Dr. John Day
Dr. Day is a cardiologist specializing in heart rhythm abnormalities at St. Mark’s Hospital in Salt Lake City, Utah. He graduated from Johns Hopkins Medical School and completed his residency and fellowships in cardiology and cardiac electrophysiology at Stanford University. He is the former president of the Heart Rhythm Society and the Utah chapter of the American College of Cardiology.
What is Happening to Your Heart with A-Fib? 3 Big Reasons Why You Got A-Fib
Most patients I see every day want to know what is happening to their hearts and why they got A-Fib. In this article, I discuss the 3 main why atrial fibrillation happens.
1. Bad Genes (Familial A-Fib)
Over one hundred genes are associated with atrial fibrillation. And new genes are identified every year. These A-Fib genes may code for any one of the various electrical channels in your heart. Alternatively, they may code for other parts of your heart cells like any number of proteins responsible for the contractile mechanism of a heart cell. And whether these genes code for cardiac electrical channels or the building block proteins in heart cells, the result is electrical disruption within an individual cell.
Testing for some of the A-Fib genes can undoubtedly be done, but your insurance probably won’t pay for them and whether or not you have one or more A-Fib genes won’t change your treatment. If you are interested in a low-cost way to screen for some of these atrial fibrillation genes, you could have your genes tested by 23andMe and then share the genetic data with a company called Promethease to get a full report. But before rushing to do the home genetic testing, please know that when I ran my 23andMe raw data through the Promethease database, I was only able to find out my status on a couple of the A-Fib genes.
How do bad genes cause A-Fib?
The first case of familial or “genetic” A-Fib was reported in 1943. While some people with familial A-Fib may only have one A-Fib gene, like KCNQ1, most patients with familial A-Fib have a combination of genes that puts them at risk for atrial fibrillation.
Just because you do have an A-Fib gene doesn’t mean you will get the disease. Genes are like a seed. For a seed to grow, it requires the right conditions. And when it comes to any one of the atrial fibrillation genes, if you’re eating junk, not exercising, stressed out all the time, or not sleeping well at night then you dramatically increase the odds of that bad gene taking over your heart’s rhythm. In contrast, by living an optimized healthy lifestyle, you have an excellent chance of forever silencing any A-Fib genes you may have.
Familial A-Fib Prognosis
So what can you expect if you have a family history of atrial fibrillation? If you have a first degree relative with atrial fibrillation, you are 92% more likely to get A-Fib yourself. However, before giving up hope, this same study showed that only 20% of the risk could be traced back to genes. In other words, the biggest reason why family history is so crucial in determining atrial fibrillation risk isn’t because of your genes but rather because you probably have the same eating habits and other lifestyle factors.
In addition to a 92% increased risk of A-Fib, studies also show that those with a first degree relative with atrial fibrillation get A-Fib, on average, five years earlier. And from this study, they are also more likely to experience symptoms. However, the good news is that a family history of A-Fib doesn’t seem to put you at more risk of stroke, hospitalization, or premature death.
Putting it all in perspective, I have seen many young and healthy patients with familial atrial fibrillation (under age 50) who show no signs of any other heart problems. Indeed, further evaluation of these patients often shows no signs of any fibrosis (cardiac scar tissue). For these patients, their atrial fibrillation may be a purely electrical disease instead of too much scar tissue accumulation in the heart (like the traditional A-Fib patient). For these patients with the purely electrical form of A-Fib, ablation generally results in what we would consider a “cure.”
2. An Out of Balance Autonomic Nervous System
The autonomic nervous system is something most people know little. After all, it is an automatic process that happens in the background. For example, you don’t have to consciously think about moving the food you just ate through your digestion system, regulating your heart rate, or remembering to breathe. It is something that just happens–something that is on autopilot. However, sometimes, the autopilot system breaks down. And when the autonomic nervous goes haywire, A-Fib can be the result.
Sympathetic versus Parasympathetic Nervous System
To better understand how the autonomic nervous system may break down, let’s take a step back and briefly discuss the two aspects to the autonomic nervous system. First, there is the sympathetic nervous system. The sympathetic nervous system is known as the “fight or flight” nervous system.
When the sympathetic nervous system is activated, both your blood pressure and your heart rate quickly shoot up. For example, I love to be in the mountains of my home in Park City, Utah. During the summer, it is not unusual for me to come across a big moose stuck blocking a mountain trail. These moose are huge animals, and when irritated are more than capable of maiming or killing a human. From first-hand experience, I can tell you that in these situations, my sympathetic nervous system has my adrenalin pumping. I’m ready to do whatever it takes to save my life.
