Cardiac dysfunction | Agents | Risk | Mechanism |
---|---|---|---|
Heart failure | Anthracyclines | Cumulative, high | Myocyte death |
Cyclophosphamide | Low | Myocarditis | |
Cisplatin | Low | Unknown | |
Trastuzumab | Moderate-high | Contractile protein dysfunction | |
Lapatinib | Low | Â | |
Bevacizumab | Low | Hypertension? | |
Sunitinib | Low | Mitochondrial dysfunction | |
Sorafenib | Low | Â | |
Carfilzomib | Moderate | Â | |
Imatinib | Low | Mitochondrial dysfunction | |
Arterial hypertension | All angiogenesis inhibitors/anti-VEGF/TKIs | Moderate, dose-dependent | Endothelial dysfunction |
Myocardial ischemia | Pyrimidine analogues | Moderate | Direct vasospasm |
Coronary heart disease | BCR-ABL TKIs(esp. Nilotinib, Ponatinib) | Moderate | Endothelial damage |
Thromboembolism | Cisplatin, All angiogenesis inhibitors, anti-VEGFs, Bcr-ABL TKIs (Nolitinib, Ponatinib) | Moderate | Endothelial dysfunction |
Arrhythmia/QT prolongation | Arsenic trioxide, TKIs, Proteasome inhibitors | Moderate | HERG K + blockage |
Atrial Fibrillation | Ibrutinib (BTKi) | Moderate | PI3K-akt inhibition |
Pulmonary arterial hypertension | Dasatinib | Moderate | HERG K + blockage |
VT/VF/Complete HB Fulminant myocarditis | Immune checkpoint inhibitors | Rare with high mortality | Co-stimulatory pathway |
Vascular Toxicity | BCR-ABL TKIs | Moderate | Endothelial dysfunction |
Premature atherosclerosis | HSCT(Hematopoietic stem cell transplant) | Moderate | Endothelial damage and inflammatory response |