Figure 1.
Electrophysiologic toxicities of cancer treatments.
Table 1.
| DRUG CLASS | EXAMPLE | ASSOCIATED ARRHYTHMIAS | POTENTIAL MECHANISM |
|---|---|---|---|
| Alkylating agents6 | Melphalan | Atrial arrhythmias | Unknown |
| Anthracyclines7–9 | Doxorubicin | Atrial arrhythmias | Free radical/toxin accumulation, myocardial damage/cardiomyopathy |
| Epirubicin | Ventricular arrhythmia | Myocardial damage/cardiomyopathy, increased ventricular repolarization indices | |
| Arsenic32,33 | QT prolongation | Potassium channel inhibition | |
| Cyclin-dependent kinase 4/6 inhibitors35 | Ribociclib | QT prolongation | Unknown |
| Fluoropyrimidines36,37 | 5-fluorouracil | Ventricular arrhythmias | Secondary to coronary vasospasm/myocardial ischemia |
| Capecitabine | |||
| Immunotherapies19,20 | CAR-T therapy | Atrial arrhythmias | Inflammatory like from CRS |
| Checkpoint inhibitors (pembrolizumab) | Atrial/ventricular arrhythmias, bradyarrhythmias | Myocarditis/inflammatory | |
| Immunomodulatory agents (lenalidomide) | Atrial arrhythmias | Unknown | |
| Platinum agents10 | Cisplatin | Atrial arrhythmias | Direct myocardial irritation |
| Taxanes46,47 | Paclitaxel | Bradyarrhythmias | Effects on histamine receptor |
| Tyrosine kinase inhibitors | Ibrutinib, sorafenib, sunitinib11–17 | Atrial arrhythmias | PI3K pathway inhibition |
| Nilotinib, sunitinib, vandetanib40–42 | QT prolongation | Impaired intracellular signaling leading to enhanced late sodium and decreased potassium currents | |
| Ibrutinib43 | Ventricular arrhythmias | Unknown | |
| ALK Inhibitors44,45 (crizotinib) | Bradyarrhythmias | Decrease If (funny channel) currents in sinoatrial nodal cells |