In contrast, the parasympathetic nervous system is the “rest and digest” nervous system. It lowers your blood pressure and slows your heart rate. Sleep or a big meal stimulates this nervous system.
To keep A-Fib from happening, you need a healthy balance of the sympathetic and parasympathetic nervous system. And when this balance is lost, the risk of A-Fib goes way up.
For the vast majority of my patients, the autonomic nervous system imbalance arises from chronic overaction of the sympathetic nervous system. One big cause is our stress-filled modern lives. Our sympathetic nervous system is designed to be turned on and then off as soon as the threat is gone. The problem is that this perceived “threat” at work or in our home life never goes away, so the threat level consistently registers high. And the adrenalin is always pumping. Over time, the heart may give up the fight against atrial fibrillation.
Stress isn’t the only thing that overtaxes our sympathetic nervous system. For example, sugar, processed foods, fast foods, etc. trigger inflammation, thereby activating the sympathetic nervous system. Paradoxically, people who don’t exercise daily also require adrenalin with sympathetic nervous system activation to get them through their day. And sleep deprivation from any cause also revs up adrenalin and the autonomic nervous system.
I have found that most of my A-Fib patients suffering from overstimulation of the sympathetic nervous system will have a resting heart rate in sinus rhythm of 80 beats per minute or faster. Their heart rate variability, or SDNN, also tends to be below 70 ms. While tracking your heart rate is easy to do, the best way to track an overactive sympathetic nervous system is with a smartwatch. Most smartwatches will not only tell you your real-time heart rate but will also give you your heart rate variability.
As most of my A-Fib patients suffer from over-activation of the sympathetic nervous system, my goal is to calm it down if we want any hope of getting their A-Fib into remission. And this means eating a clean diet, daily exercise, meditation/yoga, and sleep optimization.
Parasympathetic A-Fib: The Athletic Heart
In contrast to sympathetically driven A-Fib, you can have the opposite problem which is too little sympathetic activation or parasympathetic A-Fib. Thus, for some of my patients, a little more sympathetic stimulation (or calming the parasympathetic nervous system) is the goal.
The classic patient I see in my practice with an overactive parasympathetic nervous system is the world-class endurance athlete.
While the actual act of exercise stimulates the sympathetic nervous system, between workouts, there is a dramatic calming effect of the sympathetic nervous system, thereby allowing the parasympathetic nervous system to be firmly in control. It is for this reason that world-class marathon runners or Tour de France riders may have a resting heart rate of 30 to 40 beats per minute. And unless they are beating up their bodies from overtraining, my well-trained endurance athletes also tend to have a heart rate variability number above 70 ms.
While 99% of my patients don’t get anywhere enough exercise, I do have a small subset of patients that push their physical training to the extreme. These are usually my patients who regularly compete in marathons, long-distance bike races, Ironman World Championships, etc. A resting heart rate below 50 beats per minute is an immediate clue that they may be exercising too much. These extreme levels of exercise overstimulate their parasympathetic nervous system thereby slowing down their heart rate. And for these patients, if they can slightly dial back their training, the A-Fib usually goes into remission without medications or procedures. However, as these patients are so committed to their exercise this is often something that most are incapable of doing. And because their competition times are much slower with A-FIb or medications, we usually end up doing an ablation procedure so that they can still compete without A-Fib or medications.
Parasympathetic A-Fib: Gastrointestinal and Nocturnal A-Fib
Another group of patients that suffers from parasympathetic A-Fib are those with gastrointestinal challenges. This is often called “vagal” atrial fibrillation. The term “vagal” refers to atrial fibrillation arising from overactivation of the vagus nerve. The vagus nerve is the nerve that connects the gut to the heart and the brain. Thus, many people with vagal A-Fib report that eating a big meal, eating the wrong things, acid reflux, or even irritable bowel can then stimulate the vagus nerve to the point that an atrial fibrillation attack ensues.
The treatment for gastrointestinal or vagal A-Fib is relatively straightforward. Calm the gut, and the heart usually follows. Indeed, these patients may need temporary medications for their A-Fib until the gastrointestinal issues can be resolved.
The other commonly encountered form of vagal A-Fib is nocturnal A-Fib. For these patients, sleep (which is when the parasympathetic nervous system dominates) triggers A-Fib attacks. Often these patients will awake with an A-Fib episode.
When dealing with nocturnal A-Fib it is vital to rule out sleep apnea. Once sleep apnea is excluded, there aren’t any specific treatments as we all have to sleep. Thus, after reversing any biomarker or lifestyle factors which may be contributing to the A-Fib, these patients often require medications or an ablation. Fortunately, ablation works just as well for the parasympathetically mediated forms of A-Fib as it does the more commonly encountered, sympathetically mediated A-Fib.
