Articles, Blog

Got Rhythm? An Update on the Treatment of Cardiac Arrhythmias

September 11, 2019

Good evening and welcome. I’m Nora Cain– I’m the Director of the
Stanford Health Library. It’s my pleasure to welcome you
here this evening for a update talk on cardiac
arrhythmias, the treatment of cardiac arrhythmias. And we have the
distinguished Dr. Paul Wang speaking for us this evening. Dr. Wang is the Director of
the Stanford Cardiac Arrhythmia Service, and a professor of
medicine and of bioengineering. Dr. Wang is an expert
in the treatment of cardiac arrhythmias–
including atrial fibrillation, atrial flutter,
ventricular arrhythmias, supraventricular arrhythmias,
and sudden cardiac death. He has practiced cardiac
electrophysiology as an arrhythmia expert
for over 26 years. He was a co-inventor of
catheter cryoablation and has pioneered new
techniques in the management of heart rhythm problems. He is the past chair of the
American Heart Association Council on clinical cardiology,
ECG and Arrhythmias Committee, and is a member of
the Board of Trustees of the leading professional
society in his field– the Heart Rhythm Society. So I’m putting you in
good hands this evening to have Dr. Wang talk
about this important topic. Thank you and welcome, Dr. Wang. Thank you so much, thank you. So first, I’d like to thank
Nora and The Health Library for the opportunity to
speak to you tonight, and thanks for spending
your time with us. So in this talk,
I’d like to give you an overview of the new things
in heart rhythm management, and I hope you’ll enjoy that. So, we have a team– it takes
a village, it takes a team– and so, we have a team that’s
responsible for the care of patients with arrhythmias. So we have a mission statement
as well, and that’s– we’re dedicated to delivering
compassionate and outstanding care of patients
with arrhythmias; working with their physicians
and advancing teaching and medical research
in this field. And we tremendously
value the trust that your physicians and
their patients place in us, in terms of responsibility–
we take very seriously. So our vision is to be
one of the top recognized, as one of the top
programs in the nation. We focus on delivering state
of the art arrhythmia care, and being a leader
in innovation, translational research, and
providing outstanding service and access. So there’s a whole range of
different types of procedures that my team is involved in– we’ll be talking
about some of these. Catheter ablation,
a certain technique to treat a variety
of arrhythmias. These include atrial
fibrillation and flutter and tachycardias– what we call supraventricular
tachycardias, or SVTs, as well as ventricular tachycardia. There are other diagnostic
tests that we perform, including that of cardiac
electrophysiological testing. And then we are responsible
for the whole range of implantable devices– and they include pacemakers,
implantable defibrillators, and such things. And the management of devices– and that may be removal
at time of infection, or in times of malfunction
in other procedures, such as cardioversion,
et cetera. So one of the first things
I’d like to start this talk– and introduce the idea of– what are the things
that are warning signs? What kinds of things
need evaluation? And these aren’t specific
to arrhythmias only– many can be other signs
of other conditions, including other cardiovascular
illnesses as well. And so they may include
chest discomfort; arm or neck discomfort, particularly with
exertion; shortness of breath; other symptoms– such as
dizziness, lightheadedness; and certainly passing out,
so loss of consciousness. And then, very
frequently, arrhythmias present as an irregularity
or rapid heartbeat. And so, these are
the kinds of things that we recommend would be the
things to prompt evaluation. So let’s take a situation–
a very common one– where a woman presents
with a rapid heart rhythm. This is an electrocardiogram
of such an episode. This is a rapid
tachycardia, that we call supraventricular tachycardia. So what do we think about
when we talk about this term? Well, we talk about tachycardia
as meaning rapid heart rhythm. We contrast it
with sinus rhythm, or normal sinus rhythm–
which is normal rhythm. The opposite of tachycardia,
which is a fast heart rhythm, is bradycardia– which
is a slow heart rhythm. So indeed, we have the range of
different kinds of conditions and next we’ll come back
to this idea of where these things originate. So things are named, frequently,
by where they originate in which chambers of the heart. So if they’re in
the upper chambers, those are the atria;
or the lower chambers, and those are called
the ventricles. We’ll be using some
of that terminology, in terms of where these
rhythms originate. The other thing that we would
comment upon is the heart rate. So we’re all familiar with
the pulse being taken. So the pulse is reflecting the
rate at which the main pumping chambers of the
heart are pumping– and those are the ventricles. So when we talk
about the pulse, it’s really reflecting the
ventricular rate– the lower chamber rate– and not necessarily
the upper chamber rate. So, to understand
this better, we turn to this kind of diagram. And so, in looking
at this, we see that the upper part of the
heart, in that structure, is a structure called
the sinus node. Or, in this case,
it’s called SA node– sinoatrial node. And so, the signal
is going to travel from this top of the atrium,
through the upper chamber of the atrium, to this
structure– that I’ve highlighted with an
arrow– called the AV node. So the AV node acts as a
staircase that connects the top floor of the building–
or the heart– in the bottom floor– the ventricles. And so, that’s its purpose– it serves as a conduit,
or a controlling device, to control the rhythms that
go from the top to the bottom. And then it’ll spread
