It’s frightening to wake up in the middle of the night with the sense that something is terribly wrong. At 2 in the morning of February 27, 2001, that sensation was an odd fluttery feeling in my chest, not being able to catch my breath, and a terrifying wooziness when I tried to stand up. I was in no pain, so — at age 48 — I hoped I wasn’t having a heart attack, but since I didn’t think I was in any immediate danger (more about that later), I had my wife drive me — running a few red lights along the way — to the Baptist Hospital Emergency Room.
They take things quite seriously in the ER when you tell them you’re having heart problems, and within five minutes a triage nurse was checking my pulse. For the first time, I heard those words: “You’re in atrial fibrillation.” For some reason, that was reassuring. I’d had an irregular heartbeat for years, mainly just skipped beats here and there (called PVCs, or “premature ventricular contractions”) and this was something new. Even so, I was under the impression this was the “safest” of all the various arrhythmias.
“Oh, that’s a relief,” I recall telling the nurse. If only I knew.
The heart — along with the rest of the human body — is a truly amazing machine, as long as everything works as it should. Even a third-grader understands the heart’s main function is two-fold: circulate blood to the lungs, where it picks up the life-giving oxygen, and then pump that richly oxygenated blood to every organ and cell in the body.
But what, exactly, makes the heart beat, for most people, around 60 times a minute, 3,600 times an hour, 86,400 times a day, an astonishing 31 million times a year — for as long as you live? A cluster of nerve cells called the sinus node, embedded in the upper wall of the heart, discharges a burst of electricity every second or so. This energy is carried along the walls of the heart through invisible pathways. First, they reach the smaller, upper chambers of the heart — these are the atria — and the energy causes them to compress, pumping blood downward into the ventricles. Then, that same burst of electricity moves downward, to the larger chambers — the all-important ventricles — which pump the blood with considerable force everywhere from your brain to your toes. The slight delay between the upper and lower pulses causes the familiar thump-THUMP beat that you can hear with a stethoscope, though when you are checking your own pulse, you can only feel the harder beat of the ventricles.
All this is well and good, until you have what amounts to a short circuit, and things go haywire. In atrial fibrillation, the first electrical charge sent to the atria heads to the ventricles, but before dissipating, it tends to circle upwards again, and again, and again — causing the atria to contract each time.
Dr. Jeffrey Kerlan, an electrophysiologist — a cardiologist who specializes in rhythm disorders — explains it better: “The heart has its own electrical system, just like a house, and that energy works its way down what is essentially a highway of electrical tissue to the bottom chambers. So in a very rhythmic fashion, you have the top chambers contract, and then the bottom chambers contract — like a clock. But with atrial fibrillation, you have potentially abnormal sources that essentially interrupt this entire process.”
The regular pulse then becomes chaotic, causing the atria to beat irregularly, as fast as 200 times a minute. They are, in fact, beating so rapidly that they are actually quivering like jelly, and the chambers don’t have time to empty fully between beats. This is the fibrillation part.
If the fibrillation carried downward and reached the lower chambers of your heart, it would cause ventricular fibrillation, which is almost always fatal. But with a-fib, as it is called, the chaotic pumping is confined to the upper chambers, and the lower chambers continue to operate, though usually with some irregularity because they don’t always pick up the electrical signals sent from above.
So why is this a problem? Well, when the atria start quivering, that rather sophisticated pumping action stops working the way it should. Even though the ventricles are still working as best they can, they are no longer pumping fully oxygenated blood to your brain, and your blood pressure can plummet — causing you to feel lightheaded, woozy, dizzy, and generally miserable. Some patients in a-fib tell doctors they don’t feel a thing; I learned to hate those people. In my case, as soon as I went into a-fib, I felt miserable. Even the quivering sensation in my chest was, to me, very unpleasant, and I instantly became weak and lightheaded.
“What makes atrial fibrillation such a challenge is we have such a wide spectrum of how patients tolerate it,” says Kerlan. “We have some patients who are absolutely miserable when they are in a-fib. But I’ll see maybe five or six patients a week who go to their primary care physician for a routine screen, and he puts a stethoscope to their heart and picks up the irregular heartbeat. They had no clue.”
This isn’t a case of ignorance being bliss, because there’s the matter of strokes.
Since the atria are no longer emptying their chambers, and filling them with new blood with each pump, the blood tends to pool inside the heart. Non-moving blood has a nasty tendency to clot, and these clots form on the inside walls of the heart, and on the heart valves. This is not good. When the heart suddenly reverts back to its normal rhythm — a process called “conversion” which can happen on its own, or be induced by medicine or electrical shock — the patient can then “throw a clot” from the atria that can travel to the lungs or brain.
There’s a certain window of time for a-fib patients. As soon as you go into a-fib, you have roughly 48 hours to convert, or you are at great risk of throwing a clot. So, in addition to the physical problems, there’s the added misery of anxiety. As soon as I would go into a-fib, I would write down the time on a calendar, and just hope I would convert on my own, within that 48-window, without making another trip to the emergency room, for an uncomfortable process called “cardioversion.”
The anxiety affects you in other ways. A-fib patients live in constant awareness of their heartbeat — always worrying: Will I go into a-fib before I have to give this important speech, or before I hop in the car for a vacation trip? — or any situation at all, really. You live in a constant state of vigilance, with one eye on the clock and calendar. And, for many patients, it doesn’t take much to trigger an episode — climbing the stairs for some people, even drinking ice water in others.
