UCSF video about afib

FYI. 1.5 hours long...:-).
[www.youtube.com]

Maybe someone will watch and post a brief summary (if there is something out of the norm). I won't be watching for an hour and a half.

Quote
Ken
Maybe someone will watch and post a brief summary (if there is something out of the norm). I won't be watching for an hour and a half.

Here is the probably auto generated YouTube transcript (first half):

My name is Tommy Dewland and I'm going to cardiac electrophysiologist here at UCSF.
It is my distinct pleasure to introduce my colleague, Dr. Greg Marcus. Dr. Marcus is a Professor of Medicine and is
the associate chief of cardiology for research. He truly is a world-renowned clinical investigator
and has published nearly 300 peer review papers. In addition, Dr. Marcus is
a highly skilled and experienced cardiac electrophysiologist. Now, as students of medicine,
I am sure you have seen or will shortly appreciate that in healthcare, we often use seemingly complex jargon
to describe fairly simple thing. In this case, a cardiac electrophysiologist is
a heart rhythm specialist. We are in essence electricians of the heart. To put this career pathway into perspective,
it involves four years of medical school, three years of internal medicine, three years of general cardiology,
and then two years specifically devoted to the diagnosis
and treatment of heart rhythm abnormalities. With that, I wanted to hand things over to Dr. Marcus who
will be speaking to us this evening about atrial fibrillation. Thank you so much for the kind introduction,
Tommy. Welcome, everyone. We're very excited to have you all here and hope to provide
some interesting and hopefully useful information and get started on this talk,
which is going to focus on atrial fibrillation. This was largely motivated by
the fact there's been so many advances in atrial fibrillation. I've given a talk in this setting before,
which as many of you may know, leads to a presentation on YouTube and many of my patients Tommy,
they've seen some of these talks and I've become very aware that my last talk,
which on this subject in this forum, which I believe was in 2015 is now willfully out of date.
Also, we and others have contributed novel findings regarding the roles
of alcohol, or caffeine, of course, Apple Watches, and their relationship to
atrial fibrillation as a new development pertinent to many. We thought this would be hopefully,
again useful and interesting talk. Oftentimes people gloss right over their disclosure slides but I think
given the nature of this direct interaction with the public,
I think it's worth spending a little bit of time on these disclosures so that these are clear.
I've received research from the NIH from a not-for-profit called the
Patient-Centered Outcomes Research Institute. Another taxpayer-funded entity focused
on tobacco-related research in California, that's TRDRP. I have received funding from
a private for-profit company called Baylis, they make tools specifically related to
generally one part of the catheter ablation procedure where we cross from the right atrium to the left atrium.
I'll touch on that briefly. I've been a consultant for a startup company called InCarda therapeutics.
They make an inhaled therapeutic in the hopes of essentially delivering drugs directly to
the heart through the lung to convert atrial fibrillation. I'm also a consultant for Johnson and Johnson.
That's related to work on a steering committee related to a randomized trial.
I also do hold stock InCarda Therapeutics as in fact helped to found that company.
I'm not going to be talking about that technology or that approach, although happy to answer questions if that's of
interest about it, given time. Perhaps especially important and
especially related to what will end up being towards the end of the talk. I have not received any funding
from the food and beverage industry, which I know can be an issue when it comes to those things.
I certainly have no conflicts there. Jumping right into this common rhythm disturbance
called atrial fibrillation, what is, so, in order to understand what it is, it's really important to first understand what
the normal electrical condition of the heart is, or normal sinus rhythm,
shown here on the left, which originates in a structure in the right upper chamber,
the right atrium called the sinus node, that fires about 60 times per minute,
but it can fire 80 times per minute, 90 times a minute. It is sensitive to adrenaline,
so it goes up with more adrenaline, which can happen with exercise or excitement or anxiety, etc.
Then that electrical signal propagates through the muscle cells of the top two chambers,
the right atrium and the left atrium. They're all electrically connected. However, the atria are not usually
directly electrically connected to the lower chambers, the ventricles. Here we have the right ventricle and the left ventricle.
The heart valves, two of them are in the way and they do not conduct electricity.
In the great majority of cases, there's a rare circumstance I'll mention in a second. Then the great majority of circumstances,
the only way for that electrical impulse to get from the atrium to the ventricles is through
this structure called the AV node. That then leads to what's called the bundle of His,
which is a specialized conduction system that then breaks into the left bundle and the right bundle.
Those then lead to these Purkinje fibers that permeate the ventricles and electrically activate the ventricles,
which subsequently leads to their muscular contraction. The one rare case
that we also treat as electrophysiologists, where the atria are directly connected to the ventricle is when there's
a little thin piece of muscle that is just leftover from development in the womb
and that can lead to other arrhythmias. That can lead to something or is associated with something called
the Wolff Parkinson White Syndrome, which will not be a focus of the current talk. But again, happy to answer questions about that
if people are curious. In contrast to this, we consider the condition of
atrial fibrillation where the top chambers are very rapidly contracting in a chaotic,
unpredictable fashion, but the AV node, the His-Purkinje system,
the ventricles are still intact and they are responding as I will describe to the atrial fibrillation.
In terms of the general outline for this talk, I will focus on a little bit of epidemiology,
then talk about how we make a diagnosis of atrial fibrillation that will be
pertinent to the role of the Apple Watch and its technologies or capabilities,
as well as some other smartwatches. Then what are the consequences of atrial fibrillation?
Then a bit about how do we treat it, and then how do we prevent it, which is a new way to think about atrial fibrillation,
and which is especially pertinent, it turns out, to lifestyle factors and this is where I will discuss the role of alcohol and caffeine.
Now, as we think about this common rhythm disturbance, it's important to establish
some definitions and really a key feature of it, which is that it can be intermittent.
We call that paroxysmal atrial fibrillation or it can be consistent or persistent,
which is the formal name. Previously, what we now refer to as persistent atrial fibrillation,
meaning it is just going to continue unless we actively do something to stop it,
was also called chronic atrial fibrillation. There's another category
called permanent atrial fibrillation, which as implied means that atrial fibrillation
is just going to continue on forever. Really, that mainly occurs when there's a decision made,
ideally in partnership between the patient and the treating physician that we're
just going to allow the atria fibrillation to persist without any intended interruption.
Now importantly, the same patient can have paroxysmal and persistent atrial fibrillation
at different times. They may have an episode that is persistent and we shock them out of it back to a normal rhythm,
then they have a pyrrhiccism that lasts an hour. Although patients tend to
be either paroxysmal or persistent, most of the time, certainly the same patient can experience both conditions.
In terms of the epidemiology, the main point is that atrial fibrillation is very common.
Certainly more than five million cases, probably now, around 10 million in the US
alone expected to be 12 million, probably more by 2030.
Again, the lower end of the estimate is that there are 50 million cases around the world.
Once a person hits the age of 40, the lifetime risk of subsequently developing
atrial fibrillation is one in four. What are the risk factors for this?
Age is probably the most potent risk factor. As we grow older, we all are at heightened risk for atrial fibrillation.
If you have a room where everyone is at least 60 years of age, about five percent, if not more of them have atrial fibrillation,
a room filled with octogenarians and older, at least 10 percent of
them will have atrial fibrillation. Family history of atrial fibrillation
is an important risk factor, but it's not a classic Mendelian inheritance,
so it's not that, well, my dad had it, therefore, I have a 50 percent chance of getting it.
It's not that simple. It's much more varied and complex than that and actually, it depends on the family.
There are many genes that may be responsible for atrial fibrillation and some families have been
described where it really is Mendelian, it really is a 50 percent chance of getting a fib if one parent has it.
In most cases, it's what we call polygenic, meaning due to a combination of probably many,
many common genetic variants. It's not that someone is absolutely destined to
get atrial fibrillation or destined to never experienced atrial fibrillation, but rather dials up or down the susceptibility.
There's almost certainly environmental factors that then interact with that propensity to render
one more or less prone to atrial fibrillation. Other common risk factors include European ancestry.
Dr. Dolan and I have published fairly extensively on that subject.
Those with higher blood pressure, diabetes, heart failure, coronary artery disease, including a history of a heart attack.
Those are the obstructive sleep apnea. Those all increase the risk, and then we're recognizing more and more that there are
