Key points
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Baseline ECG in any cardiac or extracardiac tumors is mandatory since therapeutic side effects of chemotherapy on heart are proven.
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Comprehensive understanding of the cardiac effect of anticancer agents is mandatory to predict side effects and prevent irreversible damage.
Introduction
While life expectancy and quality of life have improved dramatically in this era of new oncology treatments, longer lifespan comes with its own set of issues and complications associated with new chemotherapy agents.
Although there are several techniques and modalities for detecting cardiac damage, such as echocardiography, nuclear medicine, and also measuring various biomarkers, the ECG is a simple, inexpensive, and rapid tool that can be used to diagnose clinical or subclinical cardiac damage prior to the progression of advanced cardiovascular disease. The electrocardiogram (ECG) can provide valuable information regarding the heart chambers, ischemia, and arrhythmia, among many other aspects. These alterations can be noticed prior to the onset of serious side effects from advanced treatment. For instance, anomalies in the left atrium caused by increased left ventricular end diastolic pressure (LVEDP) can be a prelude to atrial fibrillation ( Fig. 4.1 ), while a prolonged QT interval can signal Torsade de points and other dangerous cardiac arrhythmias .
Atrial fibrillation after developing multiepisodes of frequent PACs and atrial tachycardia in a patient who receives anthracycline.
There are many clues to modify chemotherapy according to ECG. These ECG changes such as frequent premature atrial contraction (PAC) or premature ventricular contraction (PVC) may be signals of further atrial fibrillation or malignant ventricular arrhythmia, respectively, which will be relieved by reducing chemotherapy drug doses. Also agents such as 5 fluorouracil and interleukin can make coronary spasm with its own changes on ECG ( Fig. 4.2 ).
Baseline and follow-up ECG
I strongly advise taking an ECG prior to initiating any form of chemotherapy so that we can compare its alterations following treatment by an oncologist fellow. Many oncologists do not trust in ECGs, yet the processes underlying chemotherapy-induced arrhythmia have become obvious in recent years. Several of the most significant and well-known mechanisms include direct cardiac injury caused by chemotherapeutic agents, biomarker release as a result of the cancer process or treatment techniques, induced dilated cardiomyopathy, and elevated LVEDP. Additionally, other factors such as myocardial ischemia and spasm can result in a variety of arrhythmogenic mechanisms such as reentry induction or aberrant depolarization with late potentials ( Fig. 4.3 ).
Effects on heart conduction system or ion channels effect with subsequent QT interval prolongation and all forms of bundle branch blocks, AV nodal or SA nodal disease are among well-known effects of chemotherapy agents. One of the common forms of these arrhythmias is sinus bradycardia which is known effect of taxanes plus its effects on other conduction system including right or left bundle branch and Purkinje system ( Fig. 4.4 ).
Although conduction delay can progress after a few hours after initiation of some anticancer drugs, it can reverse within 48 h and both oncologist and cardiologist must be aware of this kind of complication for preventing further unnecessary action.
Alkylating agents
By inducing ischemia as a result of coronary spasm, alkylating drugs such as cyclophosphamide or cisplatin might cause further cardiomyocyte damage. It is critical to assess individuals with atherosclerotic risk factors or a history of coronary artery disease for additional preventative measures against myocardial ischemia or infarction, which can further damage the heart muscle and reduce ejection fraction. Additionally, they can expand the size of the heart chambers, elevate LVEDP, and cause left atrial abnormalities with subsequent ventricular or atrial arrhythmia. Oncologists, cardiologists, and oncocardiologists must tread cautiously when treating patients who have heart failure or a lower ejection fraction ( Table 4.5 ).
| 1. Risk assessment | Tests: TTE with strain ECG, cTn |
|---|---|
| Medication-related risk | Patient-related risk factors |
| High (risk score 4): Anthracyclines, cyclophosphamide, ifosfamide, clofarabine, herceptin Intermediate (risk score 2): Docetaxel, pertuzumab, sunitinib, sorafenib Low (risk score 1): Bevacizumab, dasatinib, imatinib, lapatinib Rare (risk score 0): For example, etoposide, rituximab, thalidomide |
|
| Overall risk by cardiotoxicity risk score (CRS) | |
| (risk categories by drug-related risk score plus number of patient-related risk factors: CRS > 6 : very high, 5–6: high, 3–4 : intermediate, 1–2 : low, 0: very low) | |
| 2. Monitoring recommendations | |
| Very high cardiotoxicity risk: TTE with strain before every (other) cycle, end, 3–6 months, and 1 year; optional ECG, cTn with TTE during chemotherapy High cardiotoxicity risk: TTE with strain every 3 cycles, end, 3–6 months, and 1 year after chemotherapy; optional ECG, cTn with TTE during chemotherapy Intermediate cardiotoxicity risk: TTE with strain midterm, end, and 3–6 months after chemotherapy; optional ECG, cTn midterm of chemotherapy Low cardiotoxicity risk: Optional TTE with strain and/or ECG, cTn at the end of chemotherapy Very low cardiotoxicity risk: None | |
| 3. Management recommendations | |
| Very high cardiotoxicity risk: Initiate ACE-I/ARB, carvedilol, and statins, starting at lowest dose and start chemotherapy in 1 week from initiation to allow steady state, up-titrate as tolerated High cardiotoxicity risk: Initiate ACE-I/ARB, carvedilol, and/or statins Intermediate cardiotoxicity risk: Discuss risk and benefit of medications Low cardiotoxicity risk: None, monitoring only Very low cardiotoxicity risk: None, monitoring only | |
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