**3. Definition of CTRCD**

Myocardial dysfunction and heart failure are the most concerning cardiovascular complications of cancer therapies and cause an increase in morbidity and mortality. Different definitions of CTRCD have been used historically [5]. Guidelines from cardiac societies [4, 6] define cardiotoxicity when the left ventricular (LV) ejection fraction (EF) falls to a value below the lower limit of normal (e.g. 53% in American Society of Echocardiography [ASE] guidelines) with more than a 10-percentage point reduction. As per the ESMO guidelines, the cut-off is 50% [7], at which

**63**

*Cardio-Oncology: The Role of Echocardiography in Cancer Patients*

Clinical manifestation New onset of heart failure and LV

Effect of rechallenge High probability of recurrent

Clinical course May stabilise with heart failure therapy

systolic dysfunction

Dose effects Cumulative, dose dependent Not dose related

dysfunction that is progressive

*Abbreviation: ACE, angiotensin-converting enzyme; LV, left ventricle; EF, ejection fraction.*

*Characteristics of type I and II cancer therapeutics-related cardiac dysfunction.*

(ACE inhibitors and beta-blockers), but underlying myocyte destruction appears to be permanent and irreversible

point cardio-protection should be considered [8]. ASE/European Association of Cardiovascular Imaging (EACVI) further classifies CRTCD into either those associated with anthracyclines or trastuzumab use. Anthracycline-related CRTCD is cumulative, dose dependent and often progressive and irreversible at cell level. On the other hand, trastuzumab-related CRTCD is dose independent, does not lead to

**Type I Type II**

Doxorubicin Trastuzumab

Asymptomatic decrease in LVEF and less often clinical heart failure

Often reversible with treatment discontinuation (to or near baseline cardiac status in

Rechallenge is often tolerated after

2–4 months)

recovery

The need for a timely diagnosis of subclinical and clinical heart failure by using

Exposure to potentially cardiotoxic chemotherapeutic agents is a well-recognised indication for baseline and longitudinal evaluation of LV function [9, 10]. The most commonly used parameter for monitoring LV function with echocardiography is LVEF. Traditionally, an echo determination of LVEF is requested by the oncologists in all cancer patients at baseline and in any situation in which the suspicion of heart failure is plausible, during and after completion of the anti-cancer therapy. 2D-derived LVEF is also used to start cardio protection and to establish the interruption from anti-cancer therapies. The calculation of LVEF should be done with the best method available as per the skills and experience of the operators in a given echocardiography department. The same method needs to be maintained for surveillance during and after treatment. Importantly, the digital images obtained should be available for visually comparison with the previous studies and further discussion at multimodality echocardiographic and cardio-oncology team meetings. According to joint recommendations from the ASE/EACVI, the method of choice for LV volume quantification and LVEF calculation is the modified biplane

cardiac imaging has been addressed by the Expert Consensus of the ASE and EACVI [6] and more recently reinforced by the ESC Position Paper on cancer treatments and cardiovascular toxicity [4]. The quickest and most available imaging tool in detecting cancer therapy-related cardiac dysfunction (CTRCD) is transthoracic

**4. Cancer therapy-related cardiac dysfunction (CTRCD)** 

*DOI: http://dx.doi.org/10.5772/intechopen.93085*

Anti-cancer characteristic chemotherapy agents

**Table 2.**

cell death and is often reversible (**Table 2**).

**and echocardiography**

**4.1 LV systolic function**

echocardiography.

*Cardio-Oncology: The Role of Echocardiography in Cancer Patients DOI: http://dx.doi.org/10.5772/intechopen.93085*


#### **Table 2.**

*Advanced Concepts in Endocarditis - 2021*

ics before changes in LVEF occur.

**2. Cardiovascular complications of cancer therapy**

vascular disease, stroke and pulmonary hypertension [4].

**Cardiovascular toxicity Anti-cancer therapy**

Valvular disease Radiotherapy

Arterial hypertension VEGF inhibitors

*Cancer drug agents associated with cardiovascular toxicity.*

therapeutic regimen used (radiotherapy and/or chemotherapy).

(2D-STE) derived strain and strain rate can detect changes in myocardial mechan-

Cancer treatment can cause various types of cardiovascular (CV) complications. Different cancer therapies have different CV complications. Cancer therapy 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. **Table 1** summarises a variety of anti-cancer therapies and their associated complications, including myocardial dysfunction, heart failure, coronary artery disease, valvular heart disease, arrhythmias, hypertension, peripheral

Echocardiography is a non-invasive method that can perform a comprehensive evaluation in all stages of cancer treatment and detect myocardial, coronary, valve, pulmonary hypertension and pericardial disease complications secondary to the

sunitinib) and radiotherapy

Arrhythmias Anthracyclines, histone deacetylase inhibitors, tyrosine kinase

Pulmonary hypertension TKI (dasatinib), the TKI imatinib improved haemodynamics in

*Abbreviations: HER2, human epidermal growth factor receptor 2; VEGF, vascular endothelial growth factor.*

prolongation)

Anthracyclines (doxorubicin, idarubicin and epirubicin), anti-HER2 (trastuzumab), VEGF inhibitors, cyclophosphamide, cisplatin,

Fluoropyrimidines (5-FU, capecitabine and gemcitabine), platinum compounds (cisplatin), VEGF inhibitors (bevacizumab, sorafenib and

inhibitors (TKIs) (especially vandetanib high incidence of QT

Nilotinib, ponatinib or BCR-ABL tyrosine kinase inhibitors, radiotherapy. L-asparaginase, cisplatin, methotrexate, 5-FU and

patients with advanced pulmonary arterial hypertension

paclitaxel can cause Raynaud's phenomenon

ifosfamide and taxanes (paclitaxel and docetaxel)

Myocardial dysfunction and heart failure are the most concerning cardiovascular complications of cancer therapies and cause an increase in morbidity and mortality. Different definitions of CTRCD have been used historically [5]. Guidelines from cardiac societies [4, 6] define cardiotoxicity when the left ventricular (LV) ejection fraction (EF) falls to a value below the lower limit of normal (e.g. 53% in American Society of Echocardiography [ASE] guidelines) with more than a 10-percentage point reduction. As per the ESMO guidelines, the cut-off is 50% [7], at which

**62**

**3. Definition of CTRCD**

Myocardial dysfunction and

Vasospasm or vasoocclusion resulting in angina or myocardial

Peripheral vascular disease and

heart failure

infarction

stroke

**Table 1.**

*Characteristics of type I and II cancer therapeutics-related cardiac dysfunction.*

point cardio-protection should be considered [8]. ASE/European Association of Cardiovascular Imaging (EACVI) further classifies CRTCD into either those associated with anthracyclines or trastuzumab use. Anthracycline-related CRTCD is cumulative, dose dependent and often progressive and irreversible at cell level. On the other hand, trastuzumab-related CRTCD is dose independent, does not lead to cell death and is often reversible (**Table 2**).
