Get in Rhythm. Stay in Rhythm.™ Atrial Fibrillation Patient Conference See all conference videos, and download the slides, …
Mellanie True Hills: Our first presenter is
Dr. Adam Shapira. He is the Senior Electrophysiologist
at Advanced Heart Care and Director of the
Heart Arrhythmia Center at the Heart Hospital
Baylor Plano’s Center for Advanced Cardiovascular
Care. Dr. Shapira has co-authored a book chapter
about catheter ablation safety. Dr. Shapira
will give us an overview this morning about
afib and talk about why it’s a problem.
Dr. Adam Shapira: Good morning. Mellanie,
thank you very much for the invitation to
participate, and it’s an honor to be here
speaking with everyone. I am going to be giving
you an overview of atrial fibrillation in
defining why it’s a problem, and talking
about some of the causes that we frequently
implicate with atrial fibrillation, or the
causes that are implicated in atrial fibrillation.
First, and this may be review for many folks
here, but just to go over cardiac anatomy—this
will give us a framework for discussing all
the future topics coming up today—this is
a very simplified schematic of the heart.
[1:30] Basically, as we informally refer to
them, the top two chambers of the heart would
be the right atrium and the left atrium. The
right atrium is located over here, and the
left over here. These chambers will pump blood
into the right ventricle, and to the left
ventricle.
To give you a brief overview of physiology
and cardiovascular physiology, blood will
flow into the right atrium from the brain
and from the neck, and then blood is received
into the right atrium from the legs, the torso,
the abdomen, and all the organs in the thorax
[chest] and arrives in this chamber right
here, the right atrium. [2:15] It gets pumped
to the right ventricle, and then from the
right ventricle it’s pumped into the lungs,
and that’s where the blood gets oxygenated;
then, it returns into the left atrium from
the lungs via the pulmonary veins, and then,
it goes to the left ventricle. From the left
ventricle, the oxygenated blood, that looks
redder once it has oxygen in it, will get
pumped to the brain and all the organs in
the torso and down to your legs. So that’s
an overview of physiology. You can think back
on that as subsequent speakers talk about
atrial fibrillation and its management because
all of those elements will become relevant.
[For more details, see How Does the Heart
Work.]
[2:57] This schematic diagram is roughly what
atrial fibrillation is, and what is actually
going on. Before I get to atrial fibrillation,
let me mention normal sinus rhythm, normal
rhythm. This is the sinus node [3:10], this
little yellow dot right here in the right
atrium. Normally, electrical impulses will
emanate from that tissue, and arrive down
in this area called the AV node. From the
AV node, where the electrical system slows
that impulse down, it will conduct down to
the bottom chambers via the right bundle branch
and the left bundle branch causing the bottom
chambers to contract and pump blood to the
lungs and to the body respectively.
In atrial fibrillation, that mechanism in
the top chambers is subverted. [3:44] You
basically have a lot of chaotic electrical
signals emanating principally from the left
atrium, but also to some degree the right
atrium, overtaking the sinus node. The normal,
almost metronomic, pattern of sinus node impulses
is taken over by chaotic, random, haphazard
electrical signals coming from the right atrium,
and more principally, the left atrium. I mentioned
the pulmonary veins—our subsequent speakers
will talk more about the pulmonary veins—but
that’s a frequent target for atrial fibrillation
because a lot of this chaotic electrical signaling
that comes from atrial fibrillation will emanate
from the tissue around the pulmonary veins.
That’s, electrically speaking, what’s
going on in atrial fibrillation.
Now to define atrial fibrillation, it’s
not enough to say I have this funny feeling
in my chest, or I have some irregularity to
my heart rate. [4:37] On an ECG is where we
formally diagnose atrial fibrillation, and
this is what atrial fibrillation looks like
on an ECG tracing. Now, there are several
ways you can assess and measure and record
an ECG—this is just one line on an ECG.
Normally, on a full ECG, we have 12 lines.
[4:56] This is what it looks like; you get
this very chaotic wiggly line here between
all of these big spikes, and this wiggly line
reflects what’s going in the atria—the
right atrium and the left atrium—the top
chambers. These spikes here reflect the ventricles,
the main pumping chambers; when they contract,
they create this electrical signal. In normal
sinus, by contrast, you have this nice organized
pattern here. That’s what the definition
is of atrial fibrillation on an ECG.
[5:25]What are the risks of atrial fibrillation?
This is something on everyone’s mind who
has atrial fibrillation, or cares for someone
who has atrial fibrillation. The two principal
risks that we get concerned about are increased
stroke risk and heart failure risk.