these more readily modifiable risk factors such as obesity and alcohol use.
We'll dive more into that later. Then there are these special circumstances.
There are some conditions where atrial fibrillation might be reversible. Hyperthyroidism. When the thyroid gland is overactive,
certainly that's associated with a heightened risk of atrial fibrillation. There's some evidence, although frankly,
it's not super robust, that once that hyperthyroidism is treated,
that the atrial fibrillation may resolve. Post open heart surgery really substantially
increases the risk for atrial fibrillation. Of everyone undergoing open heart surgery without any history ventricle fibrillation,
20-30 percent of them will exhibit, will develop atrial fibrillation during their recovery.
Usually occurs about three to four days later. The thinking is the evidence suggests
that in most of those cases it actually will resolve. We still don't fully understand
their long-term risks of atrial fibrillation. Then pericarditis, which is inflammation of the heart lining,
which I think folks have become more aware of it because of myocarditis related
to COVID and COVID vaccines. Pericarditis is related to that. Similarly may represent
a reversible cause of atrial fibrillation. Now, also, people can certainly develop
atrial fibrillation in the absence of all of these risk factors. That represents about 30 percent of all cases.
Some people, young, none of the characteristics I just
described can yet still develop atrial fibrillation. This is sometimes called lone atrial fibrillation.
There is pretty good evidence that those individuals probably have more of a genetic propensity
to developing the disease. So now we will move into
the consequences of this common arrhythmia. This is a general outline for the consequences.
Then I will dig in a little bit more, especially on bullets 1 and 3. We worry about reduced quality of life.
People can be quite symptomatic. Adverse remodeling of the heart. Usually this is attributed to
prolonged fast ventricular rates or a fast pulse that can lead to weakening of the heart.
There's some more recent evidence that even in the setting of a normal heart rate,
such as when atrial fibrillation is treated with medicines, that the heart may still
adversely remodeled by adverse remodeling, I mean, can become larger, can become weaker,
can be more prone to heart failure, more prone to leaky valves as that part gets
larger and the valves are unable to close as well as they otherwise would. Then very important,
we worry about something called thromboembolism. Thrombo refers to the formation
of a thrombus or a blood clot. Then embolism means anything that is
traveling in the bloodstream from one place to the other. What can happen is these clots can travel from the heart.
They're formed in the setting of atrial fibrillation and travel to some blood vessel, block it, occlude blood flow and oxygen,
starving that tissue that receives that blood flow of oxygen, leading to cell death.
The most feared complication here is stroke. If we put a catheter in the atrium,
one of the top chambers when someone is in atrial fibrillation, the rate is incredibly fast.
This little strip here is actually from a pacemaker lead that's sitting in an atrium,
in a patient with atrial fibrillation. Oftentimes you can count these going more than 400 beats per minute,
500, 600 beats per minute. If the ventricles go that fast, that is not compatible with
life unless maybe you're a hummingbird, but certainly not in humans.
One of the important consequences of going so fast in the atria is you lose the normal blood flow,
the usual atrial kick, and therefore blood stagnates. Whenever blood sits still in one place,
it is prone to forming a thrombus or a clot. There's one part of the atria that's especially
vulnerable to this and that's this structure called the left atrial appendage.
It is literally an appendage that comes off the left atrium. This is what's called a transesophageal
echocardiogram with a view of the left atrial appendage. The esophagus is the swallowing tube,
which is in the back part of the chest behind the heart. The left atrium actually is a little
bit behind the right atrium. The right atrium is towards the front of the chest, the left atrium towards the back.
We don't get a great view of the left atrium when we put an ultrasound probe right on the chest wall.
But if we have the patient swallow that probe or under advanced that probe,
we can get a very clear, beautiful view of the left atrium and especially the left atrial appendage.
This is showing blood clots in the left atrial appendage and a patient with atrial fibrillation.
It's important to mention a concept because this is what I just described,
is the classic reasoning used to explain why atrial fibrillation,
which leads to stagnation of blood flow because of the rapid rate, then leads to blood clots.
This then leads to a common question that patients asked me all the time.
Very understandable and very intuitive. There's a somewhat counter-intuitive
answer to that question, which is why it's now important to skip ahead a little bit to treatments, which I will come back to.
That is a common question, is okay, I see what you're saying. Afib lead to blood clot, that's what leads to the stroke.
If we don't allow my atria to defibrillate, we keep my heart in normal rhythm,
that should be enough to prevent those clots. But it actually doesn't,
at least in many patients. It just hasn't been shown to be true. I'll talk a bit more about that.
When it comes to treatments, the thing that prevents the clots are blood thinners. Now, again, that's counter-intuitive
given what I just said. There's perhaps a useful way to think about this,
which I believe is almost certainly operative, at least in some patients. I can't say all patients.
But it may be that there are some atria that are prone to forming
blood clots in the left atrial appendage because there's some scar tissue there, for example.
those same atria are also prone to fibrillating. In those cases, the atrial fibrillation may be more of
a epi phenomenon or a marker to say, "Hey, this is an atria that's prone
to forming a blood clot," and in that circumstance, getting rid of the afib, suppressing the afib is not going to be
sufficient to prevent the blood clot. I've seen this in some of my patients. I think the reality is there's
probably a spectrum and that's the case. In some cases, there are other cases where it clearly really is directly related to the afib.
The other issue is that, as I described, the Afib itself lead to remodeling and, for example,
enlargement of the atria and may itself over time change the characteristics of the atria to make
them more prone to clotting. This is clearly not a straightforward issue,
but very important to appreciate. Now I talked about that AV node.
One of the key characteristics of the AV node is that it just can't conduct that fast.
It cannot conduct more than 400 beats per minute. This may be something that we evolved to prevent.
Otherwise, humans would die when they had atrial fibrillation. The AV node, in this case, really saves us,
in that it generally will conduct maybe 100, 110, 120, 130 beats per minute during atrial fibrillation,
certainly very much compatible with life. Although perhaps the ventricles will go
fast enough to make the person not feel well. But atrial fibrillation, importantly,
is not generally an imminently dangerous rhythm. It's not a true emergency,
largely thanks to this AV node. Now the AV node is heavily
influenced by what we call autonomic tone, which is this tension or balance or
harmony between the adrenaline side of the nervous system, which is called the sympathetic nervous system,
versus the vagal side, which is also called the parasympathetic nervous system, which slows things down.
If one had a lot of vagal tone, such as their resting, they just had a big meal,
the AV node will be relatively slow. That person may be in atrial fibrillation
with a ventricular rate, which will result in the pulse of about 80 beats per minute. Then they run up the stairs,
they hear the phone ringing in. The phone happens to be upstairs. They run up the stairs, they get more adrenaline and suddenly,
whereas in normal sinus rhythm, their heart rate might go 110, 120, now it's going 160, 170 due to the afib.
Now, the ventricles which generate the pulse will not only be faster than usual,
they'll also beat irregularly. This irregularly irregular pattern,
it really is random, is very characteristic of atrial fibrillation.
Another consequence of all of that is that this combination of loss of the atrial kick,
as well as the ventricles beating a bit fast as well as beating irregularly,
that all leads to less ventricular filling and a reduction in ventricular output or cardiac output,
and all of that can lead to various symptoms, including fatigue, shortness of breath,
chest discomfort, palpitations, just feeling faint and sometimes just not feeling well.
Interestingly, some people are completely asymptomatic, and we still don't completely understand why that is.
Then even the people who swear they know when they're in atrial fibrillation because they have symptoms,
if you put monitors on them in many cases you will find there having asymptomatic episodes.
In terms of the diagnosis, we use the electrocardiogram. There's a picture here, the electrocardiogram.
Very common test. Very quick. It's when they put stickers or electrodes on your chest that they connect to wires.
A normal sinus rhythm is shown here on the top, we're looking for these little waves
that are marked by these asterixis, which we call the P wave and that represents
the organized conduction of the atria. Then with the solid arrows, these larger,
more rapid waves are called the QRS complexes. Those represent conduction of the ventricles.
They're rapid because this his bundle branch Purkinje network conducts very rapidly and you'll
notice these QRS complexes are much bigger than the P waves because the ventricles generally have a lot more meat,
so they're much more substantial than the relatively smaller atria. Of note, this wave marked
by this dashed arrow is called the T wave, and represents the electrical repolarization
of the ventricles, which then might lead to the question, well, what about electrical repolarization of the atria?