through the lower chambers through the ventricles. And that’s how conduction works,
from the top to the bottom. So when we think
about fast rhythms, and we think about
particularly fast rhythms in the upper chambers,
many of these we call supraventricular– meaning above the
ventricles– tachycardias. And so, in the little
diagram you see on the left, there’s a little
circle that represents the electrical activity that is
going around and around– much like a car goes
around on a racetrack. On the right hand panel,
you see an example of a similar green outline
of where the path is going– but, in this case,
a larger path. And this is another form of a
supraventricular tachycardia. And these are examples
of the kind of rhythm, that we saw, that
this patient had. So what can we say about the
various steps of approaching such a situation? So first, we want to
establish the diagnosis. So how do we do that? So one of the
particularly, I think, unique parts of heart
rhythm management, arrhythmia management, is
that to record the rhythm is very important. And that we do using
an electrocardiogram. Now that can be a
routine electrocardiogram that you’re used to getting
in your doctor’s office– we call that a 12-lead
electrocardiogram. Or it may be something that
you’ll be carrying around– some kind of a device
we call a monitor. And I’ve listed several
of these types of monitors that are in common use. The very initial monitor
that was developed was called a ambulatory monitor. And the name of the
individual was Holter, so many people call
this a Holter monitor. And this was our very
first kind of monitor that you could
really carry around. It had a little recording
device– in those days, it was a cassette tape. And now, it’s obviously digital. Now there are longer monitors–
even things that look much more like a Band-Aid– that you can place
on, that might be good for seven to 14 days. And then other
monitors that may go for more extended periods of
time, such as a 30 day monitor. So as I’ve tried
to outline for you, this becomes paramount in
diagnosing the condition because we need to be able to
get a clear picture of what it looks like. And we do so with some form
of an electrocardiographic recording, as I’ve
illustrated here. So one of the key things that
we try to decide about is, in fact– do all of these rhythms
require treatment? And indeed, not all do. And, in particular,
the kind of condition I mentioned that
this patient has– supraventricular tachycardia. Why is that important? Well, the issue is, for
some rhythms, they’re not– by nature– life-threatening. And so for these, the kinds
of factors I’ve outlined here are really the ones that
we consider the most– and are the most– important. So the decision is made
on these various factors. So what are some of these? So some of them include
frequency of symptoms. So you may have them
very infrequently– oh, once every several years. Another patient may
have them daily. Severity of symptoms– some
patients may experience things like chest pain, dizziness,
shortness of breath– other symptoms that
are directly related to being in this fast rhythm. It turns out many
of these rhythms are self-terminating– meaning
they stop on their own. But sometimes, they continue on
and require medical attention to stop the rhythm. So medications, or a
need for medications, to stop the rhythm problem. And then there may be
other medical conditions that are relevant. So someone may have
relatively severe blockages of the arteries of the heart. Other types of heart conditions
that make us [INAUDIBLE] treat this situation in a
greater number of patients. So these are some
of the factors we would use to make
a decision to treat a condition, like a
supraventricular tachycardia. And similar principles can be
used for many other arrhythmias as well. So what are some of
the basic treatments that we can think about to
treat these supraventricular tachycardias that
I’ve mentioned? So one category is something
we call vagal maneuvers. And these are
maneuvers that we can do to stop the tachycardia– the most common, of
which, is bearing down. It’s a special maneuver
called valsalva maneuver, but it’s really
just bearing down in order to try to stop that. And it does so by changing
the properties of the AV node that may result in the
termination, or stopping, of the tachycardia. The other point that
I have on this slide is really that
medications may be useful to treat
this kind of rhythm. And in particular, as
the arrow points out, they’re directed
towards the AV node, since many of the
conditions– that are called supraventricular
tachycardias– use the AV node in order to
perpetuate the tachycardia. So these are our two
very common strategies– that is acute treatment with
bearing down by the patient; and then, otherwise, medications
that affect the AV node– that either can be given
acutely or, even more commonly, taken on a regular basis. So what are some of these
examples of medications, in terms of this approach? So I’ve listed three
categories of such medicines that predominantly
affect the AV node. They may have other
functions– they may affect blood pressure, et cetera. And, in fact, many
of these– not all of them– but many
of them actually are used as anti-hypertensives
and are used to treat high blood pressure. So what are these? I’ve listed Digoxin, which
is an older medicine– probably not as commonly used,
but still, in some patients, has value. Beta-blockers, and
examples include– I’ve listed some– metoprolol,
atenolol, and an older medication called propranolol. Or calcium channel blockers,
such as diltiazem or verapamil. Those are commonly used, again,
to [? effect of the ?] AV node. And we’ll talk
about this more when we get to a discussion
regarding other arrhythmias, such as atrial fibrillation. As an alternative to these
