2015 Atrial Fibrillation Patient Conference: Treating Afib w/ Medications: Mintu Turakhia, MD, FHRS

Thank you all. How’s everyone doing? Good. It’s a tough, tough act to follow John. It is tough. I’m going.

Thank you all. How’s everyone doing? Good. It’s a tough, tough act to follow John. It is tough. I’m going to do my best. I want to thank Mellanie and everyone at StopAfib.org for having me here. It’s a real privilege to
be here and Mellanie hit me up for two talks and I happily obliged. So you’ll have to
hear me twice but luckily you’ll have a break in between. What I’m going to do is
give you an overview on how we, as physicians who really have focused our
lives on afib think about treatment. The point is not to overload you with
information. You can read this. You’ll have the slides. The materials will be there. The point is to give you a framework of
how we think. There will be more detail than I would ever expect any audience to
to take in, but it’s there for you to come back to and digest. The reason
I thought this was important is to really lay out how the advice you’re
going to get now is even different from the advice you may have received two, three years ago. And this is true for rate and rhythm control and also for preventing strokes.
So the first thing you have to deal with when we’re dealing with afib is
which path are you going to go down? There’s a fork in the road. Rate control in afib is when you
really focus only on keeping the heart rates in a reasonable range so that you
don’t experience symptoms or other consequences, typically of the extremely
fast heart rates that can occur. And those may occur at rest. They may occur
with exercise. They may occur unpredictably and may be triggered by
many of the things you heard Dr. Day talk about in terms of triggers. And
sometimes those triggers are not just those that provoke you into afib. They
may provoke the heart rates to behave erratically as well. Rhythm control is when, as Dr. Day
said, you really make it a commitment to keep the heart in normal sinus rhythm and
thereby avoid the consequences of the fast and unpredictable variation in
heart rates that you that you have. So the problem we have sometimes is the
inherent bias that we think one side of the road is sunny and one side of the
road is cloudy, but in truth, this fork may emerge in your life multiple times.
How many of you have seen more than one doctor for your afib? How many times, every time you go to a doctor, something changes, they change something? Yeah, not an uncommon situation. So the reason we think about rhythm control is when the
afib is causing symptoms, and the symptoms vary, and all of you know this better
than your doctor or better than me. The problem is is the way we, as health
care providers, think about what these symptoms are. Sometimes what happens is, a physician who has a lot of things to care for and has to make sure that all
of you, not just your upper chambers of your heart are functioning, may not have the time, resources or understanding to go through all of the symptoms. And it’s
hard to connect the dots if you don’t know what afib could possibly cause. So
sometimes some doctors may ask you if you have palpitations, and if you don’t,
you must not have symptoms of afib, and that’s not true. What we see here is that there
are many different things that can happen. The fatigue, the weakness, the
tiredness we just heard from a patient, can be a real problem for patients. And that’s often expressed in different ways. That can be someone just
becoming irritable. I had a patient’s spouse complain that she knew when her
husband was in afib because he just got grumpy. And she commented when he was wearing the Holter monitor when he was grumpy and it tracked when he was in afib. Her notes matched spot on. So these symptoms can be very, very subtle. What we have not done a good job of is figuring out a way how to quantify
these symptoms or in some way measure them in the same patient. There are
questionnaires, scales and instruments This one comes from Europe, and many of us acknowledge that the
way the European societies have started to think about afib in some ways
exceeds the framework that we have in the U.S. There’s good and bad, and a lot of
good doctors will take some from here and some from there and piece it together.
But the EHRA scale really talks about disability and symptoms, and it’s a
functional scale of what is interfering with your daily life. So should rhythm
control be used without overt symptoms? Again, this is one of those things where
you have to connect the dots. And you’re all here because you know about afib;
it must have an impact in your lives. But in some patients, heart rates are not so
obvious if they’re out of range. Now, this is a patient that has good heart rate
control and this is a monitor that he wore, and this is the two-day snapshot.
