Interview with Dr. Emelia Benjamin on Framingham Risk Prediction Tool for Atrial Fibrillation
July 12, 2010 7:15 AM CT
In this video interview, Dr. Emelia Benjamin talked about the risk factors for atrial fibrillation, including that the lifetime risk for women is 23% and for men 26%. In order to try to prevent it, the Framingham Heart Study developed a risk prediction instrument for atrial fibrillation that includes advancing age, gender (men tend to have more atrial fibrillation than women), high blood pressure, valvular heart disease, heart failure, and a new predictor, longer PR-interval (a measurement seen on an EKG). They also looked at biomarkers and determined that C-reactive protein (CRP) and BNP (B-type natriuretic peptide) also predict atrial fibrillation.
Regarding where they are going in the future, Dr. Benjamin mentioned that they are trying to understand the contribution of family history toward everyday atrial fibrillation. Since the Framingham study is multigenerational, it has shown that if one or both parents had atrial fibrillation, the risk in the offspring almost doubled. And if one parent had it at a young age without heart disease (lone atrial fibrillation), the risk tripled. So future research is targeted toward developing a better understanding of the genetic risk factors for atrial fibrillation.
Dr. Emelia Benjamin holds the following positions:
- Director, Echocardiography/Vascular Laboratory, Framingham Heart Study
- Professor of Medicine, Boston University School of Medicine
- Professor of Epidemiology, Boston University School of Public Health
About the Framingham Risk Score Profile for Atrial Fibrillation—link to the interactive risk score calculator is at the bottom of the page
View the video:
Mellanie True Hills: This is Mellanie True Hills. I’m at Boston Atrial Fibrillation Symposium 2010, for StopAfib.org, and I have the pleasure of having with me today Dr. Emelia Benjamin. Dr. Benjamin is a professor of medicine and epidemiology at Boston University and is also very well known as the senior investigator for the Framingham Heart Study, a study that has done a lot for helping us understand heart disease and atrial fibrillation.
Dr. Benjamin, thank you so much for joining us today. You did a fabulous program, and I’d love for you to share some of the things that you talked about today in your session here at Boston Afib. So, let me just throw it to you, and I appreciate you taking the time.
Dr. Emelia Benjamin: It’s a tremendous honor to speak with you, and also to the people that you help around the country and around the world that have atrial fibrillation or have relatives with atrial fibrillation.
A lot of my interest in atrial fibrillation stems from what we know about the epidemiology of atrial fibrillation. We know that it is a common condition; we know that it increases with advancing age; and we also know that the lifetime risk is surprisingly high. The lifetime risk is on the order of 23% for women and 26% for men. And so if you live long enough, it is not uncommon that you will get atrial fibrillation.
Framingham, along with many other cohort studies, has been at the forefront of describing the risk factors for atrial fibrillation. There are many that we’re familiar with—advancing age, men tend to have more atrial fibrillation than women, high blood pressure, valvular heart disease, and heart failure.
I had the opportunity to work with some visionaries at the National Heart, Lung, and Blood Institute to really think about the prevention of atrial fibrillation. There’s been fabulous work done on the prevention of coronary heart disease and the prevention of heart failure. There’s been virtually no work done on the prevention of atrial fibrillation. My father was a southerner—we all know that an ounce of prevention is worth a pound of cure.
The question is how do you prevent a condition that has such morbidity and mortality? So we had a conference that was convened by the National Heart, Lung, and Blood Institute to really think about opportunities for prevention and what should be the research agenda to really get prevention on the map. One of the things to come out of that was looking at risk factors and a risk marker, or risk prediction, instrument for atrial fibrillation. In terms of the risk prediction instrument we went back to Framingham and we did what we’ve done for risk prediction instruments for many other conditions, like heart failure and coronary heart disease—we first tried to figure out what are the actual risk factors.
Many of the ones I already told you came up. One that hadn’t been known before was an electrocardiographic measurement, called the PR-interval, which basically is the repolarization, or the electrical activity around the atrium, and having a longer one predicts incident [new] atrial fibrillation.
