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Atrial Fibrillation and the Maze Operation
By Vincent A. Gaudiani, MD
In this document, I want to explain some basic aspects of atrial fibrillation, describe how
the maze operation works, and present our results to date. We will begin by describing
how normal sinus rhythm works, then explain what atrial fibrillation is and how it causes
symptoms, and finally proceed to the concepts of the maze operation. Here at the
beginning, let me remind you that the heart consists of two upper chambers, the atria, and
two lower chambers, the ventricles. The right and left atria are storage containers for
blood coming back from the body and the lungs respectively. The right and left
ventricles relax to allow atrial blood to flow into them, and then they contract forcefully
to deliver blood under pressure to the lungs and the body respectively. I want to explain
how this rhythmic contraction of the heart is controlled.
What is normal?
All muscular contractions, whether in your arm muscle or your heart muscle, begin with a
wave of electrical activity that causes the muscle to squeeze. In the case of the arm
muscle, an electrical signal comes from the brain and travels down the spinal cord to
nerves that distribute electrical stimulation to the muscle. If the nerves or spinal cord are
cut, electricity can’t flow, and the muscle cannot contract. Instead of relying on the
brain, the heart has its own much simpler, but highly effective electrical system that tells
the heart when to contract. This system begins with a special set of cells, called the sinus
node, in the right atrium that regularly discharge electrical messages to the heart. Each
message quickly spreads over both right and left atria causing them to contract once.
This electrical message then passes to the next key part of the electrical system, called
the AV node. This structure is a bridge that delays the signal for a brief moment and
then sends it to the ventricles. The delay is very important because it protects the
is a period during which the cells absolutely cannot be stimulated again. This is called
the refractory period. Therefore once the atria have been depolarized, they cannot be
further stimulated for a while and the electricity has nowhere to go. After this rest, the
atria regain their ability to be depolarized again so they are ready for the beginning of the
next heartbeat. But what happens if the atria are very large? Under these conditions,
some portion of the atria might recover while the impulse is still traveling through the
atria. Then the electrical impulse could always find a place that could be depolarized,
and the electrical activity would be continuous, not intermittent. That is, the electrical
impulse could always find a place ready to depolarize, and therefore electricity would
continue to wander around the atrium. The same sequence of events could happen if the
atria were diseased and therefore slowed the passage of the original stimulation through
the heart. Once again, by the time electricity spread slowly over the atria, enough time
might pass so that some part has recovered (repolarized), then another, and the original
signal could continue wandering around the atria finding a repolarized spot.
What does atrial fibrillation do to patients?
Most patients with atrial fibrillation have one or both of these problems: the atria are
enlarged and/or they conduct slowly. These problems permit an electrical impulse to
wander endlessly around the heart. The electrical energy is said to re-enter the places
where it has been on the previous beat, and thus atrial fibrillation is a re-entry
abnormality. This continuous electrical activity has several effects: first, the atria quiver
irregularly and second, the ventricles, although protected by the AV node, beat
irregularly. Let’s examine the effects of each of these on the patient. When the atria
quiver in response to continuous electrical activity, they do not squeeze effectively, blood
passes through them turbulently, and turbulent flow promotes clot formation in the atria.
When these clots are washed into the ventricle, they can end up in the brain, causing a
stroke. People with atrial fibrillation take the blood thinner coumadin to diminish the
chance of clot formation. This treatment is effective but does nothing for the atrial
fibrillation and exposes patients to the risk of bleeding. When the sinus node cannot
control heart rate, the AV node does what it can to prevent too many electrical signals
from going to the ventricles, but the normal way we control our heart rate doesn’t work,
we tend to go too fast or too slowly, and we don’t adjust to our level of activity. Some of
us sense irregular heart beats as “palpitations”. Medicines such as digoxin and the
antiarrhythmics can help, but rarely cure atrial fibrillation. Finally, when the atria quiver
they do not squeeze blood into the ventricles. This decreases the effectiveness of the
heart as a pump.
The Maze Operation
Now that you have some basic concepts about the electrical activity of the heart, I can
provide some ideas about the surgical cure of atrial fibrillation. Once you have read this,
take a look at the slide show that follows. It was written for medical personnel, so it is
more detailed, but it presents a complete view of the maze as well as our results with this
operation.
Since atrial fibrillation is a re-entry abnormality, we can cure it if we block re-entry. We
can do this by placing a series of strategically located incisions in the atria and then
sewing them up. Electrical activity cannot cross such incisions even after they heal. The
key idea in the maze is to place these incisions in the locations where re-entry is most
likely, but leave the sinus node in electrical touch with most of the atrium. In this way
the sinus node can continue to control heart rate, but re-entry is less likely. In addition,
the maze detaches and reattaches the pulmonary veins to the left atrium. This prevents
premature atrial beats that originate in these veins from initiating atrial fib. The slide
presentation will add some depth to this brief outline, and specifically credit the key
research of my colleague and friend, Dr James Cox who made this effective operation
possible.
ventricles from being stimulated too frequently. Remember that the ventricles pump by
squeezing the blood inside them and then relaxing so the next load of blood can enter. If
they are simulated too frequently, they don’t have enough time to fill or empty, so they
can’t move blood. The delay in the AV node prevents this from happening.
After a delay at this tollgate, the electrical message passes quickly to the ventricles, and
they contract synchronously to squeeze blood and thus maintain blood pressure and
provide oxygen. In very abbreviated form, this explains how a single normal heartbeat
occurs.
What is atrial fibrillation?
To understand atrial fibrillation, you have to begin with an even simpler question that
reveals a fundamental idea about the heart. Once the sinus node releases a packet of
electrical activity to the atria, why doesn’t the electricity just keep wandering around the
heart? Why does the heart quiet down after each stimulation? Every cell in the heart is
designed so that normally after each stimulation (also known as a depolarization) there