And what you can see here is that the general range of 60 to 100 is where you kind of want people’s heart rates to be, and you can see where the average is, which is a single dot, and where the range was for that day. He felt mostly fine, but he
even triggered some diary events that you can see up here and he was in afib
24% of the time. Now, this person has good heart rate control and he felt fairly well, so rhythm control may be fine, but some patients may have very fast heart
rates and feel perfectly fine. And that is a situation where, although they’re not
overtly symptomatic, we as their providers are concerned that those heart
rates can cause problems. And as part of that, the heart failure, the inability for the heart to squeeze
and work as that pump to give the rest of your body the blood that it needs, that even may
not be so obvious. Now, afib can cause heart failure a lot of ways. and the
important thing to understand is that prolonged periods of excessively fast
heart rates, and in some cases, not excessively fast heart rates, diminish
the heart’s ability to contract. And that is in the acute phase very quickly while
it’s happening, but also in the chronic phase, even after that afib episode were to terminate. And the way that’s seen is in two ways, but the most common is that the ejection fraction declines. That means your systolic function of the left ventricle, that’s what we call it, the squeeze of the heart has weakened. Most of the time, it’s reversible. and the other thing to
note is that patients who have diseased hearts for other reasons, prior heart attacks, coronary disease, maybe a thick heart from hypertension, may be the ones that are most vulnerable. And
as heart failure develops, you get in this vicious cycle where the heart
progressively becomes dependent on atrial function. So sinus rhythm isn’t
just happiness on an EKG; that means that the upper chambers, the atria, are
squeezing in synchrony with the lower chambers, and your pump is working on
four cylinders and not just two. And what happens in heart failure is that those
lower two cylinders, the ventricles, end up not working as well, so that the upper
two cylinders, the atria, need to squeeze a little bit more. And that works
in two ways. The systolic dysfunction, which is a squeeze of the lower chambers
and the left ventricle in particular, and the diastolic dysfunction, which is the
ability of those lower chambers to relax to allow the blood to come in. And if the
heart is thick from high blood pressure or other reasons, it stiffens. And when it
stiffens, it can’t relax, and if it can’t relax, the atrium has to squeeze and
supply more. This is nothing to really stare at for very long, but it tells
you the mechanisms that we now see in terms of what how the fast heart rates
can lead to heart failure. There are many ways that this happens and this is a massive
area of understanding where we’re just starting to really learn the cellular
and the energetic and biochemical mechanisms for this. And what does happen over time is you, as I said, get in this vicious cycle. The terms here are
not important, but what you have to appreciate is that afib causes heart
failure and heart failure causes afib. One can beget another, and our goal is to help you break that cycle. So how does the doctor decide what to
recommend? How does a doctor decide what fork you should take and what to advise you on? And the problem with this is that a lot of this decision making is a matter of
perspective and anytime we say it’s a matter of perspective, you have to worry
that there’s some bias thrown in there that may not really reflect an objective
decision that’s personalized for you. William Evans and Peter Swann wrote this
in 1953 after they observed 20 patients, all men. “…The condition did not
jeopardize life in a single instance and did not prove even a handicap to the
majority.” “Longevity is unaffected.” “Reassurance should be the uppermost in treatment…” “…Continuous digitalization,” digoxin, which we’ll talk about, “…is the ideal treatment,” and an urge to re-instate sinus rhythm should be suppressed.” 1953, okay? Good thing you’re here today in 2015 and not in 1953 because you know what would
have happened in terms of your treatment here. This is wrong. So the road not taken is a matter of perspective. And in some
ways, a matter of your perspective, but also your doctor’s perspective. We
looked at this and looked 163,000 patients who had a new diagnosis in the VA of afib and we’d asked a simple question. If
they went to a primary care or general medicine doctor, or if they went to a
cardiologist, which includes an EP, electrophysiologist, was the initial
treatment different? And if you adjust for everything, and we even adjust for
their travel time, how far they had to go, and balance the group so that the
distance to the cardiologist was the same as a distance to the primary care doctors.
And what you can see is that the cardiologist, if they were seen by
a cardiologist, they were almost twice as likely to be prescribed rhythm control
drugs. And the gap actually got worse over time. So it could be that some
patients self-selected themselves even though we tried to adjust for that,
but the almost 2x difference suggests that this is clearly a matter
of perspective. And what does that mean? well, perspective is how we interpret the
evidence, and how I as an EP and my colleagues as a cardiologist and even amongst us friends and colleagues, interpret in evidence is going to vary based on
the lens we’re looking through. And what has happened in some circles is, there’s
been a lot of weight on older data that really has lost relevance. This
trial is a trial that’s often quoted in circles outside of EP, the affirmed trial,
occurred almost 15 years ago now, where they looked at rate versus rhythm
control. Both groups got anticoagulation, but they looked at this
and looked to see, was there an outcome difference whether you started with
antiarrhythmics or whether you started with rate control medications, But the important thing to note is it doesn’t really generalize to
most people with afib because they threw out or didn’t enroll anybody with
symptoms. So when you look at the data of a firm and you show that, in fact, the
people who are on rate control had a trend towards better survival, you’re
missing the point because this excluded patients with symptoms. So the reason I
am passing this on to you is that you educate your peers, and sometimes your
providers, about the way we’ve moved away from some of these trials. And you’re
going to hear more about ablation and rhythm control trials in the afternoon. I
don’t want to go through too many of those drug trials because you’re gonna
hear about that later. Again, in the AFFIRM trial, they also said
there was no difference in quality of life. Well, that’s because they didn’t
have a problem with quality of life when they enrolled in the trial. So this is not relevant, but
somehow this data in this trial, with it’s catchy name, gets brought on and
