Stefan D Anker, professor of Cardiology and Cachexia Research, Department of Cardiology, Charité Campus Virchow-Klinikum, Berlin, Germany, is the 2012–14 president of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). He has been credited with establishing cachexia as an independent prognostic factor for cardiovascular illness, and he has shown that iron deficiency is a valid therapeutic target in heart failure.
What prompted your decision to become a doctor and, in particular, why did you choose to specialise in heart failure?
In truth, I never consider doing anything other than medicine. In my last year of medical school (1992), the cardiology department was getting all of the new technology and, therefore, it was the most modern and innovated department in our medical school—so, I moved towards internal medicine and cardiology. I made the decision to study in London thereafter, and I started to work in Andrew Coats’s group at the Royal Brompton Hospital, which happened to focus on heart failure and that is what prompted my decision to specialise in heart failure. The path you go down is not always something you plan; to some degree, it is chance.
Who were your mentors and what influence did they have on your career?
Number one was Professor Hans Berndt. He was actually a gastroenterologist, but he was the chairman of internal medicine at Charité Medical School at the time of my studies. I did my medical doctor thesis with him on gallstone disease. So I got to know him quite well and he taught me to think clearly and produce well-structured documents as a result of good research.
In London, there were two people—Professor Philip Poole-Wilson and Professor Andrew Coats. Professor Poole-Wilson died in 2009 and—in a way—he was my academic father. He trained me in many ways; in cardiology, from a medical standpoint and even more so in research, from a methodological standpoint. He also taught me about the redundancy of words and to not waste space in articles (or anywhere) by using words that were simply not necessary. He also introduced me into big clinical trials.
Andrew Coats probably has had biggest influence on me over the long term. He was my primary PhD supervisor (Philip was co-supervisor) and he selected the topic for my PhD, which was cachexia in heart failure. By doing that, he practically decided my fate—cachexia research. Ever since 1994, when I went first to London, we have worked together closely and we are good friends. Also, we have started to look outside of cardiology. For example, we are the scientific co-founders of a company (Psioxus Therapeutics) that is developing therapies for cancer. It is altogether very exciting.
In your view, what has been the most important development in the understanding of heart failure during your career?
Probably, firstly, the development and full acceptance of the therapeutics benefits of beta-blockers for heart failure and, secondly, the use of aldosterone antagonists. And from a device perspective, there is cardiac resynchronisation therapy (CRT). Several large-scale trials have shown that all these therapies reduce overall mortality in heart failure patients.
As someone who has been involved several randomised clinical trials, which piece of research are you most proud of and why?
I am proudest of the FAIR-HF trial (Anker et al, N Engl J Med 2009; 361:2436–48) because I worked with Philip Poole-Wilson, who unfortunately died before the study ended, on this therapeutic topic since our first contact with intravenous iron back in 2001. We were co-chairs of the steering committee and responsible for the academic side of the work—when he died, I had to bring this trial over the finishing line. I was involved in iron deficiency in heart failure from an epidemiological standpoint, then during the phase II trial, which led to the phase III study. And that was ultimately published in the New England Journal of Medicine and this therapeutic approach is now, for the first time, part of several guidelines.
What are the main research priorities in heart failure?
I think, from a global perspective, raising awareness of the problem of heart failure. Also, we need to improve the diagnosis of not only systolic but also of diastolic heart failure. You can only use the therapies that we have already developed and make a difference with them for patients, if you have awareness and diagnosis. Regarding new developments, basically, we need better therapies, better devices, and remote patient management.
I think there are more devices to come, and I think there are also much better drugs to come. One of the biggest challenges when developing new devices and drugs is prove that the “new stuff” is better than the devices and drugs that are being replaced. Therefore, comparative efficacy research will be quite important in that respect.
You’ve said in public that you are confident that we will see “significant breakthroughs” in the management of cachexia over the next 10 years. What do you think these breakthroughs will consist of?
When I refer to cachexia, l am referring to wasting disease in all chronic illnesses rather than just in heart failure. I think, potential breakthroughs will include anabolic therapies and presently there are two anabolic therapies in phase III studies. Essentially, these therapies act similar to anabolic steroids, but they are not steroids and they have a much better side-effect profile.
Cardiovascular drugs in cachexia patients without heart disease may also be useful. We know that ACE inhibitors prevent weight loss (in 2003 we published on this in The Lancet) and we know that beta-blockers prevent and even reverse body wasting. As we are already using these drugs in heart disease, we know that they will not make much of a difference to patients with cachexia in cardiovascular illness. But in other forms of cachexia, they might do.
You are the co-ordinator of SICA-HA (Studies investigating comorbidities aggravating heart failure). What are the aims of this project?
This is a European Union funded FP7 project that takes place in six countries and in 11 centres. The aim is to better understand, over a longer period of time, the factors that lead to progression of heart failure. It focuses on three areas: injury resistance, obesity, and cachexia. Basically, the goal is to better understand the interaction of these phenomena and how they contribute to poor health status and high morbidity and mortality in heart failure. We aim to establish new therapeutic targets.
As the new president, what are your goals for the HFA of the ESC?
