Chemotherapeutic classes and associations with short-term and long-term cardiotoxicities, diagnostic modalities and management/prevention
Chemotherapy cardiotoxicity | Major culprit chemotherapeutic classes (incidence) | Diagnostic methodologies | Management/prevention |
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Cardiomyopathy (with systolic and/or diastolic dysfunction) |
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Ischaemia |
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Thrombosis |
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Hypertension |
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Hypotension |
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Dysrhythmias |
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QTc prolongation |
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Pericardial disease |
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*Associated with long-term cardiotoxicity; does not necessarily apply to all agents within each mentioned drug class.
†Long-term toxicity as a function of protracted use.
‡Newer biomarkers with possible future promise include: serum galectin-3, ST-2, glycogen phosphorylase BB (GPBB), heart-type fatty acid-binding protein (H-FABP) and high-sensitivity C reactive protein (hs-CRP).81–84
§Stress test by Single-photon emission computed tomography (SPECT)-myocardial perfusion imaging, Fludeoxyglucose- (FDG)-Positron Emission Tomography (PET) scan and stress echocardiography. Of questionable utility, particularly if ischaemia is related to coronary vasospasm.
¶Deferoxamine particularly cardioprotective against anthracyclines.
Concern for chemotherapy–drug interactions with drugs that affect the cytochrome P-450 system (diltiazem, digoxin, amiodarone), as well as other QTc prolonging antiarrhythmics (flecainide, ibutilide, dofetilide, sotalol).85
Amlodipine is a very effective first-line agent for TKI-induced hypertension and proteinuria; ACE-I/ARBs are also useful (in addition to amlodipine) for proteinuria associated with these agents.
sARB, angiotensin receptor blocker; BNP, brain natriuretic peptide; ICD, implantable cardioverter defibrillator; LVEF, left ventricular ejection fraction; MUGA, multigated acquisition scan; NSAIDs, non-steroidal anti-inflammatory drugs, RNA, radionuclide angiography, TKI, tyrosine kinase inhibitor; VSP, vascular endothelial growth factor (VEGF) signalling pathway.