It is there, but it's very hard to see. Again, partly because the atria are much smaller and
probably is buried largely in the QRS. Now, in contrast to this,
we look at an electrocardiogram in the setting of atrial fibrillation where we
will have an absence of these P waves. The underlying baseline is somewhat undulating.
Now you may notice the T waves and think, "Oh wait, how do you know those aren't P waves?" But there are broader than the P wave.
They reliably follow the QRS complexes, and then the QRS complexes, again representing ventricular contraction,
are more rapid and they are irregularly irregular. This electrocardiogram, which we also refer to as
an ECG or from the German EKG, is the gold standard really the only way to
definitively make a diagnosis of atrial fibrillation. This brings us to smartwatches
and some of the new technologies that are designed specifically to identify
individuals with atrial fibrillation. To talk about how that's done, which I think is important
to understand the limitations of these smartwatches, we can consider this classic picture of
a monitor that you all may have seen on yourselves, family members, certainly on TV anytime you're in the emergency room,
certainly the intensive care unit of the hospital undergoing a procedure, you'll see something like this.
To hone in on these two rows, so this bottom row
represents a signal from a device called a pulse oximeter. This is the thing with usually red light
that's placed on typically a finger, could be placed on an ear lobe or a toe and the purpose of
this is to infer the oxygenation of the blood.
What it's doing is shining the light and then it has a little camera and it's looking at
how that light is reflected and the way the light is reflected or the amount of light reflected is
influenced by the amount of oxygen. Then the EKG we already talked about,
that's this top part. Now, smartwatches take advantage of
the fact that there is a fairly prominent pulse, right where watch is tend to
sit this radial pulses as shown in this middle picture. On the back of smartwatches that report heart rates,
so Apple Watches, Samsung devices, Fitbit, they are using the same light
based sensor called photoplethysmography, referred to in short as PPG.
The same technology used in a pulse oximeter, where it's shining a light and looking
at how that light is reflected back. Now, although Apple watches now
extensively can report on oxygen saturation, it's actually looking at the waveform change
over time to infer the heart rate. Generally these smartwatches are
again using this light based sensor on the back that is inferring the pulse from the changes in the light wave form.
It's not generally, certainly when it's reporting heart rate it's
not using anything electrical. It's not inferring anything from the actual EKG, just from this pulse waveform.
One important and fairly common way that it can be fooled is if someone
has fairly frequent early heartbeats such as something called a premature ventricular contraction or a PVC,
that sometimes can occur early enough that it doesn't generate a particularly strong pulse.
I will see patients for example, with frequent PVCs that will say, "Yeah, my smartwatch said my heart rate was 25."
When in fact their heart rate is 50, but every other beat is a PVC.
Similarly, we can infer, or this is the idea,
the presence or absence of atrial fibrillation, given the nature of the waveform. This is some raw data that we
collected as part of a research study. This is sinus rhythm, this is the photoplethysmography waveform
and normal rhythm and this is it in atrial fibrillation. In fact, before Apple and
Fitbit develop this themselves, we actually published the first study
to demonstrate that, yes, indeed a smartwatch and we did use Apple watches, this was in collaboration with
some data scientists that subsequently spun out a company called Cardiogram and they employed
a machine learning algorithm that we trained based on patients with and without atrial fibrillation.
We tested this in people undergoing cardioversion procedures where it proved to be highly accurate,
although that was a really controlled, careful setting. Then we tested it in an ambulatory population where we
noted it still was better than flipping a coin, but it wasn't terrific at detecting atrial fibrillation.
Then subsequent to that companies got really interested in doing this themselves. There have been published studies now from Apple,
from Fitbit and from Samsung. The Samsung study by the way was done by our group led by our chief for cardiology, Jeff Orgen.
Now, you might think, "Okay good, then we're going to detect more atrial fibrillation. You said that it can be asymptomatic.
You said that it can lead to stroke and blood thinners prevent stroke, so isn't this all good? We're going to detect people
who don't know they have a fib, and that indeed motivated our original study." Interestingly though, there's really
no consensus that there should be, at least from professionals and
from scientists and from clinicians, there's no consensus that we should be conducting
population-based screening for atrial fibrillation among everyone.
Now, why is that? This brings us to this concept that we
all learn in medical school that I think is really useful to share and to try to communicate and frankly,
this is all pertinent to really any evaluation of a medical test and
what we call the test characteristics. This is very classic in
any Epidemiology course or medical student course. We learn about this two-by-two table where
you imagine the disease here in the columns, presence or absence of a disease,
and you're evaluating a test whether it's positive or negative. We tend to talk a lot about the sensitivity,
which is the true positives or A here over the true positives plus the false negatives,
and the specificity which is the reciprocal, which is the true negatives over the false positives plus the true negatives.
These are not influenced by how common the disease is,
which makes sense because within this column on the left, they all got the disease, this column on the right, they all
don't have the disease. But the reality is that when we are in clinical practice and we are
confronting a patient with a positive test, we by definition do not know if they already have the disease or not.
These things, sensitivity and specificity, they can be used in a research study where you have some reference board standard
that everyone is subjected to. But in clinical medicine, we have to think about these other types of
characteristics come from evaluating the rows here rather than the columns.
Again, I'm confronted with a positive test. I'm interested in the positive predictive value,
which in this case is A over A plus B. Another way to say that is, given a positive test,
what is the likelihood that test is true? And what's important related to screening is
that these characteristics in the rows, these predictive values are highly influenced
by disease prevalence and that's just the reality. I'll give you an example.
Let's imagine we have a test that is highly accurate, so 95 percent sensitive and specific,
which as far as medical Tesco, that's really pretty good. But the prevalence of the disease is about one percent,
and it's not unrealistic to imagine that in a population of people wearing smartwatches,
which is probably will skew a little younger and healthier than even the general population.
About one percent is probably right. Mathematically, given that prevalence and
these outstanding test characteristics, if you calculate the positive predictive value,
it will be 15 percent. What does that mean? That means that 85 percent of those tests will be false positives.
This is one of the reasons that no professional society has come out to say,
"Yeah, we should screen everyone for atrial fibrillation because there's going to be a lot of false positives."
Now you might say so what, why does that matter? Well, that's going to lead to
a lot of unnecessary anxiety. Almost certainly quite a bit of unnecessary health care utilization and even
potentially unnecessary and even inappropriate prescription of anticoagulants,
which in general can provide a lot of benefit to properly selected people with AFib.
But in healthy people, there's a risk of, well on everyone there's a risk of bleeding and if you give it to enough people,
some are going to experience bleeding where they never really should have received that drug in the meantime.
I was asked to write a commentary on this Nature Reviews cardiology
and pointed this phenomenon out, this new era we're in.
Where if you consider the conventional way this works, which I went through on the left, where we first perform
scientific research that undergoes peer review that is then disseminated leads to expert consensus that informs
clinicians and the clinicians inform the patients and the general public. Now we have this very interesting situation where we have
private industry marketing devices that are making diagnoses of a disease,
atrial fibrillation directly to patients. There's no intermediary here of scientists,
clinicians, professionals, or societies. At the same time, of course, we're trying to do the research to inform these things.
But we are stuck with this situation. I've argued that we need to do
a better job educating the public, hence, a big part of the motivation for this very talk
and I think understanding what is atrial fibrillation, why do we care? What do we do about it? Is really critical and
becoming more critical given the presence of these devices. Now, there's a bit more to say about them,
and that is that they sometimes are accompanied with the actual ability to obtain an ECG,
such as many Apple watches now, this is also on the left is what's called a cardio mobile device,
which is not a smartwatch per se, but is a separate handheld device. They now have a credit card device
that you can hold that has electrodes that pairs with a mobile app. There are algorithms that will read these ECGs.
They're imperfect, but the ECGs can be saved and sent to
providers and the algorithms are almost certainly accurate
if they indicate a normal rhythm. Now, this does raise the issue of potential problems in a dating providers
with a lot of strips. But this may be especially useful for rhythms beyond atrial fibrillation.
