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Get in Rhythm. Stay in Rhythm.™ View Replays from Atrial Fibrillation Patient Conference Aug 4-6, 2017, in Dallas, TX
Get in Rhythm. Stay in Rhythm.™ View Replays from Atrial Fibrillation Patient Conference Aug 4-6, 2017, in Dallas, TX

Video Overview About Afib and Why It Is a Problem — Adam Shapira, MD, FACC, FHRS

Video from the Get in Rhythm. Stay in Rhythm.™ Atrial Fibrillation Patient Conference

Video from the Get in Rhythm. Stay in Rhythm.™ Atrial Fibrillation Patient Conference

December 10, 2013

At the Get in Rhythm. Stay in Rhythm.™ Atrial Fibrillation Patient Conference, Dr. Adam Shapira discusses what afib is and why it is a problem. Video watching time is approximately 22 minutes.


About Adam Shapira, MD, FACC, FHRS

Dr. Shapira is the senior cardiac electrophysiologist at Advanced Heart Care, is the director of The Heart Arrhythmia Center at The Heart Hospital Baylor Plano’s Center for Advanced Cardiovascular Care, and directs the electrophysiology laboratory at Hopkins County Memorial Hospital. 

Dr. Shapira received his Bachelor of Arts degree in English literature from Princeton University, cum laude. He completed his MD at the University of Louisville, his internal medicine internship and residency at UT Southwestern's Parkland Hospital, and his cardiology fellowship at the University of Louisville. Subsequently, he completed an additional two year fellowship in clinical cardiac electrophysiology at Loyola University in Chicago, where he served his final year as the chief electrophysiology fellow. He is board certified by the American Board of Internal Medicine in the fields of clinical cardiology and clinical cardiac electrophysiology. 

Dr. Shapira has a particular interest in atrial fibrillation ablation and has co-authored a book chapter about the safety concerns surrounding this procedure. He has also recently authored an overview article on catheter ablation of supraventricular arrhythmias for the journal American Family Physician. 


Knowing how important this information would be to those living with atrial fibrillation, we committed to do a two-camera video shoot of the entire conference—a very expensive undertaking—in hopes that you, the afib community, will be willing to help us defray those costs through a donation (instead of us charging you for these videos, which many of you said you were willing to pay for). You can make a secure tax-deductible donation here, or click on the red Donate Now button.


Video Transcript:  

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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Last Modified December 10, 2013

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