medicines– and these medicines make up the vast
majority of treatments of supraventricular
tachycardia– we can consider
other techniques. One which we call
catheter ablation. And, by catheters,
we mean plastic tubes that we insert in the body. And ablation refers
to this concept that delivering energy to
certain cells in the heart can kill them and,
therefore, treat the heart rhythm effectively that way. So that’s our
first topic that we talked about–
our first case was that of a supraventricular
tachycardia seen in a patient, presenting as palpitations
and rapid heart rate. So now we’re going to want you
to take another situation– and I’ll be talking about
this for the second segment of the talk. And that is regarding another
kind of condition that involves racing heart beats. And so, this is a patient
who comes in and says, I have a racing heart. And the doctor says, OK,
I better do a monitor– I better find out
what this is due to. And so, that’s what
we’re going to look at. So the monitor shows a rhythm
called atrial fibrillation– and that’s the one we’re
going to talk about next. In the little diagram
here, you see– unlike the arrow
that we saw before, which is a single
circuit, or a circle– it is going every which way. You can see the arrows
are pointing one way, and then pointing another way. And that’s our concept
about atrial fibrillation. The way I describe
it to my patients is it’s like a sand
storm, or a wind storm, blowing around very rapidly– it doesn’t have the
same organization like the car on the racetrack. So what are some of these
different symptoms to consider? And these look
familiar because many of the ones we’re seeing,
for any arrhythmia, may be seen with
atrial fibrillation. And so, these are some of
the terms many patients use. They’ll say, it feels like
a jumping in the chest; a racing heart, a very
rapid heart action. And again, there may be other
symptoms– such as dizziness, loss of consciousness,
shortness of breath, chest pain, and those kinds of things. It even may be more general
than that– less specific, in other words, a symptom. It may not be something
that we can necessarily tie to an arrhythmia. And that might be fatigue,
lack of energy, exertional intolerance– those
kinds of things. But that may be the major
manifestation of an arrhythmia and particularly
atrial fibrillation, would be those
kinds of symptoms. So one very important
thing that, commonly, I’ll have this discussion
with my patients, as to– what are
some of the factors? What are some of the
things that can precipitate atrial fibrillation? And so, we go through
a discussion of these. Maybe not talking
about all of these, but I’ve listed
a number of them. So on the top I’ve
listed, actually, something that I think is
pretty important– in terms of precipitating
atrial fibrillation. It’s some degree of exhaustion– fatigue– that,
I think, stresses the person in a particular way. That, I think, is a
very important trigger of atrial fibrillation. It may be quite surprising– the
second one– that I put down, which is dehydration. So we all have a certain degree
of hydration we’re used to and we function. But dehydration,
I think, appears to be a fairly common trigger,
or a precipitating factor, of atrial fibrillation. Now, the next two
are what we would regard as different stimulants–
so caffeinated products, alcohol. [? They ?] also may,
in some circumstances, precipitate atrial fibrillation. I’ve listed sleep abnormalities. That may be as simple as
not getting enough sleep, being quite busy,
and not getting enough in that situation. Or it may be a
sleep-related condition– something we call sleep
apnea, or another kind of sleep disorder. Something that interrupts
the sleep is the theme there. Stress– much like
exhaustion and fatigue– can be an important trigger,
or precipitating factor. And by stress, we
generalize that– that can be emotional stress,
physical stress, even a combination. And we think that could be
quite important in precipitating atrial fibrillation. Some patients are
surprised when I say, oh, a procedure or
surgery could precipitate atrial fibrillation. But that’s actually
quite common. And often, we’re
asked to comment before a procedure
or surgery, well oh, is there something we need
to look out for before we go into that procedure? And I usually am pretty
quick to say, ooh, you might develop
atrial fibrillation. That’s not uncommon,
at all, around the time of your procedure. And that could be something
as simple as a simple test. It could be something
more involved– like endoscopy or colonoscopy. Even what seems like something
unrelated to the heart– like a knee procedure,
or something like that– can trigger these
kinds of things. And this is probably for
a variety of reasons. I’ve listed thyroid. Overactive thyroid
is well-established– we’ve known about
this for decades– and occasionally, is overlooked. I think, generally, our
field is pretty clued in to look for thyroid function
tests in this setting. But occasionally, I see, oh gee,
that may be what’s going on. And that’s a very
important thing because, without the treatment
of thyroid condition, you’re unlikely to be
successful in treating atrial fibrillation. Exercise can
actually precipitate atrial fibrillation. In some patients, it does that. Even elevation– I’m asked
that frequently– oh, I’m going to go up on a
trip there and what’s that going to be like? And indeed, elevation
may be a component. So these are only
some of the factors. Clearly, there are other
things that may precipitate– other medications, things
like that; other stimulants– just to give you an idea of
the different kinds of things that might be involved in this. So going back to this concept– I said it was like a sand
storm, or a wind storm. This refers to the