The algorithms in general, using the light-based sensor, they will just comment on AFib
or something non-specific or normal. Whereas the ECG, the algorithms won't necessarily
call the specific abnormal heart rhythm. But again, if those PDFs can be saved and shared with a health care professional,
diagnosis can be made and in fact, this is where I think these devices are pretty clearly
useful and that's in patients with an established diagnosis. If you have a population of people who
already have received a diagnosis of atrial fibrillation, then your prevalence is very high, so false positives for
the same mathematical reasons I just described are much lower. This can help people with atrial fibrillation
decide when to take what's called the pill in the pocket. Some patients are prescribed a medicine to take to convert their AFib,
but the symptoms aren't always clear. Someone may just feel a little off or a little anxious and they're not sure.
Is this AFib or am I just feeling this way? Is it worth taking one of these pills? These devices may be helpful there or to determine if
a particular drug they're taking on a daily basis is working, whether they should have another catheter ablation procedure,
or to identify various triggers. Oh, it's when I consume alcohol. Yeah. The device really is showing atrial fibrillation.
Moving on now to various treatments for atrial fibrillation.
There's a big dichotomy here. These things aren't necessarily mutually exclusive,
but we often discuss them that way, and that is what we would refer to as rate control,
meaning allow that person to remain in atrial fibrillation versus rhythm control,
meaning try to get them out of AFib and keep them out of AFib. Rate control the goal is really to work on
that AV node to make sure it's not allowing the AFib to make the ventricles go too fast. Now there were several randomized trials
that were done now about 20 years ago that counter-intuitively perhaps failed
to demonstrate a clear benefit of the rhythm control strategy, meaning that let's get rid of the AFib and try to
suppress it over rate control. However, there are several limitations
to those studies that are worth emphasizing. First, there wasn't really
any evidence that the people who underwent the rhythm control generally did worse so they were considered fairly equivalent.
Second, the means to maintain sinus rhythm were sub-optimal.
We've generally recognized that this was before catheter ablation and many of these people were not necessarily treated by
electrophysiologist that understand the various nuances of various drugs available to suppress a fib.
It's also very likely that the most symptomatic patients were not enrolled. If you're a treating physician and you have
a patient that you know feels horrible, and atrial fibrillation feels great and sinus rhythm. You're not going to be very
likely to encourage them to enroll in this randomized study. Most of the studies were quite small,
and then the duration of follow-up may have been insufficient to really see the adverse consequences over time.
Now a really important lesson from these trials that relates
back to my initial discussion of the formation of blood clots in atrial fibrillation is that
a normal sinus rhythm strategy is clearly not sufficient for stroke prevention.
How do we know that? Because in these trials, especially the main one that's called a firm. Per the protocol,
if someone was randomly assigned to rhythm control and they came back to clinic and yes,
they were normal rhythm, the practitioner could stop their blood thinner and it turns out that
their stroke rate was the same as the people in atrial fibrillation. Now you could argue that well,
but it was still lower because they were authentic coagulation and indeed, there has been a question, well,
if you have normal rhythm plus anticoagulation, would that really knocked down the rate of strokes and
other thromboemboli and indeed that ends up being true. Much more recently, this trial was published,
really the first in many years to revisit this question of rhythm control versus
rate control in the modern era with ablation, with electrophysiologist caring for
these patients and really importantly, with the idea that anticoagulation
or blood thinning would be continued even in the people randomly assigned to a normal rhythm
and they found that really in every outcome, there was less problems in
the people randomly assigned to the rhythm control, meaning let's try to prevent AFib arm.
The main outcome that was statistically significant was a composite, but really each of these is lower,
so there was less death that was statistically significant, less stroke interestingly,
despite the fact that everyone got blood thinners, less hospitalization, either for
heart failure or essentially a heart attack. But sometimes a rate control strategy is
still reasonable depending on various factors and we are slowly
moving towards a rhythm control as more of a first line. One of the important caveats
of that study I just described is that these were in people with relatively new atrial fibrillation.
The one thing that everyone has in our field of electrophysiology has
agreed is it makes sense to pursue a normal rhythm control strategy in people who have symptoms in setting of atrial fibrillation.
If we imagine we've decided we're going to do rate control, we're not going to try to suppress
the atrial fibrillation or we can't suppress the atrial fibrillation, which does sometimes happen. There are a couple of drugs to help slow the AV node,
and those include beta-blockers. These are these medicines that end in olol like metoprolol, atenolol, etc.
Calcium channel blockers can do the same, specifically diltiazem and verapamil, not all calcium channel blockers per se.
Both of these classes of drugs do decrease blood pressure so that can be a win-win
when a patient already has high blood pressure, but can be limiting or problematic in people whose blood pressure is too low.
Digoxin is also useful here, perhaps is considered more second
line because it doesn't work as well. Also it may actually promote atrial fibrillation in those
who have intermittent episodes, which is less of an issue in people who are in persistent atrial fibrillation.
Now, all of these drugs, they've worked on the AV node to slow it. That's the intention.
When someone's in normal rhythm, they will also slow the sinus node. This can be a problem when
someone's in and out of atrial fibrillation, they're going too fast in atrial fibrillation hence we
give them these drugs to slow them down, then they convert to normal rhythm and now they're going to slow in a normal rhythm.
Usually that's not dangerous per se. but people can feel really tired because they can't mount
an adequate heart rate response to exercise. Sometimes people can pass out when they convert from
atrial fibrillation and it takes a while for that sinus node to recover. This is something called
Tachy-Brady syndrome or too fast, too slow syndrome and that is a indication for a pacemaker which works
very well to address this slow rate.
I want to talk about the pacemaker because of that and also another solution for many with atrial fibrillation.
Putting in a pacemaker is very straightforward. It does not entail having to open the chest.
We make a very small incision in the upper chest, just down to the muscle layer,
just under the skin, we make a little pocket. We go into a vein here, much the same way that
we go into a vein in the legs to do a catheter ablation or an operator might go into an artery to do an angiogram.
The way we do that is usually now under ultrasound or some other visualization. We'll place a needle into the vein,
get a little blood back, put a wire through that needle, take the needle out and put a little plastic tube,
essentially like a large IV over that wire, take the wire out and then we can introduce either catheters or in this case,
pacemaker leads that will look like this through those veins down into the heart under x-ray guidance.
There are a number of ways to then fixate those leads to the heart via,
for example, a screw that we can deploy with a wrench on the outside of the lead.
We connect the leads to this generator, tuck it in that pocket and sew it up but essentially this is a very common, straightforward procedure.
Now, in general, all the pacemaker can do is
prevent the heart from going too slow. It just paces the heart, activates the heart, preventing it from going too slow.
It doesn't really otherwise, slowdown rhythms that are too fast, like atrial fibrillation.
There's one exception and that is when patients have something called atrial flutter, which is related to atrial fibrillation but
is a more organized single circuit. There is one type of pacemaker were in the lead in the upper chambers so this lead,
by the way, is in the right atrium. This lead is in the right ventricle. It can sense that fast rhythm pace a little
faster and sometimes help break that circuit in the setting of atrial flutter. Now this is pertinent to this talk on atrial fibrillation
partly because of that Tachy-Brady syndrome I described, but also because of this very straightforward procedure
called an AV node or AV junction ablation. This is when we have a patient that we're trying
to rate control and we can't because the medicines aren't working. Sometimes we pile on these medicines,
their pulse is still too fast or their blood pressure is just too low on
those medicines or sometimes these are patients where we've really tried to suppress the atrial fibrillation,
but the medicines don't work. We try catheter ablation, doesn't work or things aren't tolerated, then we place a pacemaker,
as I just described. We do this actually very simple procedure where we go in with a catheter and burn the AV node,
which essentially electrically disconnects the top chambers, the atria from the ventricles.
We allow the patient to be in atrial fibrillation but the ventricles, the pulse, they just don't know it and
they never go too fast and they don't beat irregularly. They are, however, then dependent on the pacemaker.
Now I should mention the first ablation ever done in a human for an arrhythmia
was done by a doctor Melshaman, a colleague of Dr. Dolan's and myself and really a mentor of ours.