gets talked about and talked about and talked about again. And my colleague, which you’ll see, Dr. Sanjiv Narayan, I’m so glad he has called his trial FIRM and his approach FIRM, because we need to get away from AFFIRM. So the severity of afib
should also influence decision, and antiarrhythmics have inherent risks that
exceed risks of rate control, to the extent that sometimes doctors may
rightfully, or not, become concerned about using these drugs. But the
willingness to try rhythm control really is one where it depends on the potential
benefit, and the severity of afib can influence that potential for benefit. So
you have to weigh the risks and benefits of the therapy, okay? The problem was the next one, this button,
“Trust me, I’m a doctor.” So the doctor would look at the scale, figure out
what’s right for the patient and make a decision, and we’re just not there
anymore. In fact, we now have volumes of text and information talking about
interpreting benefits and risks, teaching doctors how to do this. Shared decision-making, partnering with
the patient and making that decision together. And in fact, the top-line
recommendation from the AHA/ACC/HRS, the professional american society guidelines
about what to do in afib is first and foremost, it should be a shared
decision-making process. It’s not about the individual drug. It’s not about this
or that. Some of those things are important, but top-line recommendation is
partnering with your patient. So let’s again get back to the severity issue. You heard a little bit about this from Dr. Day. The severity and the way we think about
the afib is more of an issue of how it behaves and less of an issue of how much
or how often you have it, the duration or the burden. Paroxysmal afib is when it
comes and goes on its own, but unpredictably, and that’s a huge problem.
Persistent is when it starts on its own, but as you
heard from a patient, it doesn’t go away on its own. Something has
to be done, often a cardioversion. And permanent afib is a tricky term because
there’s a judgment implied in the term and we don’t love it, but it means that
you’ve tried and tried and tried and you can’t get someone out of it. And the
reason this is defined by behavior and not burden is if someone comes to my
office and tells me that they’ve been in afib for the last six months, I’m doing a
disservice by calling that permanent. We don’t know what that is yet. We haven’t challenged it with behavior. And sometimes what we will do
in a patient who has symptoms is to see how the afib will behave just so that we
can classify this to help prognosticate treatment. In the natural time course of
afib, this is classical, every patient’s different, is you may have afib that
you don’t even know about, short, little bursts, couple seconds. Oh, that felt funny. Oh, I felt a little
flutter. Maybe it was something I ate. Maybe it was the ice cube I swallowed,
don’t know. It then becomes more symptomatic as it gets longer and then
over time, months, years, longer sometimes, become
persistent or even permanent. And we have developed the classification around
this scheme. There are flavors of how this has been modified, but this is
really how, again, we think about the behavior. Now, it’s not just about
characterizing your symptoms and how it works, but actually, these provide some
insight into the mechanisms and what’s going on, and in turn, how we might ablate it, which you’ll hear about in the afternoon. Paroxysmal afib typically occurs in
healthier hearts that are irritable and often you can succeed by taking away
the irritability. And if the irritability is gone, the heart has a tendency to
avoid going into this on its own. Once you have persistent afib, you need something, that shock to get out, you have to do more, and permanent afib may be that it’s very difficult to affect that because the heart is in fact scarred. What
that does tell us is there’s a window of opportunity for attempting rhythm
control. You really have to time this well so this also influences how we
think about what to do. Okay, what drugs can be used? There are a
lot of drugs and a lot of choices. There are antiarrhythmic drugs that are shown
here on the left. There are rate control drugs shown on the right, and we don’t
want to get into many of the details because it really varies on what you can
use. I’m going to give you a framework on how we think about it, but there are a
lot of different options here there’s no one right drug. The way we have evolved
to think about rhythm control is we look at patients and determine whether they
have structural heart disease or not. And if they don’t have structural heart
disease, you have greater latitude in using certain drugs. What has changed,
again in the last couple of years is, we’ve made a clear distinction about
what we want to use first-line, and what we want to use second-line, such as amiodarone not being used first-line. And the reason we care so much is that
there are drugs on the left, these are all antiarrhythmics used for many
reasons, they all have problems. You have a lot of serious acute and chronic
adverse effects, and we have to think very carefully about what we use. Two of
these drugs, sotalol and dofetilide, to maintain rhythm work extremely well, and
again this is informational, but nothing you should know. The point
is is that they have a lot of problems. You have to bring patients to the
hospital for dofetilide, and more commonly, we’re now doing that for sotalol for up to three days to load them to make sure it’s safe
so this doesn’t happen. This is called
Torsade de Pointes, or a form of polymorphic ventricular tachycardia that
is because the body is seeing exceedingly high levels of these three
drugs. So you have to watch these drugs and do them carefully. This is
essentially equivalent to sudden cardiac death and that’s what you of course
don’t want. So there is appropriate reservation, but as experienced capable
physicians and healthcare systems that are resourced, you can get on these drugs
and be very safe and not have problems. Let’s talk a little bit about amiodarone. So amiodarone used to be a favorite in many people. It’s
easy to prescribe, it rarely causes arrhythmias, and it’s well tolerated in
the short term. The problem is it deposits everywhere. It stays in your body
and can take months or longer to be eliminated. Every time you take amiodarone, a little bit of iodine is released in the bloodstream, and there are some dose-dependent effects, especially on the thyroid, the lung and the liver. It also
interferes with warfarin so we now don’t used this first-line unless there are no
other options really remaining, which can happen. Dronedarone is a new drug, relatively
new, that is supposed to have been amiodarone without the badness of it. It
has no iodine released. It has no accumulation effects, but now, we’re
learning it’s actually not terribly effective in most patients and can
provoke heart failure, so it’s fallen a bit out of favor in the U.S. as well.
