After nearly 18 months of work, my research group finally published our big study! It should appear in the journal of the American Heart Association, “Circulation” on April 7, 2009. This also means that I can finally talk about what I’ve been doing for the last long while.
Atrial fibrillation (AF) is the most common – and perhaps most insidious – form of heart arrhythmia (a change in the normal electrical patterns of the heart) in existence. It affects millions of people and while it isn’t life-threatening in its early stages, it eventually leads to stroke or heart attack in many of those people who are afflicted with it.
Unfortunately, the current ways of treating AF are completely inadequate. The class of medication used for treatment (anti-arrhythmics) often cause more problems than they prevent, and interventional treatment is still highly experimental. It is, therefore, all but a guarantee that the AF will become more serious over time. Patients cannot be as physically active as they used to be and eventually must adjust to the symptoms of the disease.
A great part of the reason why AF is so difficult to treat is that we lack a good understanding of what causes it. About fifteen years ago, some researchers in France recognized that the random spots of electrical activity within the pulmonary veins (which return blood to the heart from the lungs) were a likely source of the arrhythmia. As a result, there is an entire arm of interventional treatment designed to destroy these spots and isolate the pulmonary veins so that bad electrical signals are unable to influence the heart as a whole. While this is effective in some people, it doesn’t work for everyone.
More recently, other researchers found that AF actually changes the underlying tissue of the heart (a process known as remodeling), which results in other electrical and mechanical adaptations. These changes make the arrhythmia more serious as well as difficult to treat. Even though the changes are a sign that the person has a more advanced form the arrhythmia, the only way to ascertain the degree of change is to invasively measure electrical changes from the inside surface of the heart.
That is, until about a year ago. In the Circulation paper, we describe a method to determine how much the heart has remodeled by using MRI. We also showed that the degree of change is the single best indicator of how the patient will respond to treatment. While this may seem obvious, it isn’t something that could be measured easily or safely before. Now, we have a tool which allows us to see how the heart changes over time in response to AF. This will lead to a better understanding of the disease, and provide insight in how to treat it.
The image below shows an example of just how good this detection can be. The first column of images (A) shows a three dimensional model of the human left atrium. In the top row, we are looking at the back (or posterior) view of the left atrium. The pointy bits projecting to the left and right are the pulmonary veins. In the bottom row, we are looking at the atrial septum – part of the wall that divides the heart into left and right sides. The really interesting information is in the second column (B) which shows a 3D model where two different types of tissue have been identified. Healthy tissue (shown in blue) and diseased tissue (shown in green).
This particular patient has some diseased tissue, though overall the heart looks fairly healthy. What is striking, however, is how well this diseased tissue compares to the measurements made by invasive mapping (taken during a catheter intervention). On the back side (top) we can see a donut of unhealthy tissue, and on the right side (in the septum), we can see a hook of unhealthy tissue. The location and shapes of these tissue are mirrored on the invasive maps (C). And all of this can be determined without exposing a patient to radiation or needing to cut them open!
These types of MRI techniques open a whole new branch of research that can be done on the heart that has important implications for more than AF research. The remodeling and changes observed in AF can be seen in atrial tachycardia and even some types of ventricular arrhythmias. Moreover, it appears to be related to other conditions, like coronary artery disease or ischemia (from smoking, for example). More on that later, though. If interested, you can find the complete text of the Circulation article here.