Oncologic therapies associated with cardiac toxicities: how to minimize the risks

ABSTRACT

Introduction: Recent breakthroughs in cancer treatment has improved the prospects and life expectancy of cancer patients. Therefore, risk of cardiotoxicity induced by oncologic therapies has become an important determinant of patient’s survival and quality of life, independently of the oncologic prognosis.

Areas covered: This paper provides an overview of the proposed strategies to mitigate the risk of cardiotoxicity. Limitation of current approaches, the need for early detection and the treatment of cardiotoxicity are also discussed. Possible future research directions are also described.

Expert opinion: The most effective approach to minimize cardiotoxicity is early identification and early onset of a prophylactic treatment. However, the current standard of cardiac monitor identifies cardiotoxicity only when a functional impairment has already occurred, precluding any chance of effective prevention. The use of troponins to identify subclinical cardiotoxicity, and early treatment with ACE-inhibitors to prevent cardiac dysfunction and cardiac events have recently emerged, and appear to be an effective tool against this complication.

KEYWORDS:

• Cardiotoxicity
• prevention
• biomarkers
• troponin
• cardio-oncology

Article highlights

• The remarkable breakthroughs of cancer treatments of the last two decades have improved prospects and longer life expectancies of cancer patients.

• The risk of cardiotoxicity induced by oncologic therapies has become an important determinant of the patient’s survival and quality of life independently of the oncologic prognosis.

• The identification and the management of cancer patients at high risk for cardiovascular events has resulted as one key strategy to reduce morbidity and mortality from cardiovascular toxicity related to cancer therapy, which may thwart its effectiveness.

• Several strategies for the prevention of cardiotoxicity have been developed to minimize cardiac morbidity and mortality related to it. In particular, the use of available less cardiotoxic regimens with similar oncologic effectiveness, early diagnosis, and prevention – primary or secondary - with cardioprotective agents should be encouraged (Figure 1).

• There is promising evidence that the prevention of cardiotoxicity is a possible objective, but it requires a multidisciplinary approach and close collaboration between cardiologists and oncologists.

• However, the current standard of cardiac monitoring identifies cardiotoxicity too late, only when a functional impairment has already occurred, precluding any chance of effective prevention.

• Probably, cardiotoxicity is a unique and continuous phenomenon starting with myocardial cell injury, changes in myocardial strain, followed by progressive LVEF decline that, if disregarded and not treated, progressively leads to overt heart failure

• At present, we can identify cardiotoxicity at a preclinical phase, very long before heart failure symptoms onset, long before the evidence of LVEF drop.

• The most effective strategy to minimize cardiotoxicity is its early identification and the early commencement of a prophylactic treatment. The use of troponins to identify patients with subclinical cardiotoxicity combined with early treatment with ACE-inhibitors to prevent LVD and related cardiac events occurrence appears to be an effective method against this complication.

• However, the optimal approach to minimize the risk of cardiotoxicity, the best tool for its early detection, and the most effective medical treatment regimen to prevent it, is still a subject of debate.

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Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties

Reviewer disclosures

A peer reviewer of this manuscript declares receiving honoraria for lectures and advisory boards for the following companies: Amgen, Astra-Zeneca, Celgene, Daiichi Sankyo, Eisai, Lilly, MSD, Nanostring, Novartis, Pfizer, Puma, Roche. The other peer reviewers on this manuscript have no relevant financial or other relationships to disclose

Additional information

Funding

This paper was not funded.