Let’s talk about rate control. How do we decide what to use first-line? This is
highly variable, and you need to ask your doctor why they are recommending what
they’re doing because there is not a ton of evidence in terms of whether
beta-blockers, metoprolol, atenolol, others, or calcium-channel blockers, diltiazem,
verapamil, are better. It’s a personalized decision based on how well someone’s
going to tolerate them and in some cases, whether heart failure is a co-existing
condition. So again we think about how to do afib rate control the same way. We have certain first-line
drugs based on other accompanying diseases, and we try to avoid amiodarone, which rarely can be used just to control the rate. So this again is a
matter of discussion and personalization. What about digoxin? Well, digoxin’s got a lot of press lately. We’re partly to blame for that. We did a big study that got
some press back in last August where we looked at a 160,000 patients and found, in newly diagnosed afib, not long-standing AFib, but new AFib, and we wanted to see if there was a problem with the drug. And we found an
increased risk of mortality with digoxin. This was not a randomized trial, and you
don’t prove that it was definitively the cause, but it got a lot of press, and
there’s been a lot of studies afterwards. And the point of this isn’t that you
should stop your digoxin. It isn’t that it’s going to necessarily
kill patients. It’s an observational study. There are many potential causes. The point
of this study is to have a conversation amongst us as physicians and amongst our patients and us as physicians about what really are the best choices. Maybe this
is right, but could there be other options that could do just as well, if
not a better job. How fast or slow should my heart beat? There’s no right answer.
It’s highly individualized based on symptoms and avoidance of extreme heart
rates. And the trials of strict and lenient control just haven’t been very
good. So we have guidelines, and again, I’m showing this to you to give you insight
on what we think what we’re held to in terms of accountability. In patients with
afib-related symptoms during activity, the adequacy of heart rate control should be
assessed during exertion, adjusting treatment as necessary to keep the rate
within physiologic range. Don’t just look at your resting heart rate, see what it
does with exercise. So I’m going to close here. There is a lot to digest and we’re gonna have a little bit of time for questions. I will be at the break, but the
choice of rate or rhythm control is a highly, highly personalized decision that
is guided by symptoms, which may not be apparent, quality of life and now, the
impending risk of heart failure. That’s something that’s relatively new. So one is, are you in tune with your symptoms? Are the things that are nuisances in your life there, and could they be associated with afib? And the
second point is more important. Is your doctor in tune with you to personalize
this decision. And within each of these strategies, there are numerous drugs they
could be chosen based on individual circumstances. There’s no decision, this
is not a permanent fork in the road. You may revisit this many, many times over
the course of your life. So no decision is final, none irrevocable, and the best
decision here really is one that’s made through a shared decision-making process
with you and your doctor. Thank you.

2 thoughts on “2015 Atrial Fibrillation Patient Conference: Treating Afib w/ Medications: Mintu Turakhia, MD, FHRS”

  1. Would appreciate more info. on the relationship of AF, obesity, diastolic dysfunction and heart failure.
    I have read about recent studies that have found that a low glycemic/low carb diet and major weight loss can reverse fatty infiltration and fibrosis of the heart, in effect reversing AF & DD.
    None of my docs has ever volunteered even a mention of weight loss as a potential solution for AF.
    And I noted this speaker also did not address obesity per se as a causative factor. Why do all the EP's skirt lifestyle issues in dealing with AF?
    Pills for ills is still the orthodoxy.

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