electrical signals. So that’s the way in which the
electrical signals are going about in the upper chambers. That’s what makes it
atrial fibrillation. So just to say a word about
it’s importance as a condition– it really affects
millions of patients. And I think, in
general, these are underestimations– we think now,
in terms of, how many people have atrial fibrillation. The other thing we
notice is it indeed– it does get more prevalent
as we all get older. There is also an associated
increased risk of stroke, and we’ll talk
about that further. And it may have
important effects on other cardiovascular
mortality. So I use this slide
frequently because it gives us a very visual image of,
really, the patients that develop atrial fibrillation. In the dotted line, is
the US population by age. And so, you can see there’s
a little bump there– that’s kind of the baby
booming plus group, I guess. And you can see that,
in the green, the bars– those are actually patients
with atrial fibrillation. So you see, in fact, that
atrial fibrillation is largely a condition from 60 to 85– the vast majority of
patients are in that bin. And so we notice that, as our
patient population clearly is aging, that we see
more and more patients. So you can see, indeed, we’ll
have quite a lot of business in the future, in terms of that. So one thing, in
terms of terminology– if you talk to your
physician, if a family member has atrial fibrillation,
that they might use this word– is persistent versus paroxysmal. So when we talk about
atrial fibrillation, we have a very specific
meaning in mind. Paroxysmal atrial
fibrillation is really atrial fibrillation that
can come and go on its own. It literally is going inside the
door and coming back and forth, and it just goes as it pleases. Persistent atrial fibrillation,
however, generally requires some intervention. There needs to be something
to reset the rhythm back to normal– get it to go back to
the rhythm previously. And that usually takes
some medications, or an electrical shock we
call electrical cardioversion. So some intervention
that’s, typically, necessary in persistent
atrial fibrillation. But we’ll talk a
little bit about that, so I thought it was important
to mention the difference. So back to what is the
cause of atrial fibrillation in its manifestations. To understand that,
one has to recognize that the atrial rate– that is how many beats are
circulating around and going very rapid in the atrium– is basically beyond counting. It’s in the 300,
400, 500 plus range. And so, therefore, it’s
really not possible that you really get a clear
count of how many beats there are. However, we’ve already talked
about the way, in which, impulses get from
the top chamber to the bottom– from the
atrium to the ventricle. And we said it was that
structure in the middle– the staircase–
called the AV node. So that’s the same thing
for atrial fibrillation– its got to go from
the top to the bottom. So when we talk about heart
rate in atrial fibrillation, we’re talking about how
fast the lower chambers go. So what [? determines ?] that? That’s the statement
in the middle– the AV node prevents
from most of the beats from getting from the
top to the bottom. So it acts as a blocker– a filter, you could say– to prevent many of the beats
from coming from the top to the bottom. And that’s the basic concept
we have, in terms of thinking about the heart rate we call the
ventricular rate, in this case. So one of our first jobs,
as we evaluate patients with atrial fibrillation, is
to do what’s illustrated here– to assess the ventricular
rate, meaning is it too fast? Do we need to slow it down? Are there things that we need
to do that will be helpful? And so, these are going to look
very familiar because they’re the same medicines that
we talked about being used for other conditions– such as supraventricular
tachycardia. They’re medications that
affect the AV node– Digoxin, beta-blockers, and
calcium channel blockers. And so, why is this valuable? We can often see a remarkable
improvement in patient symptoms simply by controlling
the rate better– making sure that the heart
rate is not nearly as fast as it was previously. The next topic is that of– well, what can we do beyond
controlling the heart rate in atrial fibrillation? And that’s where these come in. So I’ve written here that,
if the patient remains symptomatic– that is despite
keeping the rate better controlled– that you may use
certain medications. And these are six
anti-rhythmic agents. So, as the name implies, that
the anti-rhythmic agents work against the atrial
fibrillation– they try to bring
it back to normal and maintain normal rhythm. And so, we can select among them
for various different reasons. And so, there are a
variety of reasons– whether it’s kidney
function, other factors about the patient– we could select among the
six that I’ve listed here. And as you see, they’re
highlighted in red– Flecainide, or Propafenone;
Sotalol, or Dofetilide; Dronedarone, or Amiodarone–
are those six medications. So we may pick among
them and choose one that’s right for
the individual patient. So the next topic, before
we continue our discussion about rhythm control,
is to talk about stroke. So we talked about there
is a risk of stroke that can be increased
with atrial fibrillation. And there’s great– meaning
significant– data that lead us to believe
that we can markedly reduce the risk of stroke. And so, these are some of
the very pioneering studies that showed with
warfarin, or coumadin, that you can go from the
yellow bars to the aqua bars, in terms of the risk of
stroke in atrial fibrillation. And that’s whether you
have many factors– risk factors– for stroke. And regardless of your
age, it reduces it to quite a low level. So we’ve recognized that
for quite some time. Now this field