There are several goals, but maybe the most important aim is to increase awareness of heart failure on a global level. Also, we want to increase the understanding of heart failure among healthcare professionals. As well as achieving this through our annual congress and through our journals, we also have ongoing online education initiatives to provide information on heart failure.
Finally, I want to further strengthen the HFA and, basically, make it strategically ready the next 10 years—from a structural and economic angle and from a membership and an academic angle.
What are the key themes of the 2013 Heart Failure congress?
Its motto is “the cardiologists of tomorrow” and our focus is the education of the new generation of cardiologists. We want to get them interested in heart failure and show them how exciting it can be. Devices and biomarkers will also be important areas where innovative research will be demonstrated and discussed. Professor Burkert Pieske from Graz (Austria) is chairman of the congress and his research specialty is heart failure with preserved ejection fraction, so that will be also an important focus of the congress.
Another goal is reach out to national and international societies—we aim to establish HFA and its Annual Congress as the premier place to exchange ideas and to learn in the field of heart failure.
What has been your most memorable case and why?
Back in the mid 1990s, when I was working in London, I had a heart failure patient who had lost 15–20kg [about 2.5–3 stones]. At the time, cholesterol was already established as being the “bad guy” no matter what, and this patient was fixated on reducing his cholesterol because his GP told him to do so, despite him having a relatively low total cholesterol already. I had to tell this patient that in addition to his heart disease, he now had another much bigger problem—he was now cachectic because of all the weight that he had lost. In fact, he and his wife (who was with him) realised that a lot of his symptoms (such as breathlessness, weakness and fatigue) were related to the loss of leg muscle. He asked me what he could do, so I told him to go back eating bacon and eggs for breakfast [rather than continue on the strict low cholesterol diet he had been on]. In my opinion, the effect of his weight loss was a much bigger problem than his low density lipoprotein (LDL) level could possibly be. On hearing this, he and his wife suddenly had this marvellous “shining light” look in their eyes. He could eat what he wanted to eat and she could cook him the food that she wanted to cook him. Therefore, it was almost like providing marriage counselling when giving this medical advice!
Later in 2003 we published on what I had told this patient, ie. that heart failure patients indeed have a better survival when they have higher rather than lower cholesterol or even LDL levels (Rauchhaus et al, J Am Coll Cardiol 2003).
Outside of medicine, what are your hobbies and interests?
A few times a year I play tennis or golf—but there is much too little time. I like collecting sculptures, particularly anything “skinny or thin”. The majority of the artists of whom my wife and I have sculptures, we know personally. They provide a different perspective on life. We use pictures of some of the sculptures I collect as the cover art of Journal of Cachexia, Sarcopenia and Muscle (JCSM), of which I am founding editor-in-chief.
2002–present Professor of Cardiology and Cachexia Research, Department of Cardiology, Charité Campus Virchow-Klinikum, Berlin, Germany
2012–2014 President, Heart Failure Association of the European Society of Cardiology
Editor-in-chief, Journal of Cachexia, Sarcopenia and Muscle
Founding president, International Society on Cachexia and Wasting Disorders
Co-ordinator, studies investigating comorbidities aggravating heart failure (SICA-HF) project
1987–1993 Charité Medical School in Berlin, Germany (MD) 1998 National Heart & Lung Institute, London, UK (PhD)
1. Anker SD, Ponikowski P, Varney S, et al. Wasting as independent risk factor of survival in chronic heart failure. Lancet 1997; 349:1050–53
2. Niebauer J, Volk H-D, Kemp M, et al & Anker SD. Endotoxin and immune activation in chronic heart failure: a prospective cohort study. Lancet 1999; 353:1838-42
3. Anker SD, Negassa A, Coats AJS, et al. Prognostic importance of weight loss in chronic heart and the effect of treatment with angiotensin-converting-enzyme inhibitors: an observational study. Lancet 2003; 361:1077–83
4. Sandek S, Bauditz J, Swidsinski A, et al & Anker SD. Altered intestinal function in patients with chronic heart failure. J Am Coll Cardiol 2007; 50:1561–69
5. Anker SD, Comin Colet J, Filippatos G, et al. Ferric carboxymaltose in patients with heart failure and iron deficiency. N Engl J Med 2009; 361:2436–48
6. Maisel A, Mueller C, Nowak R, Peacock WF et al & Anker SD. Mid-region pro-hormone markers for diagnosis and prognosis in acute dyspnea: results from the BACH (Biomarkers in Acute Heart Failure) trial. J Am Coll Cardiol 2010; 55:2062–76
7. Anker SD, Koehler F, Abraham WT. Telemedicine and remote patient management in heart failure. Lancet 2011; 378:731–39
8. von Haehling S, Schefold JC, Jankowska EA, et al & Anker SD. Ursodeoxycholic acid in patients with chronic heart failure a double-blind, randomized, placebo-controlled, crossover trial. J Am Coll Cardiol 2012; 59:585–92
9. Koehler F, Winkler S, Schieber M, et al & Anker SD. Impact of Remote Telemedical Management on Mortality and Hospitalizations in Ambulatory Patients With Chronic Heart Failure: The Telemedical Interventional Monitoring in Heart Failure Study. Circulation 2011; 123:1873–80