We then said, OK, well let’s understand if we can predict in an individual what their risk would be knowing these risk factors—what their ten year risk would be—so we developed a risk prediction instrument. It’s available on the Framingham Heart Study web site, and I’d love to have you go and use it.
What we have are standard clinical factors, not fancy stuff that costs a gazillion bucks to measure that requires a special tertiary care hospital, but simple things that a physician or a care provider can obtain in the office. Things like, “how old are you”, “do you have heart failure”, etc. You can go to the web, and you can look at what your risk is, and you can compare it to an individual of the same age and sex who has low risk factor burden, and that helps people understand what their personal risks are.
Now, part of the motivation for developing it was to give people a realistic sense of their risk, but one of the biggest motivators for me is—I think all of us are aware—there’s a huge health care problem in terms of financing. I’m an associate editor for the cardiology journal Circulation, and it’s not uncommon that every week we get submissions for this risk factor or this risk marker. And the question is, “how much do these risk factors or risk markers add to our understanding of the actual risk of developing a condition?” So we first developed the clinical risk marker, a clinical risk factor index, and then we added C-reactive protein and BNP, two biomarkers, to see if they help predict the onset of disease. It turns out they did, and we did some fancy tests to figure that out, the details of which are not important.
Where are we going in the future? Hopefully we’re going to also understand what is the contribution of family history. What is it that we at Framingham, and other people—Iceland, Dr. Ellinor at Mass General, and people at the Mayo Clinic—have published, that there is a familial component to atrial fibrillation. I think all of us know there are those kind of unusual families where everybody has atrial fibrillation at a young age with no heart disease. That’s unusual.
At Framingham, we asked the question, “What about everyday atrial fibrillation?” Not fancy tertiary care hospital, but stuff that we see in the community. And because the Framingham Heart Study is a multi-generational study, we were actually able to not only look at an individual’s risk, we were able to look at whether their parents have had atrial fibrillation. It turns out that if one or both parents had had atrial fibrillation, it almost doubled the risk of having atrial fibrillation in the offspring, just common atrial fibrillation. And if one’s parent had it at a young age and didn’t have any heart disease, then one had a tripling of the risk. The logical extension of that is figuring out, “What are the genetic factors that do contribute?” And we, and Dr. Ellinor, and Dr. Heckbert at the Cardiovascular Health Study and a number of us got together, and said, you know, we could all just compete with each other, but we actually could collaborate, do some great science, and have some fun.
Luckily, we chose the latter, and we’ve all been working together to try to understand what are the genetic risk factors for atrial fibrillation. These require huge, huge studies. There’s advances in technology where you can actually get markers across all the human chromosomes, and then when you have these large studies with large numbers of people with atrial fibrillation, and good controls, which you do have in a cohort setting, then you can actually say, “Well, wow, you know, this really has a very, very tiny risk, but it’s very robust, we know that it has it.” Because the kind of genetic risk factors that happen in the community aren’t those 2, or 3, or autosomal dominant [where you only need to get the abnormal gene from one parent]—you know, where everybody gets it if you have that marker. They’re not mutations; they’re common, they’re markers that have a little bit of risk associated with them, and you can only find them if you look at lots of people.
So is that going to make any difference to the patients that follow your website? Probably at this point, 1 or 2 markers isn’t, but just say we get to the point where we had many, many, many different genetic markers. Well, then, we may be able to bring them together and figure out, does it help with risk prediction, or not, over and above what we know clinically. And more importantly, it gives us more opportunities to design drug targets and understand the pathophysiology of atrial fibrillation.
It’s an incredibly exciting time in atrial fibrillation research. It’s really marked by incredible advances, and also tremendous cooperation across multiple centers across the world. And I feel honored to speak to your organization. Thank you.
MTH: Thank you Dr. Benjamin. It’s all so fascinating, and we appreciate the contributions that you and your colleagues are making to helping us really understand atrial fibrillation, and we know that this is going to make a huge difference going forward. Thank you so much for taking time to join us today. This is Mellanie True Hills, for StopAfib.org.