The first example of cardiac cancer treatment toxicity was described in relation to anthracyclines more than fifty years ago. The concept that chemotherapy (CT) and radiotherapy (RT) may induce potentially deadly cardiovascular (CV) side effects developed progressively and cardiologists were charged with the management of patients with these complications. The complexity and the peculiarity of the CV toxicities of cancer therapy evolved quickly, requiring specific formation and skills: C-O was born. In a few short years, C-O has shown huge growth and development. The reasons are:

• The progressively ageing population with an increasing incidence of cancer patients and patients with CV diseases (CVD) and the consequent increase of the prevalence of patients suffering from both conditions.
• The increasing survival from cancer and CVD with an increase in the prevalence of these two conditions combined.
• Most survivors from cancer therapy develop or die from CVD, more than from cancer recurrence.
• Patients cured for cancer should not die of a CV complication.
• Patients suffering from cancer may have CVD risk factors and/or a pre-existing CVD, often concealed, enhancing the toxic effects of CT and RT. An adequate and aggressive risk factor control and CV diagnostic work-up strongly enhance survival.
• CT and RT toxicity may develop many years after treatment. Tight follow-up protocols to avoid long-term cardiac side effects are essential for adequate treatment.
• Cancer-cardiac patients may undergo different treatment if managed by a separate approach of care by oncologists or cardiologists, due to a more or less aggressive treatment of the two conditions separately. The best treatment may be achieved if cardiologists and oncologists are interacting properly, building a C-O expert team.

So, the probability of every physician facing cancer and CVD patients is high. Everyone should be aware of: 1) the toxicity of a CT agent or of RT, 2) the risk factors and pre-existing CVD predisposing to cardiotoxicity, and 3) the use of preventive and curative measures during possible cardiotoxic therapy.

Oncologist and cardiologists should undertake the therapeutic option for a cancer patient by:                  

• Planning the optimal treatment regimens to minimise cardiotoxicity without compromising anticancer efficacy.
• Detecting CV effects when potential cardiotoxic agents are used, with particular attention to subclinical signs and symptoms.
• Preventing CV side effects with a careful CV work-up before using therapies with significant cardiotoxicity, paying attention to the patient’s comorbidities that should be controlled.

CT toxicity is related to the mechanism of action of the drugs, the doses, the manner of administration, and the underlying predisposing factors such as cardiac conditions, genetic pattern and age, and it can manifest itself immediately or many years after the treatment.

Concomitant CT and RT treatments may interfere in toxicity, with mutual potentiation.

Irreversible cytotoxicity or interaction with functional aspects of the function of cardiac cells not primarily cytotoxic may lead to ventricular dysfunction. Furthermore, different mechanisms may lead to arterial hypertension, venous and arterial thromboembolism, myocardial ischaemia and infarction and arrhythmias with several CT agents.

Acute toxicity may appear very rarely or quite frequently with different drugs.

Also, the incidence of chronic toxicity is variable and may develop over a long period of time.

Clinical signs and symptoms, electrocardiographic modifications, cardiac imaging tools (mainly left ventricular ejection fraction [LVEF] and strain assessment), troponin and natriuretic peptide elevation may identify early CT toxicity.

Several strategies are available for the prevention and treatment of toxicity of the different CT drugs, based on accurate patient selection, short- and long-term monitoring, and on therapies which may prevent and delay cardiac dysfunction in this setting.

Possible CV complications of CT and/or RT are [1]:

• Myocardial dysfunction and heart failure (HF)
• Coronary artery disease (CAD)
• Valvular heart disease (VHD)
• Arrhythmias – acquired LQT syndrome, atrial fibrillation and atrioventricular (AV) blocks
• Arterial hypertension
• Thromboembolic disease
• Peripheral vascular disease and stroke
• Pulmonary hypertension
• Pericarditis

CONCLUSION

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ALPINE
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Journal of Molecular Oncology Research
Email: oncology@openaccessjournal.org