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Heart failure stimulates tumour growth

14 August 2018

A failing heart , e.g. as the result of a heart attack, pumps blood less efficiently and secretes substances that may stimulate tumour growth. This has been revealed by research with mouse models, supported by data from the PREVEND population study, conducted by Professor Rudolf de Boer and his team of the UMC Groningen. He has published on this topic in the scientific journal Circulation.

Heart failure is a very common condition - about hundred and fifty thousand people in the Netherlands suffer from it. Heart failure develops in response to injury to the heart and is characterized by a deficit to supply the body with sufficient blood. People may suffer heart failure after a heart attack, or as a result to long-term hypertension or valvular heart disease.

The concept that a link between heart failure and cancer could exist has been around for some time – it has been noticed that a disproportionately high number of cancer deaths were observed in registries of patients with heart failure. It was not clear, however, if a direct causal link exists. De Boer for the first time demonstrates scientific evidence of this in the publication.

He conducted research with mouse models with a genetic predisposition to colorectal polyps and cancer and observed significantly increased growth of polyps in the colon of mice in which heart failure was provoked as compared to the mice with healthy hearts.

De Boer discovered elevated levels of various proteins in the mouse models. The levels of these proteins turned out to be also elevated in the blood of human patients with heart failure . Finally, epidemiological research with data from the PREVEND population study, which measured classic heart failure biomarkers (signal substances), revealed that healthy individuals with elevated levels of these biomarkers (so with possible early heart failure symptoms) were more likely to develop cancer or colorectal cancer over a period of 10 years.

De Boer: ‘Our data validate the suspicion and provides scientific proof that patients with heart failure appear to be at greater risk for (colorectal) cancer. Whether this also applies to other forms of cancer needs further study – the indications are certainly there. Our results should raise specialists’ awareness of this risk so they can act accordingly, for example by offering patients with heart failure low-threshold and perhaps timely screening for colorectal cancer.’

De Boer and his team worked on this research together with the departments of oncology, gastroenterology, pathology and internal medicine of the UMCG and with the University of Innsbruck, Austria.