continues to evolve, as many parts of our field. And this is the very latest. In the last year or so,
the United States guideline shifted to this score called
the CHADS2-VASc scoring system. So what does that all mean? So in the little table
that I’ve illustrated here, you get the number
of points that are listed on the right side. Well, the more points,
the higher the risk we think of having a stroke
in atrial fibrillation. So by making this
scoring system, the idea is that we
can assess that risk and, therefore, advise
people about therapy. And so currently, and
this is still under– I think it’s going to
be adjusted and revised, as these guidelines are
revised in the future– but currently it says that,
if you have a score of zero, that no therapy is
necessary, or obligatory. If you have a score of one,
you can be any of the options– that is have no therapy beyond
an anticoagulant or aspirin. And if your score
is two or more, you’ll want to be on an
anticoagulant in most cases. So this is a practical
scoring system. Clearly, there are limitations–
every individual is different. But, indeed, we have some way to
describe and guide caregivers, in terms of what
would be necessary, in terms of anticoagulation. So what are our options
regarding this anticoagulation choice? So, it could be warfarin. And many, many of our patients
remain on warfarin– they’ve been on warfarin for one,
or more, or several decades. And they’ve remained on it. I illustrate one
thing here that there are some newer technologies– not in warfarin, but in
terms of the monitoring. We call it the INR, or
international normalized ratio monitoring, which
are blood tests. So previously, you had to go to
a lab and get the blood tested. This is a home unit where
you could just prick yourself and get a little small sample. And it’s very convenient. And many of my
patients who travel– like to be free of
going to a laboratory– really find it useful. Then I’ve listed the currently
available FDA approved oral anticoagulants, and
I’ve listed them here– dabigatran, or Pradaxa;
rivaroxaban, or Xarelto; apixaban, or Eliquis;
and edoxaban, or Savaysa. And so, these are
newer agents– and I’ll talk a little bit
about that as well. So back to our
discussion about what rhythm management should be. I mentioned that there
is a procedure called catheter ablation– catheter,
being these plastic tubes; ablation, using energy
to kill islands of cells responsible for
the heart rhythm. And so, the principle
here is, if the patient remains symptomatic– despite having these
medications that we’ve already talked about– they might be limited to
exertion, shortness of breath, or other symptoms. That patient is the
typical candidate for catheter ablation. So what are our target sites? So this is one such example– these are structures
called the pulmonary veins. These connect the lungs
to the left atrium and are felt to be
the most common– not the only– but the most
common triggering areas. That is– we think that that’s
where the atrial fibrillation is starting, and it’s
responsible for the initiation of atrial fibrillation. I say it’s like a match
you put into the fireplace, or to get the fire going. What are the
different– the latest, in terms of our development? So radio frequency, or
radio waves, is approved; freezing, or
cryoablation is approved; and then laser
has been approved, and is in the process of
being rolled out and released. So these are different
techniques that have been used, and are currently being used,
in terms of catheter ablation of atrial fibrillation. So I’ll show you some
of these studies. This is the very first FDA study
for any radiofrequency ablation for atrial fibrillation. And in red is the use of
the catheter ablation, and the blue line is
that of medications. And so, you can
see that comparison was, in terms of recurrence– there were more
recurrences, clearly, and quicker in the patients on
medical therapy in this study. And that’s pretty much what
most studies seem to show. This is the freezing, or
cryoballoon, you see here. It’s a balloon
that’s positioned– see in the middle here– around the pulmonary veins. And you see a very,
almost, identical graph that you see the upper
line for cryoablation; bottom line for drug therapy. And again, showing a
gap between the two. What’s happened in the
successive years is, gradually, the techniques
have been better; the tools are better;
and the success has gone up, in terms of the
freedom of atrial fibrillation following catheter ablation. This is a recent study that
compared cryo, the freezing, versus the radiofrequency,
the radio waves. And in the overall study,
they were superimposed. There are some subgroups, which
favor one versus the other– that’s for the
re-hospitalization, for example. Cryoablation seemed to be
superior in this study. And similarly, need
for repeat ablation seemed to have the same effect. But again, other studies
are being conducted as well. So what can we
think about the risk in the success of
catheter ablation for atrial fibrillation? So indeed, the risk is
higher for catheter ablation of atrial fibrillation
than, say, other arrhythmias– such as
supraventricular tachycardia. It’s probably in the 2%– maybe 3%– of serious
complications. We think that, for the
patients with paroxysmal atrial fibrillation, that the freedom
of atrial fibrillation at one year is up to 80%
or so, but still may require a second
procedure, and then lower success if you have
persistent atrial fibrillation. There may be some early atrial
fibrillation the first three months– most of the time,
that goes away. There are some new arrhythmias
that can be created. Again, most of the time,
they settle out on their own. The larger the atria
appears, as well as being persistent
atrial fibrillation, seems to be a predictor of
less likely to have success. Not [? absences ?]
