Heart Failure Correlates with Increased Cancer Risk

Age-related disease results from the underlying cell and tissue damage that causes aging. Different people accumulate that damage at modestly different rates, the result of lifestyle choices and exposure to infectious disease. Thus the presence of a sufficient burden of damage to produce one age-related disease will be accompanied by a raised risk of other age-related conditions. The conditions themselves need not have any direct relationship with one another, but can be distinct outcomes of the same root causes. Here, however, researchers propose that heart failure may provoke increased cancer risk via inflammatory and other signaling pathways. This may or may not be the case. The inflammatory signaling certainly exists, but it is always a challenge to determine the relative significance of the many possible contributing mechanism in the onset and progression of age-related disease.

Our study demonstrates that heart failure patients have a significantly increased incidence of cancer in general and of each individual cancer type studied. The data - based on a collective of over 100,000 heart failure patients - confirm the results of previous evaluations in smaller study populations. The data do not prove a causal relationship but instead show a statistical relationship between heart failure and cancer. Nevertheless, these results allow us to speculate that there may be a causal relationship between heart failure and an increased cancer rate.

The particularly high incidence of oropharyngeal carcinoma in heart failure patients suggests that common extrinsic risk factors such as nicotine are a possible trigger of the co-morbidity. In this regard, one limiting factor of our study is that our database does not provide data on nicotine use or alcohol consumption. In addition to these external risk factors, cancer in general and cardiovascular diseases share common risk factors such as obesity and diabetes. As our data are adjusted for these risk factors, our highly significant results cannot be explained by these factors alone.

One possible explanation could be the occurrence of certain pathomechanisms such as chronic inflammation or increased free radical formation, which may interact with a certain genetic background to connect both heart failure and cancer. Another interesting hypothesis suggests that heart failure is an oncogenic condition. This means that the failing heart may promote tumourigenesis or tumour growth. New data from animal studies suggest that the secretion of certain proteins may be up-regulated in failing hearts, promoting the secretion of certain tumour growth factors.

Supporting evidence comes from a study demonstrating that serum levels of heart failure markers such as N-terminal pro-brain natriuretic peptide and troponin T were elevated in cancer patients even before the application of anticancer therapy, suggesting that subclinical myocardial injury exists in cancer patients. The specific interaction of cardiac stress-induced proteins with oncogenic signalling pathways is a relatively new branch of research with great potential. Some of these potential heart failure / oncogenic pathway interactions may be organ specific. In this context, studies such as ours that link large collectives of heart failure patients not only to cancer development in general but also to individual organ systems may be helpful.

Link: https://doi.org/10.1002/ehf2.13421

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