3. Age and Lifestyle-Related Fibrosis of the Heart
Of the three reasons why people get A-Fib, age, and lifestyle-related fibrosis of the heart is by far the number one reason I see every day. Indeed, at least 90% of my patients develop A-Fib primarily from progressive scarring of the heart (fibrosis) rather than purely genetic or autonomic nervous system driven A-Fib. Indeed, A-Fib didn’t just start. Instead, the fibrosis was accumulating decades before you ever had your first A-Fib attack.
Fibrosis, or cardiac scar tissue, damage electrical pathways in the heart leading to atrial fibrillation and other arrhythmias. You need each heart cell as healthy as possible to keep your heart in normal rhythm. Thus, the more fibrosis you pick up over time, the higher your risk of atrial fibrillation. Therefore, it should come as no surprise that the earlier you can be treated and make the necessary lifestyle changes to stop or even reverse the fibrosis, the better your chances of putting A-Fib into remission.
Studies show that as atrial fibrillation worsens over time, people correspondingly have more and more fibrosis in their heart. This finding has led to the common saying that “A-Fib begets A-Fib.” In other words, the more episodes of A-Fib you have, the more scarring takes place, and the more A-Fib attacks you can expect in the future. This is something we discussed in a published manuscript. Just 5 minutes of A-Fib is enough to start changing the way electricity is conducted within your heart. And five weeks of A-Fib is enough to start laying down new scar tissue (fibrosis) in your heart.
What Causes Fibrosis?
If we want to stop fibrosis, we need to know what causes it in the first place. Sadly, some degree of fibrosis happens from age-related changes. And while we can’t stop how many birthday candles are on our cake, we can slow down the biological aging process. Indeed, “old-appearing” 40-year-olds will often have more cardiac fibrosis than young appearing health conscientious 60 or 70-year-olds.
Rather than just looking at how old someone looks on the outside, you can measure this at the cellular level. As we age, the telomeres on the ends of our chromosomes shorten. Telomeres are like the caps on shoelaces. When shoelace caps wear out, shoelaces unravel. The same is true of our DNA. We need these telomeres to protect our DNA.
As telomere shortening is a marker of biological aging, it should come as no surprise that research from our hospital has shown that short telomeres significantly increase your risk of A-Fib. And the key to slowing down the aging process is the same recipe for stopping A-Fib in the first place. Eat a 100% clean diet, avoid weight gain, exercise daily, and optimize your sleep and stress levels.
In addition to aging, many other things cause cardiac scarring. For example, eating the “Standard American Diet,” being overweight, not exercising, always stressing out, not getting enough sleep or sleep apnea, high blood pressure, diabetes, other heart problems including not getting enough blood flow, valve problems, or heart failure, etc. are all well-known causes of cardiac fibrosis.
How Can You Measure Fibrosis?
There are many tests you can do to determine how much fibrosis there is in your heart. While a cardiac MRI is the most accurate way, you can also tell by the simple echocardiogram (ultrasound of the heart). If your right or left atrium are enlarged, you probably have a fair amount of scar tissue. Indeed, studies show that the size of the upper chambers in your heart is a powerful predictor of how well you will respond to treatment of your A-Fib. And if your A-Fib ultimately requires an ablation, depending on what technology your electrophysiologist chooses to use, they may be able to tell you the degree of fibrosis you have.
A Window of Time to Stop the Fibrosis
It is a race against time if you are to stop atrial fibrillation. At some point, if you develop too much fibrosis, you will no longer be able to maintain a normal rhythm. Exactly how long you have before atrial fibrillation becomes permanent is unknown as it varies from person to person. In a study of over 4,000 patients, we showed that the longer one waited from the time of atrial fibrillation diagnosis to an ablation procedure, the worse their long term freedom from atrial fibrillation.
While “bad genes” or an out-of-balance autonomic nervous system may certainly make atrial fibrillation worse, the primary driver is progressive cardiac fibrosis. Thus, the key to beating A-Fib for most people is to stop the fibrosis before it is too late. Fibrosis can be stopped, but it will probably require a lifetime commitment to healthy eating, daily exercise, optimizing stress levels and sleep, as well as a possible ablation for those wanting to avoid a lifetime of cardiac rhythm drugs.
Disclaimer Policy: This website is intended to give general information and does not provide medical advice. This website does not create a doctor-patient relationship between you and Dr. John Day. If you have a medical problem, immediately contact your healthcare provider. Information on this website is not intended to diagnose or treat any condition. Dr. John Day is not responsible for any losses, damages or claims that may result from your medical decisions.