Who’s new at OHSU? Maros Ferencik, M.D., Ph.D.

Maros Ferencik, M.D., Ph.D., is a clinical scientist whose research focus is cardiac imaging. He joined the faculty at OHSU in January 2014.

Where are you from originally?
Slovakia. I went through medical school and earned my Ph.D. there.

Where were you before coming to OHSU?
I did my initial medical training in Slovakia for three and half years. During that time, I also spent a year on a research fellowship at the University of Massachusetts. I returned to the U.S. after my training and spent twelve years at Massachusetts General Hospital in Boston in the Harvard system. I did almost five years of research and my internal residency and cardiology training there.

Crater Lake, Oregon

Crater Lake, Oregon

What brought you to OHSU?
I was looking for new growth opportunities, mostly on the research front, and when I interviewed with Sanjiv Kaul, I realized there was a lot of support here for growing the cardiovascular research program within the Knight Cardiovascular Institute. In addition, my wife is a hematologist oncologist, and she was offered a position here, so that also factored into our decision.

How do you balance your clinical practice with your research?
My goal is to spend three-fourths of my time on research, though that’s not always possible. But my research is clinical research, so it melds together with some of my clinical imaging duties. My research focus is in imaging, primarily cardiac computed tomography (CT) imaging, which I also do as part of my clinical work.

What specific applications of cardiac CT imaging are you exploring?
I would summarize my research focus as exploring the use of cardiac CT for more efficient use in clinical practice to improve our ability to both detect disease and predict future events. As such, I have a few areas of interest. I work closely with colleagues at Mass General and the clinical trial center there on ROMICAT II, a large randomized trial involving people who came to the ER with acute chest pain. In this trial, we are looking at patients with acute presentations and using cardiac CT to better understand their diagnosis as well as prognosis. I also work with another large trial, PROMISE—again using cardiac CT—involving people with stable chest pain who present in an outpatient setting.

Traditionally, in cardiology, we look for stenosis, or narrowing of the arteries, to identify heart problems. With CT, in addition to imaging the stenosis, we can actually see the plaque, the wall of the artery, the disease that’s causing the problem. We’re learning more and more that characteristics of plaque are predictive, incremental, and independent of stenosis, and other factors, in predicting whether people develop acute coronary syndrome. Our recent work shows that what we refer to as “high-risk” plaque features are associated with worse outcomes. This goes along with histological data drawn from analyzing the plaque of people who have died. These plaques contain a lot of cholesterol, have a necrotic core, and grow outwardly, a process often referred to as “extensive remodeling.” Because CT can characterize tissue to some extent, we can identify these low-density plaques that predict poor short-term outcomes. But we are also looking to see whether these plaques predict future events. In the PROMISE trial, we’re looking at patients two to four years after they were initially evaluated to see whether certain plaque characteristics, beyond stenosis, can tell you which people are going to have cardiac events. We hope we’ll be able to provide better risk stratification to see who we should focus on with preventive measures, or, perhaps in the future, even move directly to interventional treatments.

Because CT is much more sensitive and accurate in predicting events compared to what we have traditionally used—stress testing—our notion about how many people are actually at risk has completely changed. When you run stress tests on a population of patients with stable chest pain, 80 percent will have negative results (no narrowing), but we’re learning with CT that only 50 percent are completely clear of plaque. People with plaque are at increased risk, so roughly 25 to 30 percent of the population actually has plaque without narrowing, causing blood flow obstruction. These are people we didn’t even know about and hadn’t identified with traditional risk factor assessments. Though this subset has lower risk than those people with stenosis, they still have disease and should be reclassified.

In both of these trials, we are trying to develop the most efficient use of CT by not only identifying people with disease but also by identifying those that don’t require treatment. Over-treating patients with statins is both expensive and can cause patients discomfort. CT can help identify those who need pharmacological treatment and those who don’t.

Another area I’m exploring is a combination of imaging and other methods. Imaging using contrasts carries some risk, so how can we minimize imaging at the initial evaluation? Highly sensitive serum assays that are used in Europe, but are not commercially available in the U.S., can detect even very small levels of cardiac troponin, proteins that signal necrosis in myocardial tissue or other types of damage. Over the years there have been vast improvements in the sensitivity of detection as well as the speed with which we can detect cardiac troponin. The problem is we can now detect troponin in almost everyone, and that presents a challenge. With increased sensitivity you get decreased specificity, so it comes with a cost. We don’t have a societal agreement about what the tolerable risk rate should be. If you increase sensitivity you have more expensive testing, hospitalizations, invasive procedures, etc. On the other hand, when you aim for high specificity, you end up sending some people home who will have an event. We know these patients are at high risk for dying and worse outcomes than they would be if they were in the hospital. So, what should the thresholds be? What is the ideal combination of these serum marker measurements, combined with the clinical risk factor assessments that help us decide who to safely send home and who to send for further testing (CT)? We’re trying to create an algorithm around evaluation protocols that use both biomarkers and imaging for more efficient use in the emergency department. The future of this depends on how the U.S., and the FDA specifically, will deal with the highly sensitive troponin assays.

What other aspects of cardiac CT are you involved with?
I’m very involved in the Society of Cardiovascular Computed Tomography (SCCT) – the international society dedicated to the field of cardiovascular CT. I’m on the board of directors and also serve as an associate editor for the Journal of Cardiovascular Computed Tomography. I’ve enjoyed being part of this organization and watching it grow. When I came to the U.S. in 2002, cardiac CT basically didn’t exist. But my mentors and colleagues in Boston saw this was an emerging field, and I was able to be a part of its expansion. I just returned from the 10th annual SCCT scientific meeting with almost 1,000 in attendance. A great deal has happened in this field in the last 13 years!

What do you like to do for fun?
Another reason my wife and I decided to come to OHSU was that we were attracted to Portland. We have a six-year-old son and a four-year-old daughter, and we wanted them exposed to nature and to spend time outside. When we do manage to have some free time, we love skiing, hiking, and biking. We love the closeness of the mountains and the ocean — it’s a wonderful place to raise a family.

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About the Author

Julie Rogers is Research Development Associate in the Office of Research Funding & Development Services.

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