necessarily, but just a lower than for paroxysmal
atrial fibrillation. So one of the key things,
as I described to you, is that the field
has tried to learn about– where is it that we
should focus our ablation tools? And I mentioned that there
are these structures called the pulmonary veins– the
little areas that I said were like the fire that
you put into the fireplace. So this is a little
color map that was drawn by one of my
colleagues, Sanjiv Narayan, who has developed a new strategy. And the idea is to be able
to find other places that are responsible– that
are the key sites– that we might be able
to ablate our approach. And so, this is what
we’re kind of looking for. We’re looking for like a storm– a little area that
we can see a pattern. And this is what we call a
focal impulse, or a rotor map. There’s a little movie
in the left hand corner– which is kind of cute. You can see a little
bouncing ball move around. And that’s the
computer-generated computational analysis
of electrical signals. And you can see that
there’s a pattern you can see in this patient. And so, this would be
an example of an area that we specifically
would target– where the little bouncing
ball is going around. And so, that’s felt to be an
important mechanistic addition to our understanding
of atrial fibrillation. And these studies are
underway, but it’s something we do in regular practice now. These are some of the initial
studies showing the difference in benefit, using
this technique. And again, more studies are
underway to really elucidate the degree of
benefit, et cetera. One other topic that we
always want to mention is that atrial
fibrillation is a spectrum. And indeed, you can kind
of see it outlined here. They may be at the
very top– that is paroxysmal
atrial fibrillation, have a very normal size atrium. And then, as you get
farther down into the red, you see larger
atria, longer periods of atrial fibrillation–
meaning they’re persistent; they continue on for
more than one year. And that leads to a
more advanced situation. And so, the same
techniques may not be as successful for
the bottom, compared to the top of the groups. And so, we’ve really tried
to find other options. So this other option, that
I’m describing to you now, is something that we call hybrid
surgical-catheter ablation. By that, we mean that
the surgical colleague, that we have, puts little ports
between the ribs in both chests and then applies the energy
on the outside of the heart– doing very similarly what
we do from the inside, but from the outside– with very specially
designed tools that are made to be
used on the outside. And that’s one of
the examples of what we call a hybrid
surgical-catheter ablation. The second part of
which is, we then go– in a separate setting
typically– from inside and will then do the ablation. It is a longer hospitalization–
that’s mainly the time it takes to re-inflate the lungs– but we think it probably
has higher success. So that’s another
variation on this approach of ablation– in
this case, a combined surgical-catheter approach. This is some of the early
data from a combined series in the Netherlands
and in Virginia– which kind of show you both
with antiarrhythmic agents and without; success
is in the type 80%. There’s a clinical
study that we’re starting that’s a national
study that is examining this. And the hope is that this
will lead to a specific FDA approval for this
procedure for patients with atrial fibrillation. The tools are FDA
approved already, but what they want
to be able to do is to demonstrate the degree
of success using this approach. One particularly important
topic that we, generally, have overlooked in our
field is prevention of atrial fibrillation. Pretty much all
I’ve said, so far, is really diagnosis
in management of atrial fibrillation–
not how we can prevent it. We touched upon a little bit,
in terms of the precipitating factors. But here, we’re going
to talk about what causes atrial fibrillation–
what are some of the things that we can do? And so, we’ve listed
some of those– treatment of hypertension, we
think, is extremely important; treatment of diabetes, metabolic
syndrome, hyperlipidemia, excess lipids or cholesterol. Obesity– weight loss
is, therefore, important. Sleep apnea and, therefore,
treatment for that– that’s important. Various kinds of
stress are important. Smoking cessation,
decreasing alcohol intake are probably all important in
managing atrial fibrillation. So this is a little
nice figure that was from a group that’s a leader
in this field in prevention– they happened to be on the
other side of the globe, in Australia. And they’ve done some very
aggressive work regarding this, and I’ll show you some of that. So this is their work. It shows that, on
the left hand panel, even if you do not do ablation
or drugs, the patients who had weight loss– those are in the red– did far better than the people
who had minimal, or no, weight loss. So even without
using medications, they were able to– with a very aggressive
intervention– all those things that we talked about. In particular
here, weight loss– they can show a very
important impact, in terms of the
success in treatment of atrial fibrillation. When you add ablation and
drugs, to the right hand side– clearly, all the boats rise. But the patients who have
a significant weight loss– indeed, its successes
were even better. And this is even
with– if you can look at even– single
ablation procedure versus multiple