In my own case, that initial run of a-fib — the one that sent me in a panic to the ER — lasted 18 hours. Months passed, and then I had another run, this lasting about 20 hours. Only a few weeks passed before another episode. In fact, I was experiencing a specific type of a-fib called “paroxysmal” or “lone” atrial fibrillation. In these cases, like mine, there is no structural defect that causes the problems; the a-fib comes on suddenly, and just as suddenly goes away. But the episodes became more frequent: They started occurring once a week, then every few days, and then I began going in and out of a-fib several times a day.
In the beginning, cardiologists generally treat a-fib patients with a variety of medicines at their disposal. Drugs called beta-blockers, which have some control over the heart’s pumping action, are usually the first choice, because their side effects are, in most cases, not dangerous, but they tend to lower your blood pressure and your heart rate. Mine would drop into the 40s (normal is around 60) so I would feel miserably tired. Unfortunately, as with many medicines, your body builds up a tolerance to these meds, so next the doctors usually try the so-called anti-arrhythmic drugs, which directly affect the electrical conductivity of the heart. The problem — and it’s significant — is that these medications tend to cause heart rhythm problems on their own — a condition called proarrhythmia — and some of these can be dangerous, so the patient needs to be monitored carefully while taking these drugs.
Surely, there had to be a better way.
In the 1980s, cardiologists began experimenting with different cardioversion procedures. They discovered that if they actually got inside the heart — and this required open-heart surgery, they could score lines across the inside of the atrium, which would build up a “barrier” inside the heart that would block these so-called “aberrant pathways” that were causing a-fib. This was known as the “maze” procedure, but since it involved major surgery, it was only reserved for the most severe cases. Later, electrophysiologists began trying the same approach, but using catheters — instruments threaded up inside the heart, through the femoral artery that runs inside your leg. They did this by using radio-frequency, or RF ablation. In terms we can understand, they were essentially using a soldering iron to burn a line on the wall of your heart, causing scar tissue to build up, which blocked the improper electric signals.
This procedure, as you might imagine, carried very definite risks, which could result in — and I’ve always loved this term — a “negative outcome.” Meaning: You die. The normal way to reach the femoral artery is through the groin, since it’s close to the surface there. So, the EPs would make a deep incision, thread a catheter all the way from your groin to your heart, snake it around inside your heart, find the exact spot that was causing the problem, burn away that area, and then withdraw all this equipment. This sounds tricky enough, but remember that they are doing all this while your heart is filled with blood and beating. It would be like working on the valves of a car, while the engine was still running.
If they missed the spot, or if the catheter snagged on something, well, that was a big problem. Another risk came from the heat caused by that “soldering gun” inside your heart. It seems your esophagus runs directly behind your heart, and actually presses against it. In rare cases, if the heat radiated through the heart muscle, it had an unfortunate tendency to “weld” the esophagus to the heart, or even to burn a hole between them. Blood pouring from your heart down your esophagus tends to cause a very negative outcome.
Some dozen years ago, physicians came up with a different procedure, using liquid nitrogen — pumped into a tiny balloon which was then inflated and pressed against your heart wall — instead of the RF energy used in the “hot” approach. The balloon is then withdrawn and removed. The procedure that cured me is called a Pulmonary Vein Isolation. It seems that the most common problem area inside the heart is the opening around the four pulmonary veins that feed blood into the left atrium; for some reason, the heart’s electrical system tends to “short out” right at those round openings.
The curved surface of the balloon quickly affects a larger area, so the EPs don’t have to dab away at tiny areas, trying to build up the scar tissue. “If you imagine each of those veins like a hose or a tube,” says Kerlan, “then this balloon, inflated at the entrance to those vessels, creates a circular freeze or isolation area that essentially blocks those signals.” The scar tissue also tends to be more uniform, so the heart — your body is alway searching for ways to repair itself — isn’t as likely to form new pathways through it.
I met with Dr. Kerlan at Stern Cardiovascular Center in October, who determined that I was an excellent candidate for the procedure. He cautioned me that, as with anything else in medicine, it’s usually 80 to 90 percent effective, and I was willing to take those odds. And, even better, insurance companies are paying for these procedures. Years ago, they might have been considered experimental, but Kerlan tells me that he and the four other electrophysiologists at Stern perform more than 500 ablations every year now. That gives you an idea how prevalent atrial fibrillation can be; it is considered the most common of all the various rhythm problems that can affect the heart.
I underwent the procedure at Baptist Hospital in Memphis in December 2014. Nurses first shaved and briskly scrubbed just about every square inch of me so they could attach all sorts of patches and electrodes and gauges so they could monitor my heart and other organs during the two-hour procedure. They wheeled me into the EP lab — an ice-cold room cluttered with monitors and tubes and gleaming tanks of liquid oxygen — I had a feeling I had zoomed into the future — where the ablation takes place. After a few minutes, where I confess I thought, “Hmmm, maybe this isn’t such a good idea after all,” somebody pressed an oxygen mask over my face, and the next thing I knew, I woke up in a hospital bed, my heart thumping normally.
I spent the night in the hospital and went home early the next morning, without any monitors whatsoever (that made me nervous, but I soon learned that, yes indeed, the procedure worked). The only problem, for me, came from the incision made in one of my femoral arteries. They don’t sew those shut; instead, they close the opening with pressure bandages, and one of mine started to leak. It was nothing serious, but within days a yellowish-black hematoma the size of a football spread around the incision site. This was nothing to be concerned about, they told me, but it certainly looked awful.
But that was it. I returned to Stern for followup visits and EKGs to monitor the results every two or three months, without anything unusual to report. What had become a weekly nightmare had vanished. I haven’t had a single episode of atrial fibrillation in more than two years. And since I tend to be a rather difficult patient — I always “enjoy” the side effects of medicines before any of the benefits can kick in — I consider the success of this procedure almost miraculous.