Anker first studied medicine at the Charité Medical School, Berlin, completing his MD in 1993. But it was at the National Heart & Lung Institute of Imperial College in London, UK, where his academic teachers were Philip Poole-Wilson and Andrew Coats, that Anker first became involved in HF research, looking at the pathophysiology of body wasting in chronic HF and its survival impact. He completed his PhD in that field in 1998. “Learning from Philip [Poole-Wilson] changed my outlook on clinical research and life. He was a great man and I feel privileged that for almost 15 years he was my mentor and became a good friend.”
Today, Anker works at Charité Berlin, where, since 2007, he is a Professor of Cardiology and Cachexia Research, taking pride in the fact that his team’s interests bridge across a wide spectrum of disease areas from heart failure to cancer, kidney disease, COPD and stroke.
Anker’s notable contributions include the FAIR-HF study, published in the New England Journal of Medicine in 2009, where together with Piotr Ponikowski, previous president of the HFA, and Poole-Wilson, he showed that HF patients with biochemical evidence of iron deficiency receiving intravenous iron did much better for symptom status than those receiving placebo, regardless of whether or not they also had anaemia.
“Mitochondria of any muscle cell – whether in the heart or in skeletal muscles – need iron to generate energy, which could be the explanation behind the observations that the treatment results were similarly positive in patients with and without low haemoglobin levels (i.e. anaemia),”explains Anker.
He rather likes the fact that his early interest in gastroenterology (his original MD thesis at the Charité was on gallstone disease) has come full circle, with his work in HF. Anker’s endotoxin hypothesis proposed that abdominal congestion (caused by HF) leads to increased gut permeability, allowing endotoxins (i.e. lipopolysaccharide, LPS) produced by gram negative bacteria to enter the circulation and to trigger production of proinflammatory cytokines. Recently, Anker’s group has used a strategy to unspecifically bind LPS by using ursodeoxycholic acid (UDCA) – a drug typically used to resolve gallstones – and in a randomised controlled trial in CHF patients they have shown some improvement in limb blood flow (JACC 2012;59:585-92).
In his wide ranging research career Anker has also been credited with establishing cachexia as an independent prognostic factor in chronic HF, for defining the pathophysiology of tissue wasting in HF as an imbalance of catabolic processes going up and anabolic processes going down, and finding that the pathophysiological mechanisms of cachexia are similar across many illnesses.
As coordinator for the European Commission’s FP7 funded “Studies Investigating Co-morbidities Aggravating Heart Failure” (SICA-HF) project, Anker now hopes to provide further insights into the links between cachexia, diabetes and heart failure. The project - which aims to recruit over 1,600 patients from Germany, UK, Poland, Italy, and Russia - is focusing on co-morbidities contributing to disease progression in HF. This includes patients at the extreme ends of the body weight spectrum (i.e. patients with cardiac cachexia or obesity), as well as patients with type 2 diabetes mellitus.
“By collecting biomaterials such as blood samples, adipose tissue and skeletal muscle biopsies from patients who’ve undergone clinical investigations, we’re hoping to understand better the pathophysiological connections between these different complications,” he says.
Cachexia is a condition that affects 5 to 15% of patients with chronic HF. “Yet currently only around 20 to 30 research groups in the world focus on cachexia, creating a mismatch between the degree of attention awarded and medical need,” he says. No specific treatments are available for cachectic patients, but recently Anker has been heartened by an “explosion” of research activity with studies using anabolics like selective androgen receptor modulators, myostatin antibodies or ghrelin. “Over the next five to 10 years I’m confident we’ll see significant breakthroughs.”
Anker first joined the Heart Failure Association in the days when it was a Working Group, becoming a Member of the Board in 2006, being appointed Treasurer in 2008, and in 2010 was chairman of the scientific committee for the congress in Berlin.
As President, he is now spearheading the development of the Association’s online education platform. “The advantage of online education is that it can reach out to everyone, regardless of whether they attend congresses or not. The programme, which contains case presentations, testimonials and interviews, with a strong focus on guidelines, follows our newly developed heart failure curriculum,” he says.
He also hopes to raise public awareness of HF as a major healthcare problem requiring more research, clinical testing, political attention, and innovative therapies. “Raising awareness would undoubtedly help patients achieve a quicker diagnosis, and encourage more young physicians and scientists to enter the field” he says.
Anker is optimistic that new drug and device based therapies, together with telemedical interventions, will improve outcomes for patients with CHF. An increased focus of activities, he adds, should be directed at hospitalised HF patients.
Anker is renowned for his focus and love for life. Even his hobby of collecting sculptures revolves (to a large degree) around cachexia. “My wife Cornelia and I found our first sculpture on holidays in Burgundy. It showed a really skinny old man holding up a heart in his hand. The artist said it depicted ‘the heart you have to give to receive love’, but to me it provided the perfect representation of cachexia in heart failure,” he says.