Second half:

It was done at UCSF in 1982 and it was this procedure.
They used a different form of energy, but it was essentially this AV junction or AV node ablation.
Moving on to other therapies and imagining now we do want to obtain and maintain a normal rhythm.
A common way to do this in those with persistent atrial fibrillation. It's not breaking, they're not reverting on their
own to normal rhythm is to do what's called a cardioversion. This is the same procedure you see on
TV where they put on pads and they yell clear and they deliver a shock that is
usually in a scenario of a ventricular arrhythmia, a deadly arrhythmia, in this case,
is a very calm. We really do help clear after
charging and before we shock but it's a very common procedure. We often do four of these on any given day at
UCSF and hospitals all over do this frequently. It works very well to
convert someone from atrial fibrillation to a normal rhythm but it doesn't do
anything to prevent the atrial fibrillation from coming back. The most important determinant of the success tends to be
how long the atrial fibrillation has been going on. If it's been present for years and years,
sometimes even the cardioversion doesn't work. We can sometimes facilitate that by adding medication,
sometimes trying an ablation but it usually works and the challenge tends to be the recurrence of
the atrial fibrillation down the line. That brings us to various drugs called anti-arrhythmic
drugs that are designed specifically to suppress the atrial fibrillation.
There are several. They all have their pros and cons. None of them work perfectly, of course, for any given individual,
they may work especially well but in a general population with atrial fibrillation, you give these drugs,
50-70 percent of them will be able to maintain a normal rhythm at about a year. Certain drugs are contra,
indicated in the setting of certain disease states, especially in people who have
any blockages in the arteries supplying their heart or a history of heart attack or heart failure then we're a little bit more
limited in terms of the drugs that we can give. Now, the other option as I've
referred to is catheter ablation. This is a more complex ablation than simply burning the AV node.
The goal here is to render one free of atrial fibrillation.
The way this works is we do something called a transseptal puncture. This comes back to my disclosures I mentioned of
that a company Baylis they make tools to help us traverse the septum and the point of
that is to burn or freeze the opening,
the ostia, or just outside these veins that come from the lungs,
hence pulmonary, into the left upper chamber.
I should mention, these veins have little sleeves of muscle that conduct electricity.
If we put a catheter like this, what we call lasso catheter that has these electrodes on it,
into the pulmonary vein we can measure signals that are conducted from the rest of the atrium.
It's been demonstrated that if one can electrically isolate those veins, generally by burning around them
or delivering this what's called a cryo balloon, essentially freezing the tissue surrounding them,
you can free the majority, not everyone but the majority of people with atrial fibrillation.
Now, how does that work? What are these pulmonary veins have to do with a fib?
That's actually an area of ongoing study, but there are several potential explanations
and they may vary depending on the individual person. This approach was really first described by clinicians in Bordeaux,
France that noticed that some people with interim-in-nature fibrillation seemed
to have the rhythm triggered by these early beats called premature atrial contractions originating
inside the pulmonary veins. The first procedures they were going in for the pulmonary vein,
they were trying to hunt down these rare early beats and burn them and they showed that that could work.
But the problem was then other premature atrial contractions which show
up elsewhere in other pulmonary veins and burning inside the vein could lead to narrowing of the vein,
which led to problems with shortness of breath, etc. That subsequently led to this idea of,
maybe we just need to electrically isolate all the veins and none of those triggers can get out. That's one potential explanation.
Another there is what's called a Cox-Maze procedure developed by a surgeon
with the theory that atrial fibrillation represents these partially re-entrant wavelets that
require a certain amount of tissue to perpetuate and to be
sustained such that if you cut up the tissue, cut up the atria, you created lines of
scar or electrical block these wavelets couldn't coexist, and therefore normal rhythm would take over.
It's possible that with our ablation, we're also making the atria a bit smaller,
providing less room for these wavelets. Then third, there's this idea
that maybe we're influencing the autonomic tone that I referred to earlier specifically,
there are nerve fiber bunches where it's mainly the vagal anti-adrenalin input
on the heart that happens to sit right next to and right outside where we tend to burn or
freeze when we're trying to get rid of atrial fibrillation and isolate the pulmonary veins.
Indeed sometimes with these procedures as we're burning, we'll see the heart slow way down because we're
irritating that vagal bundle of nerves called a ganglia. It's not uncommon after an eighth of ablation that
individual's heart rate to go up a bit and we think again, that's because we've disrupted this vagal atrial connection
and there's some evidence also that if you activate those ganglia, especially in animal models, you can induce atrial fibrillation.
It may be that one of these things is active in various patients or it's a combination.
Again, the point is that we know empirically in randomized trials
that this does tend to work. This ablation procedure is the most effective means to maintain normal rhythm.
In studies that have compared this to drugs, it tends to win out. Interestingly, it's especially useful in
heart failure patients with some evidence, especially those whose hearts are weak rather than simply stiff.
With some evidence from at least one randomized trial that ablation in those patients can actually reduce mortality.
The success rate is probably on average 60, maybe 80 percent,
perhaps as high as 90 percent. Repeat procedures probably do increase that success rate.
The risks are generally low altogether 3-5 percent. But importantly, the great majority of
that 3-5 percent are things that either take care of themselves, they're not going to result in permanent disability.
The risk of death, permanent disability, something that's really going to be negatively
life-altering is substantially less than one percent. I have become much more sanguine about this procedure.
The last time I spoke about this in 2015. I'm certainly doing this procedure. I've been doing it since I was a fellow,
I started my fellowship 18 years ago. I've been doing it ever since I started on the faculty 16 years ago.
I have been performing this but I've tended to err on the side of being quite conservative. I tend to approach things with
some healthy skepticism and we'll say that the tools have really improved.
They've made the procedure, I think safer, more effective, faster and I've seen
more and more anecdotal success that has accompanied randomized trial data demonstrating
good results with this in select patients. It's not necessarily indicated for everyone and again,
happy to talk more about that in the Q&A. The best candidates are those that are
symptomatic and especially those that are symptomatic and that have failed drugs. The individuals who are
not the optimal candidates tend to be those with a very long-standing atrial fibrillation for years and years.
Sometimes it can help those individuals, but we know the success rate is not as good. Older patients tend to experience more risk factors.
Once we get into the mid, certainly the 80s, and definitely, mid 80s, 90s, I would tend to shy away more from this procedure.
Now, very important to talk about preventing thromboembolism.
This means, by the way, it's not just stroke, which is what we mainly talk about with atrial fibrillation
appropriately because it's so important but remember, there's no reason these blood clots necessarily just go to the brain,
there's now evidence that people with a fib are at a high risk for heart attack worsening kidney disease.
It may also not just be these big clots that lead to a stroke, but perhaps small or tiny clots that
aren't manifest in any way in an immediate sense, but over a long period of time may lead to dementia.
Really this can lead to harm to various organs and prevention of thromboembolism is meant
to prevent all of these things. The mainstay there is to use what we
call anticoagulants or a particular type of blood thinner, which are highly effective
in preventing these complications. Randomized trials have shown less death with them,
as well as substantially less stroke and these other complications. Now we use the term anticoagulant,
mainly in distinction to what are called anti-platelet drugs such as aspirin or Plavix.
Those are also blood thinners and that they block platelets. This blood clots can
have within them platelets and clotting factors, certain types of blood clots,
especially those for example that form in coronary arteries from a ruptured cholesterol plaque
that lead to a heart attack. Those tend to be quite platelet rich and therefore drugs like aspirin or
Plavix are useful for that. The sort of clot that forms in the setting of atrial fibrillation,
seems to be much less platelet related and more related to these clotting factors
that these anticoagulants block. Therefore, aspirin and Plavix don't work particularly well
to prevent all these complications and atrial fibrillation. Interestingly, with these new anticoagulants,
the risk of bleeding however, is about the same as with aspirin, for example.
The first-line drugs we're talking about here, which are also referred to as no acts
for novel oral anticoagulants. NOACs as opposed to the older,
mainstay of warfarin or DOACs for direct oral anticoagulants include Apixiban,
Dabigatran, Rivaroxaban, and Edoxaban I've listed the trade names there as well as Eliquis,
Pradaxa, Xarelto, Sayvasa. Warfarin is also an option. Warfarin is also called Coumadin.
It does work well, has been studied in large randomized trials, but isn't considered second line to
the drugs listed above due to inconvenience since you have to constantly check
for how thin the blood is and potentially adjust the dose. There's a higher risk of bleeding inside the head with
Warfarin or Coumadin compared to these newer drugs. There are some circumstances
where the newer drugs, again, those listed above are not indicated in the setting of atrial fibrillation,
such as when someone has what's called mitral stenosis, which is almost exclusively
caused by rheumatic heart disease. That's a narrowing of the mitral valve or
mechanical heart valves or sometimes people do develop clots
while on these perhaps more gentle NOACs or DOACs and then we give warfarin and can then
dial up how thin the blood is. I just wanted to address
some common concerns that seemed to come up fairly frequently and that I hear from
patients especially when I first introduced the recommendation to start one of these. One is, while they're
new they haven't been studied enough. My response is they've been around now for a decade.
In the randomized trials alone included 10s of thousands of people.
Now we have data from literally millions of people in the real-world, all with very consistent findings
of the benefits of those drugs. Another concern as well, they're not reversible, but there are now antidotes available.
Frankly, even before the antidotes we could control the bleeding. These are gentle enough that we are now performing
procedures on uninterrupted, no NOAC or DOAC. Oftentimes when we put in a pacemaker,
certainly pretty much every time we do an eighth of ablation, including puncturing the veins,
puncturing the septum between the top two chambers were doing it in people who have taken their eloquence or Xarelto that morning.
In general, when indicated, the risk of not taking them exceeds the risk of taking them.
There's a saying that I learned from older investigator that I really like, which is patients don't call you in the middle of
the night to thank you for not having a stroke. Sometimes it's too easy to imagine why I'm doing this thing it's going to lead
to bleeding and it's harder to fully appreciate the absence of something happening.
But of course, we can all recognize that's not necessarily rational per say
just because it's easier to imagine doesn't actually mean it's more probable and the data clearly