Stroke risk is the most important element,
in my view, and I know Dr. Prystowsky is going
to talk about this. What’s going on is when
the top chambers, the right atrium and left
atrium, are in atrial fibrillation, they are
not contracting as well as they normally would
in sinus rhythm. When they don’t contract,
the blood doesn’t slosh around—it doesn’t
move around—very much in the top chambers,
and when the blood doesn’t move around a
lot, it can form a clot relatively quickly.
[6:12] If a clot were to form, it then gets
sent to the right ventricle or left ventricle.
And from there, the muscular chambers of the
heart, the ventricles, will pump that blood,
including that clot, out into the body. It
can go to the lungs, it can go to the brain,
and it can go anywhere in the body. Most concerning
is that if it goes to the brain it can cause
a stroke. That’s where a lot of attention,
and I think, the most important element of
atrial fibrillation management, lies—in
preventing stroke.
[6:37] Heart failure can also arise. This
is another, the second cause of morbidity
and mortality, or risk, in atrial fibrillation
because when you’re in atrial fibrillation,
the top chambers will drive the bottom chambers
very fast. If the bottom chambers are going
fast for a long period of time—several months
or sometimes years—that can weaken the bottom
chambers and that can lead to heart failure,
and that’s a major cause of risk of death.
[7:16] There are two ways that we can look
at stroke risk in atrial fibrillation. There
is something called the CHADS2 score, which
is a little bit older risk modification scheme
to assess someone’s risk of having a stroke.
So, if someone has heart failure, if they
have high-blood pressure, if they are 75 years
of age or older, if they have diabetes, or
if they’ve had a stroke, they get a certain
number of points. You get one point for everything,
except for stroke history, where you get two
points. And then you can look on the right
hand side of the screen and tally up the score.
Your score can go anywhere from 0 to 6. As
you see the more risk factors you accrue—the
more clinical parameters that are identified
on the left hand side of the screen that you
accrue—the higher your risk of having a
stroke.
This annualized stroke risk will help determine
whether we anticoagulate someone with just
an aspirin, or with something more potent
like Coumadin or some of the newer antithrombotic
agents that are out. Some of the subsequent
speakers are going to be talking about some
of those options because those are good questions
a lot of people have now as to which anticoagulant
they should be on.
[8:25] This [CHA2DS2-VASc is a newer score
that drills down on a couple more clinical
elements, and is felt in some ways to more
accurately define stroke risk, but it’s
not yet incorporated in formal guidelines.
[UPDATE: The CHA2DS2-VASc score was formally
incorporated into the new afib guidelines
that were released on March 28, 2014, and
the CHADS2 score was no longer recommended.]
To give you an introduction to this, you see
some of the familiar faces from the prior
slide; you have heart failure, high blood
pressure, age, stroke history, but also vascular
[heart] disease, and then age is broken up
in a little more detail between 65-74 years
of age, and then being female gender will
also confer higher risk. This gives you a
little bit, I’m not going to say more accurate,
but a different perspective on stroke risk
right now.
[9:06] The questions that always come up are:
What did I do to cause this? Why do I have
atrial fibrillation? Quite honestly, a lot
of times—and most of the time in my practice—there’s
really no good answer. So, there are a lot
of things that can contribute to the development
of atrial fibrillation, and I’ve listed
a lot of them here.
[9:24] You can have valvular heart disease—where
the valves in the heart are not functioning
as well as they should—and you can get backwards
blood flow or you can get lack of blood flow
across from one chamber to another, and that
can cause pressure changes and dilation of
the chambers that can lead to atrial fibrillation;
[9:40] high blood pressure; diabetes; heart
failure; thyroid abnormalities can lead to
atrial fibrillation; alcohol use; nervous
system abnormalities where the nerves that
innervate—that go through the heart—release
an abnormal amount of chemical neurotransmitters
that can predispose someone to atrial fibrillation;
genetic factors; cardiac surgery is a very
common cause of atrial fibrillation; chronic
kidney disease; obesity; metabolic syndrome;
hypertrophic cardiomyopathy, which is a big
long term that basically refers to thickening
of some of the heart muscle walls; coronary
disease; and inflammation. So, there’s a
whole host of these things, and it’s not
uncommon to have a patient that has multiple
elements that you’ve seen listed here.
[10:26] Genetics. Mellanie wanted me to mention
the role of genetics, and this is a little
bit unclear right now. This diagram is not
anyone who has atrial fibrillation; it just
shows you what we’re looking at when we
consider genetics in someone with a medical
condition. This would be a man, and this would
be a woman, and this reflects their offspring.
You can see some of their offspring marked
by the black box are affected by the condition,
a generic condition in this case. It might
be atrial fibrillation. But the bottom line
with genetics, in my view, is that it’s
not really completely understood right now.