ablation procedures, you see that still holds. So this group has been a leader
in the country, I would say, in terms of trying
to demonstrate this. And I think the rest
of us are really trying to embrace this as well. And now, we’re just starting
a program at Stanford and getting going to
look at prevention of atrial fibrillation as well. And this is that AF risk
modification program. And also, there’s a mindfulness
study that’s underway by one of our nurses– who
is a PhD candidate– that’s going to be running
our programs in that area. So, in this second segment
of atrial fibrillation, what are my messages to you? So, generally use rate control– that is to calm the rate down. We generally use
antiarrhythmic agents to improve symptoms– to
decrease atrial fibrillation recurrence. We know that catheter ablation
of atrial fibrillation has been shown, compared
to antiarrhythmic drugs, to reduce symptomatic
recurrences. That’s quite important. Anticoagulation for
patients at risk may, in fact, be
important in reducing risk factors for stroke. Addressing the various
things that I mentioned that are involved in
atrial fibrillation– such as hypertension, diabetes,
metabolic syndrome, obesity, sleep apnea, stress,
smoking et cetera– may be important in decreasing
atrial fibrillation. So in the last part
of the talk, I’d like to shift gears
a little bit– and this is about a totally
unrelated condition. So in the yellow here, it has
these mysterious letters– SCD. And so you kind of think,
well, what is that? So you look and say, well,
I’ve heard of AIDS or HIV. You’ve heard of breast cancer,
I’ve heard of lung cancer. Clearly heard of stroke. But I’m not sure
I’ve heard of SCD. But look at the
numerical numbers– these are deaths in
the United States. About 300,000– 1,000 a day– in the United States
alone, patients die of SCD. So what is that? So that’s sudden cardiac death. So it is a condition that is
one of the most important causes of death in our society. And yet, as you
probably surmise, I think the recognition of it as
a condition is not very large. And so, when I give
talks like this, I really try to
educate the community about how big a problem
it is, and how we can all work together to fight it. So what is the reason for this? Why do so many people die
of sudden cardiac death, or cardiac arrest? So the reason why is that–
so survival, even in 2017, is 10% or less. That’s extraordinary. There aren’t many
conditions that can happen– when you flick a switch,
that have a mortality of 90%. And the reason, in
particular that’s true, is that survival declines
about 10% with every minute after the cardiac arrest occurs. So within 5 to 10
minutes, the success of resuscitation– we would say
revival from cardiac arrest– is quite low. So time is of the essence. This is why, currently
throughout the world– the United States– now all of you, I
think, have seen and are aware of what
a automatic external defibrillators is. Indeed, they’re around us,
luckily, at this point. And that’s due to many factors. American Heart
Association was very proactive in disseminating
these, making sure that manufacturers
would have a market so they could
significantly reduce the cost from the initial
$10,000 to, now, $1,000 for each of the AEDs. And the ability of technology
to provide something that laypeople
now can use– it’s not made for the trained
personnel necessarily. And so, the way in
which it does that is it has visual and voice commands. So it literally talks you
through the resuscitation. And when people
have done studies, they’ve done analyses of
patients that get resuscitated. They found that, for
example, in O’Hare Airport– one of our busiest airports in
the country, if not the world– more people are resuscitated by
people passing by than people employed by the airport. So you know that, now, we
have the technology that’s really designed
for the layperson to be able to do this. They even did a study– they
put, in a room, 13-year-olds. And they said, here– they didn’t give you
any instruction– they said, do what it says to do. So someone figured
out how to turn it on, and it started to talk to it. And they did it perfectly. So it’s really possible
for the lay public to be a major factor. And that’s really
what we need to combat this important condition– to be
aware and involved in treating this kind of condition. So that’s really one of the
major take home messages. This, I always
think this produces a little bit of a chuckle– so where is the
highest likelihood of survival of cardiac arrest? So we say hospital, airport,
airplane, casino, sports arena. So the funny part– or
I guess we would say– is it’s dramatically a casino. And so, I reasoned that,
not only is it humorous, but it actually says
something very critical, in terms of the mechanism
of this condition. In particular, how
survival can be increased. And these studies– they’ve been
duplicated a number of times. The survival of patients who
get resuscitated in casinos is very high. And the reason why is that
it’s a matter of time– we already mentioned that. So time requires
people to recognize what’s happening very quickly. So recognize what’s happening,
get help immediately, bring the AED over, and perform
successful resuscitation. So in the casino,
as you can imagine, someone’s watching
every single person in the casino every minute. I don’t think it’s
for this reason, but it’s for other reasons