show that generally these tend to lead to better outcomes. Now I mentioned properly selected people.
What do I mean by that? Even among people with atrial fibrillation, there's clearly a spectrum of risk of stroke and
thromboembolism and we use the scoring system called the CHADS VASc. We used to use something called the
CHADS2 score but in general, younger patients and those
without any other cardiovascular risk factors. No high blood pressure, no diabetes, no history of stroke,
no heart failure maybe at sufficiently low risks that it makes sense to not prescribe a blood thinner.
Probably especially selling those who have fairly rare atrial fibrillation.
I will say that given the convenience of these newer drugs and how well they work, the field seems to be moving a little bit more towards
erring on the side of generally recommending them. In the next few slides,
I'll move to this new way to approach atrial fibrillation that has to do with prevention,
which of course is always preferable rather than delivering some therapy for
a disease that someone has to first suffer not to mention the hassle and the risks of the various therapies.
I will say it's been very interesting when I was a medical student and even a resident, we didn't think about preventing atrial fibrillation,
we didn't think about preventing electrical problems we certainly thought of that when it came to heart attacks,
reducing cholesterol, stopping smoking, but atrial fibrillation was just bad luck could just happen to people.
More and more, we're starting to recognize that perhaps at least in many, probably not everyone,
especially those for example who have strong genes that make them susceptible. But in many, we might be able to
prevent the disease and also use lifestyle factors to reduce the risk of recurrence.
In fact, these are figures from on the left the American Heart Association,
which now considers Lifestyle Risk Factor Management one of the pillars of treating
atrial fibrillation along with Anti-coagulation, Rate Control, Rhythm Control. On the right here, this is a statement
regarding research priorities from the NIH, the NHLBI. I was fortunate to be part of this group
related to secondary prevention of atrial fibrillation. Meaning that once it occurs,
what are the things we can do to actually prevent it from happening with a major focus on lifestyle.
One of the leaders in this has been a colleague, Sanders, who's in Adelaide,
Australia, where they do a lot of oblations and they had a long waiting lists.
The story goes that they add all these patients that were waiting a really long time for their ablation and they wanted to help them,
wanted to figure out what can we do in the meantime. They ended up examining the effect of fitness training and weight loss,
especially in obese patients. This is a very famous randomized trial
where individuals are randomly assigned to a Weight Reduction and Cardiometabolic Risk Factor Management Strategy
versus just letting them be and they showed that indeed if they can lose weight, become more fit, that
their atrial fibrillation burden went down substantially. Now alcohol has long been
considered a possible trigger for atrial fibrillation. This was a meta analysis now over a decade ago,
and you can see that the findings and individual studies with
equivocal will be where this solid line of one is favoring a relationship between alcohol and AFib.
and we'd be on the right side of this line. One of these studies was mined from actually some work I did as a fellow at UCSF,
but the general conclusion was those who tend to drink more tend to be at a higher risk
of atrial fibrillation which then leads to the question, well, if you've been drinking is the cat out of
the bag or can you still influence the risk-free of it? We published this study where we leveraged
a large prospective NIH funded cohort and we looked at the people who used to drink and then quit,
and found that those people actually did have a lower risk of afib compared to those that continue to drink.
This was one of several studies that the first author here; Aleks Voskoboinik, who we had the privilege to
help train in his cardiac electrophysiology training is Australian. A very clever study
that he did and he's kindly referenced the slide I just showed is one of the inspirations for this study.
So this was part of his PhD with another electrophysiologist named Peter Kistler in Australia where
they took patients with atrial fibrillation who drank pretty heavily, and they randomly assign them to try to convince them,
try to stop drinking versus didn't really tell them anything. They continued to drink. Those randomly
assigned to abstinence exhibited a substantially reduced risk of recurrence and atrial fibrillation burden.
Now what are the mechanisms here? What's going on with alcohol? There's this common conception
that alcohol is good for the heart. There is some evidence that alcohol when consumed in moderation;
meaning about a drink a day, there may be beneficial cardiovascular effects. There could still be a reduced risk of AFib.
This is very controversial, really unknown. I'm happy to talk about this in the Q&A. We're trying to get a major study funded here
when not consumed in excess, but there's also evidence that in people who already
have afib that even a drink might be enough. I'll tell you about that a little bit later. Now the protective effects tend to be attributed
to maybe beneficial effects on lipids, and maybe it thins the blood a little bit which helps prevent heart attack,
but the mechanism by which alcohol may lead to atrial fibrillation has largely been not understood.
We did a randomized study where we took patients undergoing afib ablation. They had catheters in there hearts so we can
measure the electrical activity and characterize the electron activity inside the atrium and we randomly
assign them to a [inaudible] of alcohol titrated to a breath alcohol concentration
of 0.08 percent versus a double-blind must placebo. We found that in the alcohol group
the refractory period of the pulmonary vein electrical activity became substantially
shorter only when people were exposed to alcohol not in the placebo group. That shortening of atrial recovery is something that is
thought to render the atrium more prone to fibrillate. If you imagine those multiple wavelets I described more of them can
co-exist if the tissue is recovering more rapidly. We thought it was especially interesting
that this was found on the pulmonary veins which are the target of our ablation.
We also showed in ambulatory people with paroxysmal atrial fibrillation that if we put sensors on
them and continuously to monitor them for their heart rhythm as well as an alcohol sensor that when
they consume the alcohol their risk of a discrete atrial fibrillation event went up substantially in the next few hours.
This was really the first time that these acute effects were shown. All the previous data had to do with long-term effects,
alcohol as a risk factor for the development of the disease or the burden of the disease
but this was the first evidence that there may be immediate effects of alcohol on AFib.
The hopeful thing is if that's true that also suggests that if you stopped drinking alcohol then fairly immediately you're going to
reduce your risk for a given AFib episode. It was very gratifying to see that study I just
described was covered in The New York Times and they talked about very generally alcohol
affecting the heart even though it was about atrial fibrillation whereas in the past I think again all the alcohol,
heart disease media attention has focused on heart attacks as well as
strategies to prevent the disease. Just to cover a couple of other lifestyle factors.
Smoke along with many other horrible things that can happen from smoking tobacco,
there's now evidence smoking also does increase the risk for atrial fibrillation. We showed that actually
secondhand smoke can be a risk factor for the development of atrial fibrillation and then we just recently
published this study looking at records from more than 23 million Californians seeking
healthcare and found that various substances: methamphetamine, cocaine, opioids, and even cannabis,
actually increase the risk for atrial fibrillation. You may be lamenting, Oh man,
I can't drink alcohol, I can't use cannabis, or Dr. Marcus is telling me I shouldn't use cocaine,
that's all fairly pretty true. What about my coffee? Don't take away my coffee.
I do have better news here. There is this conventional wisdom that coffee leads to a arrhythmias and there's even
professional society guidance without really substantive data that warn
against caffeine consumption to avoid arrhythmias. We were interested in looking at this and just
looked at common early heartbeats. This is in a population-based NIH funded study.
We could find no relationship between how much coffee one said they tended to
consume and the frequency of those early beats, and then more recently we published
a study using data from the UK Biobank. This is from several hundred thousand participants
in the UK. Actually it found that those who drink more coffee experienced a lower risk
of various arrhythmias, and that lower risk was largely driven by a lower risk of atrial fibrillation.
Now these are observational data and not randomized data. We tried to address that by
performing something called a Mendelian randomization studies, so we looked at caffeine related genetic variants
that are at least ostensibly somewhat randomly assigned. There we didn't find a heightened risk of atrial fibrillation,
but we also didn't find a lower risk using these genetic markers
as surrogates for random assignment to at least caffeinated products.
I will end here with these conclusions and then look forward to hearing what you're
curious about and hopefully answering your questions. In conclusion, atrial fibrillation is very common.
We make the diagnosis using a electrocardiogram, also called an ECG or EKG.
Not to be confused by the way with a echocardiogram, and a echocardiogram that's
the ultrasound of the heart and that electrocardiogram needs to be over-read by healthcare professionals.
We shouldn't rely on smartwatches by themselves to make that diagnosis.
Smartwatches can identify those with atrial fibrillation, but we still need to figure out how to
optimally use them in the general public. They perhaps have the greatest utility among
those who already have a diagnosis of the disease. The goals in treating atrial fibrillation are to improve quality of life,
to avoid adverse remodeling, weakening the enlargement of the heart, and to prevent stroke and other thromboemboli.
There are many effective options to address each of these, often working in concert.
Now we recognize that staying physically fit, especially among those who are obese,
as well as minimizing alcohol and avoiding tobacco and illicit drugs may all reduce the risk of atrial fibrillation.
When it comes to coffee, I'm not recommending anyone start to consume coffee because there's
no randomized control trial evidence for that. However, if you enjoy your coffee,
then I certainly would not discourage its consumption.
That is all I have. Thank you so much for your attention. I hope this has been interesting and useful.
Great talk, Dr. Marcus. Thank you. We go through some of the questions here in the Q&A.
There's a number of questions regarding the risks to some of these procedures that you described with regard to
atrial fibrillation ablation here with device implantation. Maybe you can just touch on what are some of the risks
of atrial fibrillation ablation? What are some of the risks of poking a hole to perform this procedure?
Maybe two holes in the heart. Any problems with these leads
in the ventricle of the heart in traversing a valve when we put in a pacemaker defibrillator?
Great question. The most common complication of the ablation procedure is where we go into the veins.
That can result in various issues. Again, that makes up maybe 2-3 percent of all of those complications,
perhaps even as high as four percent. That rate, by the way, is probably now lower. We used to do this based
purely on what we knew about anatomy. We would feel the pulse of
the artery and we would go next to it to get the vein. Now we use ultrasound, so we're visualizing the vessel as we go in.
We use very small needles what are called micro puncture needles and very small wires to initially access the vein.
Usually, if that's a problem, it will manifest as a collection of blood or even a connection between an artery and vein.
Many times those things just take care of themselves. If that becomes an issue, usually, the scenario is not generally the patient is unstable,
