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Developments in anti-cancer treatments have significantly improved patient survival; however, there is evidence that a growing number of cancer patients present with impaired heart function as a consequence of their treatment. This phenomenon is known as cardiotoxicity. All anti-cancer treatments affect the heart to some extent, though the symptoms and their severity vary from one treatment to another.  

What is cardiotoxicity and how serious is it?

Anti-cancer treatments are not designed to be toxic per se, but to selectively target aspects of cancer cells that support their growth and survival. However, identifying a treatment target that is specific to the cancer cell is very challenging.

For example, HER2 is a protein overexpressed in several cancers. Its overexpression is associated with aggressive tumours that often have poor patient outcomes, making HER2 a logical drug target. However, HER2 is expressed in other cell types, including cells in the heart. Treatments designed to selectively target HER2, such as the antibody‑based therapy Herceptin®, cannot distinguish between cancer cells and healthy cells that express HER2, and therefore target all HER2‑expressing cells, which can lead to unwanted effects. If these effects occur in the vasculature or heart cells, this can cause cardiotoxicity (i.e. impaired heart function).

The symptoms of cardiotoxicity can range from fatigue, shortness of breath, chest pain, swelling and hypertension, to an irregular heartbeat and even heart failure (an inability of the heart to pump blood around the body). These symptoms have been observed in patients with no known heart conditions prior to cancer treatment, though increasing age, smoking, or pre-existing health conditions can increase the risk of experiencing treatment-related cardiotoxicity.

How is cardiotoxicity managed in the clinic?

In the clinic, cardiotoxicity is managed by modifying treatment regimens, promoting regular exercise and a healthy diet, and by closely monitoring individuals that may be at risk of developing treatment-related cardiotoxicity. Patients can be monitored through blood tests to detect biomarkers of abnormal heart function, and through assessing how well the heart contracts, as reduced contractility can be an early sign of heart failure.

Depending on the anti-cancer treatment, cardiotoxicity may be reversible by stopping treatment, allowing cardiac function to return to pre-treatment levels within months. However, stopping treatment halts the intended anti-cancer effect. Therefore, patients will have to switch to another therapy to disrupt tumour growth, which will also have its own cardiotoxic risk. Because treatment-related cardiotoxicity is not always reversible, cardiovascular medications (like the ACE inhibitor Elanapril) can be used to alleviate persistent cardiac effects and to control cardiotoxic symptoms that may arise during continued cancer therapy.

How can research help combat cardiotoxicity?

Research is starting to uncover how these anti-cancer treatments damage heart cells and lead to cardiotoxicity. This knowledge can then be utilised to develop strategies that can reduce or reverse these cardiotoxic effects, though the variation in mechanisms of cardiotoxicity across cancer treatments make a universal solution unlikely.

Currently, Dexrazoxane is the only available drug used to prevent cardiotoxicity. It is used alongside the chemotherapy drug Doxorubicin and has been shown to reduce, and in some cases prevent, cardiotoxicity in patients receiving Doxorubicin treatment. Further research is needed to identify new ways of preventing cardiotoxicity from other anti-cancer treatments, similar to the protective effect of Dexrazoxane. After all, preventing cardiotoxicity is far more effective than treating symptoms once they have occurred.

Is it all doom and gloom?

Although cardiotoxicity is a significant problem facing cancer patients and clinicians, it is undeniable that modern cancer treatments have significantly improved the outlook for patients. This includes prolonging patient survival – but does this come at a cost of heart function?

A 2011 study by an American research group investigated the leading cause of death in women diagnosed with breast cancer, over the age of 65. By the end of this 12-year study, half of the patients had died, with the leading cause of death being cardiovascular disease (CVD), closely followed by cancer. The study showed that over time, deaths from cancer decreased while death from CVD increased, and that pre-existing health conditions and increasing age increased the risk of CVD-related death. Notably, in this study only a quarter of women who died from CVD already had heart disease when diagnosed with cancer – the majority developed CVD during or after chemotherapy treatment.

Although this study observes heart disease to be the leading cause of death in these patients, it is important to acknowledge that approximately half of these women were still alive 12 years after diagnosis – which would not have been possible without modern therapies. As people live longer, they will face age-related health issues, which include a gradual decline in heart function and increased risk of CVD.

Though some cancer treatments can affect the heart, patients are now living long enough for these delayed cardiotoxic effects to become apparent, which itself reflects the significant progress in cancer care. The challenge ahead is to develop strategies that can lessen or even reverse these cardiac effects, helping to further improve long-term health and quality of life for survivors.