We don’t really do anything to target genetics
in atrial fibrillation, and its role in atrial
fibrillation. But, it in all likelihood has
some causal role.
[11:11] The role of sleep apnea. This is another
common thing that we see in folks that have
atrial fibrillation, the presence of sleep
apnea. What sleep apnea is is a lack of normal
air flow through the nasal passageway into
the back of the throat. You can see in the
diagram there that when the nasal passage
or the tongue falls back on the airway, you
don’t get as much air into the lungs and
the decreased oxygen quantity in the blood,
and pressure changes in all these things,
can lead to atrial fibrillation as well. I
just wanted to mention that because it’s
a common player with atrial fibrillation.
[11:45] What does atrial fibrillation feel
like? Well, it can feel like just about anything.
There’s no real specific way it feels. Some
people feel palpitations, some people feel
“fluttering” sensations, some people feel
a skipped beat, and some people feel things
that aren’t related to the heart at all.
It could be anxiety, or sweating, or fatigue,
or nausea. It’s really all over the place,
and just because you have one of these elements
or symptoms doesn’t mean you have atrial
fibrillation; but by the same token, your
atrial fibrillation, or someone’s atrial
fibrillation, could manifest with one of the
symptoms. Symptoms aren’t terribly helpful;
but if they’re debilitating and they’re
a problem, that’s what we’re targeting
when we’re trying to get someone back into
sinus rhythm with some of the therapies that
we have.
[12:26] How do we diagnose it? Well, I mentioned
ECG before. Symptoms are sometimes a player;
if someone has symptoms and we document that
they’re in atrial fibrillation when they
have those symptoms, then moving forward that
can be a reliable marker that, “Hey, I’m
in atrial fibrillation” or “Hey, this
person is in atrial fibrillation again.”
Holter monitor and event monitors are more
long term ECG monitoring techniques where
you go home and wear a couple of stickers
on your chest with some wires that are attached
to a little pager, and that can monitor for
the presence of atrial fibrillation.
[12:57] Types of atrial fibrillation. These
terms may come up during subsequent talks.
Lone atrial fibrillation—we really don’t
use that term much anymore, but I put on here
just because some of you all may have heard
it. Lone atrial fibrillation is atrial fibrillation
that has no underlying cause; it is really
occurring in the absence of any other significant
medical problems. The more commonly used terms
are paroxysmal atrial fibrillation, persistent
atrial fibrillation, longstanding-persistent
atrial fibrillation, and chronic atrial fibrillation.
Basically, paroxysmal atrial fibrillation
comes and goes. It is formally defined as
more than two or more episodes of atrial fibrillation
within one week, and these episodes can typically
last up to 24 hours—but they don’t have
to—but the bottom line is that paroxysmal
comes and goes on its own.
Persistent atrial fibrillation. We really
need to do something to get someone back into
normal rhythm. So you have a cardioversion,
or you have to have medication or shock, or
medication to get someone back into normal
rhythm.
Longstanding persistent has been there for
a long time, but it hasn’t quite gotten
to the point where someone has said, “We’re
just going to leave you in atrial fibrillation
all the time”, or “I just want to be in
atrial fibrillation all the time”.
That’s what chronic [permanent] atrial fibrillation
is—people are in it all the time and we’re
not going to do anything, and they’re not
going to do anything to try to get themselves
back in normal rhythm.
[14:13] Moving forward for the rest of the
talks, I thought this might be a helpful framework
for thinking about atrial fibrillation. One,
what are we going to do to anticoagulate someone?
And that’s based on that CHADS2 score or
CHA2DS2-VASc score that I mentioned before.
Two, what are we going to do to make sure
the heart rates don’t go too fast [rate
control] and don’t lead to excessively rapid
heart rates for many, many months leading
to heart failure? You see, stroke and heart
failure are the first two elements here. Three,
rhythm control is more of the symptom control—and
that’s more of a soft end point here in
terms of management of atrial fibrillation.
What do we do to make someone feel better?
As you hear the rest of the talks throughout
the day, and as you think about atrial fibrillation,
this, as an electrophysiologist, is the way
that I think about atrial fibrillation. I
think it’ll be a helpful way for anyone
who has atrial fibrillation to think about
it: What are the three things that I’m doing
to target afib on these three fronts?
Mellanie True Hills: Let’s open it up for
questions. Does anyone have a question for
Dr. Shapira about understanding atrial fibrillation
and what are the risks of atrial fibrillation?
Melissa is walking around with the microphone
to allow you to ask your questions.