but rather they go home. They say, "Yeah, the pain there is not getting better,'' or are
they notice it's swollen. We get an ultrasound, we consult our vascular surgery colleagues.
They will often say just keep an eye on it and get another ultrasound in a few weeks. Once in a while,
about less than one percent of the time they'll actually have to go in and fix it. In terms of other complications,
the poking of the hole between the septum, between the right and left atrium that we do deliberately,
that seals up in about, we think it takes about a month. In fact, we published a paper a long time
ago showing that when you do a repeat ablation, getting back across a little bit more difficult so
that it heals up really very well. There is a very interesting phenomenon
that hasn't been very well studied, but it's been pretty extensively described that in that first few weeks,
some people can develop migraines, especially visual migraines, and there's also evidence that people with
migraines may more often have a little hole there. We all have little holes there when we're in the womb,
and then when we're born, there's a little flap that closes. About 20-30 percent of the population,
there's still a little hole there. We don't necessarily go through that exact spot, but very close to it when we do our transseptal puncture.
The idea of these migraines, that mechanism that's purported,
is there some substance that normally is filtered by the lungs that comes back to the right side of the heart,
when there's a little hole there, it goes directly to the left side and that causes the migraine. Interestingly, those symptoms
reliably go away after three or four weeks, demonstrating that we think that that hole is closing.
Now one of the other more feared complications that remains relatively common,
maybe as high as one percent, is a unintentional hole in the heart,
which usually manifests as bleeding outside the heart, which patients undergoing
these procedures are at high-risk for because we're giving very potent blood thinning, because we're on the left side of the heart and we
want to avoid any blood clots forming there. Should that occur,
the solution that works the great majority of the time is we enter in just under the rib-cage to drain that blood.
That hole usually just seals up again and the key is just draining the blood from outside the heart or
getting into the sac that lines the heart. Usually those patients,
they spend the night with a catheter sitting in there and that can be uncomfortable. But the great majority of the time,
that's less of an issue. Another final complication I'll mention that is really
the worst complication and is extraordinarily rare and it's so rare that it's actually quite hard to study.
To my knowledge we've not seen this among any of our patients ablated at UCSF,
although we certainly care for these patients at UCSF that are transferred from elsewhere, where a hole forms
between the esophagus, the swallowing tube, which, as I described, is directly behind the heart and the back of the left atrium.
One of the things that is especially pernicious about this, or it makes it really difficult,
is that that doesn't form immediately, it comes up three weeks later and can present in unusual ways.
And so we take several measures to make sure we really try to avoid that.
These days, and different colleagues do some different things. I've been using a device
where we put down actually a device that cools the esophagus and prevents it from getting heated
up while we're burning the back of the heart. To quickly move on to the pacemaker question again,
I will defer most of that to Dr. Dolan's talk in hopes of motivating many of you to attend that,
but most of the time it's not an issue.
The heart is unbelievably forgiving of many of the things we do, but it can sometimes lead
to difficulty about tricuspid valve that we traverse with the lead that
goes into the lower chamber closing and that can be an issue sometimes usually over a long period of time.
How about cardioversion? There's question on that as well. Yes. The risks of cardioversion are very low.
It is an incredibly safe procedure. It's been around for a very long time. The most common adverse consequence of it are skin burns,
which again are mitigated by the nature of the pads we use. We see that very rarely.
The other risks would be shocking the heart into another dangerous rhythm,
and that can broadly take two forms. One is we can shock into a dangerously fast rhythm.
There is something that we do to synchronize the shock with
the timing of the way that the heart depolarizes to prevent that.
But in that worst-case scenario, the solution to that is essentially to shock the heart again. There is also a risk of shock
the heart of someone in atrial fibrillation and their normal sinus rhythm comes back very slowly,
and then we would give medicines to speed up the heart. We can also use those same pads actually to
pace the heart from outside if needed. A couple of questions regarding stroke and atrial fibrillation,
including any concept of how or any idea of how long it takes for
one of these clots to form in the heart? Then with catheter ablation,
do we have any idea of whether the ablation procedure long term
helps impact the risk of stroke or lowers the risk of stroke with those individuals that have an ablation?
Yeah, two great questions. I'll answer the second one first I think.
The honest answer is we don't know. There's some controversy in the field.
There is observational data, so there's not yet randomized controlled trial data
which we try to rely on the randomized data, mainly because that's really the only way to
fully mitigate against confounders.
But there's some observational data that those who undergo ablation may experience a lower risk for stroke.
Some will sometimes then stop anticoagulants. In my practice, if
someone's stroke risk based on their other factors is sufficiently high,
even if all the evidence is they have just a normal rhythm I tend to favor continuing a blood thinner.
If their stroke risk isn't terribly high, I'll have a discussion with them sometimes obtain a monitor to make sure there's
no asymptomatic afib and what we call shared decision-making with the patient,
I will sometimes stop the blood thinner. I usually give it about a year
though to make sure it's gone. Then there are the people who, as I mentioned, are so low risk of stroke that it's not
clear that they would even need a blood thinner and those folks, I do often stop it.
Sorry. What was the first question? How long does it take to fully recline presumably once an individual is in atrial fibrillation?
Thank you. There is a convention that we think it
takes about 48 hours at a minimum. However, there are cases that have been
described where the evidence is that atrial fibrillation has been present for
a shorter period of time and yet strokes can occur. Interestingly, cardioverting the heart
heightens the risk for stroke, mainly because after cardioversion the moving from atrial fibrillation to rhythm,
that seems to stun the left atrial appendage and make the blood even more stagnant.
That is not a property of the electricity we deliver. It's a property more of the conversion
from the atrial fibrillation to the normal rhythms. Whenever we do a cardioversion, especially if it's been more than two days,
we always make sure someone has to be on uninterrupted anticoagulation for at least ideally a month afterwards.
Now, it's also important to mention, and I tell my patients this frequently that we don't think just as I described,
that it may not always be the afib that's directly causal to the clot. It's also not the case if you take
someone for example that has paroxysmal atrial fibrillation that, now they're in afib, "Oh no, now I'm going to have a stroke."
It doesn't work like that and I don't want people to be alarmed when they're in atrial fibrillation.
That's suddenly now at that time they're at this very high risk for stroke, I think it's more helpful and more reflective of
the reality to think of it more like treating high blood pressure or treating diabetes,
that the reason to take a blood thinner in the setting of atrial fibrillation, even when it's coming and going,
is to reduce the risk of stroke over years and years.
Everyone with atrial fibrillation and they're not on anticoagulation,
on average their stroke risk is about five percent in a year.
It's not five percent for a given afib episode is certainly not 20, 30 percent. We're talking a longer timeframe.
It's important to understand, as I mentioned earlier, these are not emergencies when you have an afib episode,
you don't need to rush to worry about it. It's treating it over the long period of time. A question came up about
alcohol and I think this is on a lot of people's minds and you've done a lot of research in this area.
There's pretty good evidence that heavy alcohol consumption increases the risk of atrial fibrillation.
How do we weigh mild alcohol consumption given that there is perhaps
some data to suggest that it may be reduces things like heart attacks or some forms of cancer.
How do we weigh the overall risks and benefits of it when atrial fibrillation is
the problem but there's all these other things that we have to worry about? Fantastic question. We don't know and it's,
I think very important. There's even some evidence, as I may have alluded to.
There's one big observational study that suggested that in people without afib, those who drink just one drink a day have a higher risk
of afib compared to those that don't drink. That was from continental Europe.
I think Germany, but I don't remember the country. There's other data from the UK that people who
drink one drink a day may have a lower risk of atrial fibrillation. As Dr. Dolan mentioned,
there's evidence that people who drink a drink a day, there's even a randomized trial evidence may have a lower risk of diabetes,
and they may have a lower risk of leukemia lymphoma. They may have a higher risk of breast cancer, colon cancer if there's a lot of uncertainty there.
We've actually, I mentioned this, I think earlier. We're trying to get a major study funded that
would actually compare a drink a day to near abstinence. A colleague of mine at Harvard
Ken Mukamal who is also really a leader in alcohol-related research, and I have to keep trying
for this one grant mechanism that would work for this. Unfortunately, and we don't want industry funding,
we want to be completely unbiased. We're trying. It's a great question.
We think it's incredibly important and we're trying to do that study.
We would love to do that study and we think it could be super informative and helpful to countless numbers of people.
I would mention more than two drinks a day, almost certainly harmful even
when it comes to heart attack and we've shown that when it comes to all these outcomes.
I tend to recommend to my patients without atrial fibrillation. I tell them, I don't know. I would generally recommend not consuming more
than a drink in a 24-hour period on average. Have you noticed that some of these medications over time become less
efficacious and what happens to the patient whose maybe failed medications,
failed a catheter ablation procedure. Is there anything wrong? Yeah. Treating atrial fibrillation is often very iterative.
It's really a trial and error thing. I really try to also emphasize to my patients that their quality of life is so
important because I know it can often happen that we prescribe a medicine, patients don't feel well on that medicine,
but they say, well, my doctor said I got to take this medicine. I always encourage them, please let me know.
If you're not feeling well, the whole point of this is to help you feel better. Now, the anticoagulants they don't necessarily help
you feel better say hopefully preventing a stroke. But day-to-day, that's not their purpose.
The day-to-day of the drug is to suppress afib, they really should be helping you feel better. If they don't, you need to try something else and yes,
it's interesting for some reason. First of all, some people's given atrial fibrillation
just never is susceptible to a given drug. Sometimes a given drug will work for years and
years and then the afib comes back despite that. Then we go, it's iterative.
We can then try a different drug. We can then try ablation. Sometimes you try ablation. Patient does really well for a couple of years and
the afib comes back, then you try drugs. As I say, it's a fairly constant trial and error,
I say fairly because there are some patients who are on the same drug for decades, never have any more afib.
Or we do a catheter ablation, no drugs and they're free of afib for many years.