that they’re doing that. So what it means is– what
they’ve done, actually, is really, I think,
terrific in casinos– they’ve actually trained
their staff to, in fact, go on the walkie talkie and say,
someone’s down, go get them. And so, they go to the place
and they bring the AED over, and they resuscitated
the patient, again, very successfully. And so, the point I have to
make is– it’s about time. It’s about getting to the
patient quickly and one knowing– so education
is very important– that there is an AED, when you
should be using AED, et cetera. And this is really– as you know, AEDs are
now in every fitness club in the state of California. They’re obviously in every
airport and every airline. And they’re increasingly in
other public areas as well. So, as we have a greater
dissemination of AEDs– in my opinion, that’s going
to be a very important step in increasing survival. So related to this– this is
another part of this puzzle, you could say. So this is a woman who,
I’ve highlighted in yellow, has had a prior heart attack– comes in for a routine
test, is doing well, has a good stress test, is
on excellent medications. But, my question is– what piece of
information do we need to know beyond she’s doing well,
and all these things are good? So it’s something called
the ejection fraction. So ejection fraction is a very
common, readily available, number that’s used routinely
to assess the pumping strength of the heart. It’s the percentage
of blood pumped out with every heartbeat. That’s normally 60%. So when it gets down to
about half that value– 30% to 35%– we’ve
recognized now that patients are
at much higher risk to have sudden cardiac death. And so, for these patients,
we’ve elucidated– in these patients with this
lower ejection fraction– that, in fact, they
have this risk. So they have a
increased risk of sudden life-threatening collapse,
due to these ventricular arrhythmias. And therefore, the
solution is really that of a special
pacemaker-like device called an implantable cardioverter
defibrillator, or ICD. And so, that’s being
used now for several– over almost two decades
in this kind of role. There’s a little picture
of the defibrillator– it’s like a pacemaker. And it gives a shock to the
heart if it needs to have that. And this is, again,
just like an AED, but it does so automatically. So you don’t have to wait
for somebody to come. You don’t have to
wait for somebody to recognize that you’ve
developed this rhythm. The device does so rapidly– within seconds– and is
able to convert the rhythm. So the success of resuscitation
with a defibrillator is over 95%. So it went from less
than 10% to over 95%. So that’s really what it is. So we’ve talked about
a lot of conditions. We’ve talked about
atrial fibrillation– over 2 million for sure. Sudden cardiac
deaths– over 300,000. There are many
other conditions– myocardial infarction,
heart failure– and over 5 million
people in the US. And so, these are all
the kinds of conditions where we do recommend people
seek medical attention. Another common question I get
is evaluation prior to sports. In general, what we recommend
for any individual– history and physical
examination; and selectively electrocardiogram. And if there are other
symptoms– dizziness, passing out– we typically do recommend
a more extensive evaluation such as echocardiogram,
things like that, to look for certain
structural abnormalities. For patients that are older– in fact, starting an
exercise program– we’ll often recommend
a stress test. That’ll be another thing
prior to participation. So those are some of the
guidelines we look at– particularly screening
for individuals that might be at risk to have
arrhythmias and, in fact, even a serious risk. So what are your
take home messages from this last part of the talk? I would say– know
your ejection fraction. If you, or your
family members, had a heart attack or documented
coronary artery disease, know the options– these include implantable
defibrillators. We really would
really encourage you to support the use of automatic
external defibrillators in our community. And, as we’ve talked
about, patients that are specifically– oh actually, we didn’t
talk about this last part– that some patients with
poor pumping function can benefit for certain
special devices that can improve pacing, through
pacing their heart function. So with that, I’d like to
tell you about your role. So, just as you’re doing
tonight, learn more. Be active in prevention of
these conditions– including, particularly, sudden
cardiac death. Spread the word of what can
be done and become more aware. And support the
important advances that are done throughout
the country and the world in advancing our understanding
of cardiovascular disease. So these are the kind of things
I would like to leave you with. Again, I’m very grateful
for your attention today– hope you found it
instructive and enjoyable. Thank you very much.

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  • Reply Steven Stoffers February 24, 2018 at 7:53 am

    20:03 the baby boomers are in their 20's and 30's…. the "plus" generation???? huh? where did the WW2 boomer cohort go… that was a huge one? they died???

  • Reply shortn0w July 23, 2018 at 8:45 pm

    Chiropractic can treat. This specialist says not one word about structural pressure on the spinal nerves that actually create the sinus node pulses in the first place. Just saying.

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