Question: I have aortic stenosis, and I’m
moderate. I’m currently under investigation
for afib with an event monitor. I’ve had
a little bit of sensations of all of this
going on, but I had sort of a little emergency
after I started taking an increase of Niaspan
[extended-release niacin]. It seemed to happen
almost right away. Is there a possible correlation?
Dr. Shapira: A lot of times, correlations
with starting a certain medication and then
you notice immediately afterwards that you’re
having more palpations, or more whatever symptom,
in all likelihood there very well may be a
role in linking the two. However, and I tell
this to folks all the time, atrial fibrillation
is so common, in particular in the setting
of valvular heart disease, that it may have
happened anyway. There’s not really going
to be a clear-cut way to link the two. However,
if you stop the medicine and it goes away,
then it might be that that medicine is causing
it. But niacin can frequently cause flushing
and a sensation of warmth rushing to your
face and head. Atrial fibrillation, for some
folks, can feel the same way. So, unfortunately
with afib, we are dealing with a bit of a
chaotic element, and as the electrical pathways
and patterns in atrial fibrillation are chaotic,
the clinical manifestations of it, meaning
how it shows up and how people experience
it, can also be a little random, too.
Question: Can you speak about afib triggers,
including some more popular medications that
are prescribed? Foods that we might eat, and
alcohol.
Dr. Shapira: That’s a very good question.
A lot of people will note that when they eat
a certain type of cold food, or they drink
a cold drink, or they have alcohol, or they
exercise, or they do whatever activity or
eat some sort of food, they always go into
atrial fibrillation, or they notice more palpitations
when that happens. I mentioned in one of the
slides that there are nervous system abnormalities.
There’s a nerve that runs from your brain
down through your entire digestive system—it’s
called the vagus nerve. That basically refers
to the vagal nerve and its role as vagal tone.
The vagus nerve runs right by your esophagus,
and it runs through a lot of your digestive
system, as I mentioned. It’s postulated
that when you drink cold water it can sometimes
cause excess triggering of this nerve, and
the release of neurotransmitters from this
nerve can sometimes lead to atrial fibrillation.
In fact, when we do afib ablations, we target
the pulmonary veins, which I mentioned before,
but we also target these plexi, or plexus,
where the nerves come together, and a lot
of the nerves come together on the back wall
of the heart. The ablation also will target
that tissue as well. We can’t really define
where that tissue is as readily as we can
define where the pulmonary veins are, but
to speak to your question now, some triggers
you mentioned that I come across, such as
drinking cold water, can sometimes trigger
that area. Now certain medications have certain
chemical components to them that can alter
other neurotransmitters or other chemicals
in your body that may make it more likely
to go into atrial fibrillation. It’s something
that has the same effect as caffeine in your
body. You’ve heard of the fight or flight
response that kind of gets everything revved
up in your body—in terms of the human body
is scared, so it’s going to run away from
something—well the same thing can activate
the heart and cause the heart rate to increase
and can sometimes trigger atrial fibrillation
in some folks. And thyroid abnormalities,
for the same reasons—the chemical components
in the blood stream—can sometimes trigger
atrial fibrillation by mainly affecting neurotransmitters
and nerve-ending chemicals.
Question: In your opinion, how high does a
score need to be before you think it’s necessary
to have the more pricey alternatives to aspirin?
Dr. Shapira: There are two elements to that
question: there’s the priceyness question,
and then there’s the movement from aspirin
to another. Well, if you go by the old score
[CHADS2], if you have a score of zero, I don’t’
think you’d come across a lot controversy
in terms of going with an aspirin. When you
start hitting the score of one is when we
start moving into the wiggle room of does
someone need to be on a more potent blood
thinner or do they need to be on just an aspirin?
That is modified by your risk of bleeding;
if someone’s risk of bleeding is higher
than their risk of having a stroke, then we
favor not being as aggressive with anticoagulation.
If someone has a very low risk of bleeding,
then we recommend going ahead and putting
them on an anticoagulant.
Question: I want to know whether or not the
ejection fraction plays any kind of role in
giving you clues?
Dr. Shapira: It does. Anyone who has heart
failure is at risk of having atrial fibrillation.
So there’s an increased risk of atrial fibrillation
in someone who has heart failure. And the
ejection fraction, for those who aren’t
familiar with that term, is an index or percentage
of blood that’s ejected from the left ventricle,
the main pumping chamber of the heart, per
heartbeat. When that ejection fraction starts
to decline—normally it’s about 50%-55%,
in that range— that indicates heart failure.
Folks that have heart failure are also at
risk of having atrial fibrillation. So, to
answer your question, yes, the ejection fraction
does play a role in determining someone’s
risk of atrial fibrillation.
Mellanie True Hills: Thank you so much, Dr.
Shapira.

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