hopefully, he start working on that.
If he's exercising two to three times, maybe we can work on
getting that weight loss a little bit.
Third is we talked about mind over the body, right?
What are his sleep patterns? Which we'll be coming into the questions of variables.
What are the tools available to this 45-year-old
who can modify his sympathetic and parasympathetic
tone? I think that's where I think the key is.
He's going to drink, he's going to drink.
As I said, a drink or two is not going to cause much AFib.
But how is this 45-year-old person
aging? That is where actually the key is,
where everything else comes to point.
Your supplements, your GLPs, your HRVs, your exercise.
That's what I think the answer to your question should be.
So,
your GLPs like Ozempic and Wegovy, they reduce
weight.
Mm-hmm.
And fasting can be used to reduce weight, too.
Is there any data on fasting and reducing the risk of AFib?
There is no direct data that I was able to pull up, but again, if the
fasting reduces your weight, reduces your inflammation, I would
assume that there should be some positive impact.
If nothing else, at least, changes your heart rate variability.
Again, balancing the sympathetic-parasympathetic system.
But I do not have the evidence directly.
Is there any data on meditation?
There is some data. There is the famous study, it's a very tiny, small
study on yoga.
Mm-hmm.
Which is obviously exercise, which is mind-based.
There is a study on cognitive behavioral therapy.
Mm-hmm.
That study did not show any big change in development of atrial
fibrillation. There's an ongoing yoga study, it's a randomized trial going
on, patients with atrial fibrillation with yoga versus just routine of
care. That study is ongoing. But yoga has shown, or the small
study has shown, the more meditative you get, you change your heart rate
variability. Your resting heart rate comes down, your blood pressure comes down.
You feel better. You change your depression.
Remember, depression and anxieties are all linked.
Mm-hmm.
So I think the numbers are small-
Mm
... and we don't have a good one particular
tool that we can prescribe to a patient, "Okay, do this kind of yoga-
Mm-hmm
... and you should benefit." But
in theory, it does make sense that if something makes you more meditative
and brings your resting heart rate down and makes you more calmer,
I would assume that should translate into some kind of arrhythmia
modulation.
Thank you. That was very insightful.
So,
as a part of our conversation, we want to go through
at least one tech device every so often to tell our
listeners about this. There are many.
Tech is coming into health in a big way.
Correct.
So, I just saw you wear Whoop.
Yep.
I wear the same. So, I just want to go through it.
What's your experience from a cardiologist standpoint
when you have Whoop database, what do you see how useful it is?
I think I should reverse the roles here because you are much better at
Whoop data, or you have a good analysis of all these variables and
things like that. But whatever, these devices are helping,
giving some insight. Remember, all these devices are a
window
to your autonomic nervous system.
And how do we measure that? One of the things I keep saying is the heart rate
variability, and we talk about it, which is-
So can we tell people what heart rate variability is?
It basically is how fast or slow
each and every heartbeat will change to your body's external
environment. So, if you're in fight or flight, your heart rate's
supposed to go up. When you're resting, your heart rate is slowing down, when
you're sleeping. So how fast that beat-to-beat
variation can occur is a term called heart rate variability.
So just to clarify, even when your heart rate is regular,
every beat is not equally spaced.
Exactly.
There is always that variation.
Variation. Now, that variation is in milliseconds.
We talk about one-thousandths and thousandths of a second.
But for each heartbeat, that matters. And there is mathematic tools.
These devices, they're called SD and N, standard deviation, and root
mean squares. All these are tools to actually figure out that variability.
So Apple Watch generates a number, Whoop generates a number.
Most variables are generating that number.
Again, they're looking at your variation in every pulse, and that creates the heart
rate variability.
So coming back to the point, any of these tools are giving
you insights.
Whoop gives you sleep data. We talk about the various
phases of sleep. Are we focusing on the sleep?
So at least now you have a tool which tells you how good your sleep is, how deep
your REM sleep versus non-REM sleep is.
But the second question is how are we going to use the data?
Mm-hmm.
That's even more important than just getting a variable.
So, in terms of sleep, I feel knowing
is half the job, sleep or exercise.
So Whoop gives you calculated variables on strain and recovery.
Strain is their kind of algorithmic calculation, which takes into account
your heart rate, your activity, your respiratory rate,
your body temperature-
Temperature
... the whole thing, how well you recover.
Correct.
So it's more for
athletic sort of performance, but your day-to-day as well.
And I particularly like the idea of total strain
because even when you're sitting in a busy boardroom
conversation,
you are under a certain amount of strain, and if that's high, that still puts
a toll on your body.
Correct. I agree with your point because Apple Watch has all the data, too.
But then you have to use individual-- You have to piece them together.
Mm-hmm.
If we're all busy, who has time to look into all these things?
So if that tool gives you, "Okay, today was my strain full.
This is a strain day, this is not a strain day." And you can pinpoint what caused.
For me, I don't drink alcohol, but every time I
do, even a glass of wine, my sleep is gone.
My heart rate variability is
down the drain. So
to me, it's definitely helping me.
Even what tiny things I'm doing is making big changes to my health.
And over time, remember, it's not one day.
This is going to collectively, if I keep getting data again and again and again,
hopefully, I'll have enough impact on my behavior.
And that's what we want for our patients.
Mm-hmm.
These are devices which are easily accessible for most patients now.
So I think variables are here to stay.
And then the key is, one, to know the data, and number two is how can we
tell our patients how to use the data.
Exactly.
As far as accuracy is concerned, you're talking about mid to
high 80s in terms of accuracy in sleep detection for Whoop-
Correct
... from what I understand.
And
it's good for broad sleep stages compared to the gold standard, which is the sleep
study.
Right.
But from what I could find as more accurate for REM sleep, it may overestimate the
deep sleep a little bit.
The Whoop, you mean?
Yes, the Whoop. But coming to that, of
course,
I don't think you want to use these as
the dictum, "Okay, I got this much today." I think this is consistency of
wearing and seeing which way your data is tracking day-to-day-
Right
... as opposed to an isolated data.
Right. It's the trend.
Exactly.
Are you hitting the right trends? That's what more important is.
And the other reason I particularly like this is, of course, there is no screen,
so no distraction.
Correct.
The data goes straight to-
And it's easy to wear. You can sleep with it at night.
I could not sleep with an Apple Watch, believe me. I tried.
Well, nothing against that. We use Apple products, but-
Yeah
... I particularly like this in terms of fitness tracker.
We'll talk in our future episode about
other variables like Oura Ring and see how these two compare.
Right.
But all in all, it was a great conversation.
Thank you so much for taking the time, and
hope to talk to you soon. Next time we'll talk about pacemakers.
Thank you for having me. Appreciate it.