Geesh! 90 minutes of watching vice 25 minutes of reading. Oh well,....

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gloaming
Geesh! 90 minutes of watching vice 25 minutes of reading. Oh well,....

Here is the very short summary from a scan:

Don't drink or don't drink more than 1/day.
Anticoagulate with elevated CHA₂DS₂-VASc score
Treatment is iterative:

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The day-to-day of the drug is to suppress afib, they really should be helping you feel better. If they don't, you need to try something else and yes, it's interesting for some reason. First of all, some people's given atrial fibrillation just never is susceptible to a given drug. Sometimes a given drug will work for years and years and then the afib comes back despite that. Then we go, it's iterative. We can then try a different drug. We can then try ablation. Sometimes you try ablation. Patient does really well for a couple of years and the afib comes back, then you try drugs. As I say, it's a fairly constant trial and error, I say fairly because there are some patients who are on the same drug for decades, never have any more afib. Or we do a catheter ablation, no drugs and they're free of afib for many years.

Nothing really new for most of avid Afibbers.org forum readers, but it's an interesting talk.Thanks for posting !

In this video he stated Caffeine is not a bad thing for Afib patients. I used to drink one cup of coffee in the morning, then a few cups of green tea during the day. I gave them up because caffeine is deemed as a trigger for Afib. Now I want to have my coffee and tea back, perhaps limiting to one cup of each per day and see if it affects my Afib. I started to learn what may trigger my Afib, so far, I know to avoid stress, eating too late, eating too much, deep breath, sleep on left side. My last trigger (two days ago) was cold drinks from fridge, never had this problem before, so this is new to me.

Caffeine has been shown in a couple of studies to actually be slightly helpful for afib. The idea that it's a trigger dates back decades to doctors simply thinking any stimulant would be a trigger for afib. They had no actual reason to think that but it became ingrained in everyone's thinking and still persists today.

The takeaway for me, having read tons across the www, is that it really is incumbent upon each AF sufferer to manage their own disorder. It's a learning experience, and each experience is going to be at least partly unique. For example, I haven't found that caffeine is especially intrusive, but I also know that an irritable heart is not going to take too kindly to more than about 80mg of caffeine spread over 8 hours. For me, that is.

I also know that, in my case, sleeping on the left side only works when I am quiet, have been in bed and asleep for about an hour or until the first dream, and at which my heart has almost certainly reverted to NSR (I awaken every day with a pulse of between 46-60, so clearly NSR). My heart is always experiencing ectopic beats when I get into bed, and turning onto my left side is sure to mean a long night lying awake. Later, though, no problem. Instead, after the first couple of jerks, I notice my heart has calmed a lot, amazingly reliably, at which I turn onto my right side and fall asleep inside of 10-15 minutes most often.

Stomach distension, acidic burping, these can all set me off, as can inner abdominal tension when under stress. Alcohol, less so, at least so far. But I have never drunk excessively, at least not in the past 25 years. Alcohol has never been a problem, and I can thank my parents for modeling correct consumption. But people can develop sensitivities to almost anything. My son-in-law can no longer drink beer because his gut is intolerant to a component commonly found in beer...whatever it is.

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gloaming
My son-in-law can no longer drink beer because his gut is intolerant to a component commonly found in beer...whatever it is.

Hoping it's definitely not water !
All joking aside, you're right saying we've to find what works or not for us.
I think we're a lot here not really knowing what's really good or Bad. Just guessing based on some personal events, while trying not being misled by just coincidences.
And I fear there's rarely a single culprit. It's likely a combination of things that don't do anything wrong when checked individually.

I wonder if someone successfully managed to avoid all his/her triggers (I know it's hard but presumably), will he/she be able to put Afib into remission?

Yuxi, because it is a progressive disorder, I think it's pretty much all wishful thinking, no matter how successful we are with avoidance, patience, optimism, and various medical interventions or miracles.

Mine is up an down every ten minutes, and has been since New Year's Eve. I can look at my watch at 0900 and see that it is at 115 BPM. I'm surfing the web, and have been for 30 minutes, inactive, but my heart rate says I'm out for a walk. Then, at 0908, it will show 55, or 46, or 85...take your pick. At 0930, it will be back up to 131. You should see the ECG graphic depiction that my Samsung Galaxy 4 wristwatch shows me if I take a reading during the higher rates. It's horrible.

The point is, apart from some half-n-half coffee or tea, or maybe laughing during a sitcom, I am doing nothing particularly onerous, and I am not under duress or stress. I'm just laughing, and my watch jumps from 85 to 116 while I look. I eat small meals, usually only twice a day, and don't drink alcohol. We did purchase a Toyota Highlander the afternoon my heart went on the fritz again, so it must have been the stress of writing the check. There was no dickering (not in today's market), and the sales person was very nice, long in the tooth, and there was absolutely zero pressure to purchase. It all came from my wife and me. Or, maybe it was when I learned that new owners of Toyotas only get one digital key fob. The second comes months later. They need all the fobs they can get to sell the limited stock they have for sale. At the time, our dealership at exactly two Tacomas, a single Tundra, two RAVs, three Highlanders, and one of their new all-electric SUVs. It's the same for all manufacturers...no chips.

So, I dunno what is going to set my heart off, but it could be anything, any time...or nothing at all. Luckily, Ablation The Second is going to happen for me on the 14th. I just hope it works this time.

Very cool trick George. How did you do it? Thanks!

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Yuxi
I wonder if someone successfully managed to avoid all his/her triggers (I know it's hard but presumably), will he/she be able to put Afib into remission?

Avoiding triggers may be difficult, but likely far easier than identifying them. Most people here struggle finding triggers.

George, I forgot to thank you for your efforts to put it all in place for us. Thank-you!

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Yuxi
I wonder if someone successfully managed to avoid all his/her triggers (I know it's hard but presumably), will he/she be able to put Afib into remission?

This is a bunch of stories put together in 2007 by member Peggy Merrill. It is kind of hard to find since the website got reorganized a few years ago. Here are other things from that time: [research.afibbers.org]

I'll have had afib for 19 years in July. In my first four months, had a 2.5 month episode. Prior to that had 6-9 hour episodes every 10-14 days. I determined my path to afib was chronic endurance fitness. During the 2.5 month episode, my EP said I was doing well out of rhythm and suggested I stay out of rhythm (my afib heart rate was < 100 BPM). I suggested a "Plan B" that included detraining, electrolyte supplementation and a script for flecainide on-demand to convert me when I went out of rhythm. He accepted. I've been following this plan, in a broad sense since. My afib burden in the first 4 months was 57%, subsequently in most years it has been 0.02%. 2021 was a bad year with 15 episodes and a 0.7% AF burden.

Some things I've learned. If I don't supplement with enough potassium and magnesium, anything can be a trigger. My exercise trigger is generally the product of intensity times duration. Long duration high intensity bad, Long duration low intensity OK, Short duration very high intensity OK. In 2012, I learned that excess calcium (for me) made many more things a trigger (cold drinks, laying on left side, the time immediately after orgasm and more). By restricting calcium in my diet, those added triggers went away.

In 2004, I weighed 205#'s. I was very fit but heavier than needed. When I detrained, I started to gain weight, so adjusted my diet (keto adapted in 2009) and dropped to my current 168#'s. Recently figured out that my 300 mg dose of flec for conversion was probably more than I needed and dropped it to 200 mg with better results. This is probably because my weight dropped (as an aside someone should weigh more than 154 pounds (70 kg) for 300 mg of flec).

So I would not say I'm in complete remission. I've kept afib burden very low and certainly a dramatic improvement from 57% in the beginning. Also, as I described, different things can be triggers depending on the status of other factors in the system. Not suggesting that what works for me is a template for others.

George, thanks for sharing your experience and the links, this is really helpful

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gloaming
George, I forgot to thank you for your efforts to put it all in place for us. Thank-you!

You are certainly welcome!

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Yuxi
George, thanks for sharing your experience and the links, this is really helpful

As well, you are welcome!



Edited 1 time(s). Last edit at 02/05/2023 03:13AM by GeorgeN.

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PavanPharter
Very cool trick George. How did you do it? Thanks!

Assuming you mean the transcript. On a computer (Mac in Chrome in my case), there are three dots ... next to Share below and to the right of the YouTube video. Click there and select Show Transcript. I turned off the timestamps to make it a little smaller to copy/paste as our software here was not happy with the amount of text, which is why it is split in two parts.