Table 1.
AF induced by anticancer therapy.
| Classification | Drug classified | Drug | Incidence of AF | Mechanisms and actions | References |
|---|---|---|---|---|---|
| Anticancer drugs | Targeted therapies | Ibrutinib, 7-hydroxy-staurosporine, |
6.1% | PI3K–Akt pathway, the BTK and tec protein tyrosine kinase (TEC) | Honigberg et al., 2010; Herman et al., 2011; Burger et al., 2015; Byrd et al., 2015; Wang et al., 2015; Gertz, 2017; Shanafelt et al., 2017 |
| TKIs | Cetuximab, Crizotinib, Sunitinib, sorafenib |
3.3% | QT interval prolongation, decrease of nitric oxide signaling, increase of endothelin-1 production, inhibited AMPK and potassium channels, enhanced accumulation of lipid, ROS production, mitochondrial disorders, and apoptosis | Lara et al., 2005; Moslehi, 2016 | |
| Anthracycline agents | Aclacinomycin A, doxorubicin, adriamycin, 7-con-o-methylnogaril. |
6.6% | Cx43/Cx45 junction channels, CaMKII, Ca2+ ATPase, ST segment elevated, inverted T wave, long QT intervals, ROS, mitochondrial dysfunction, and apoptosis | Kluza et al., 2004; Chu et al., 2007; Lai et al., 2011; Lau et al., 2011; Xin et al., 2011; Zhang et al., 2011; Doherty et al., 2013; Kawabata et al., 2015; Varga et al., 2015 | |
| Alkylating agents | Cisplatin, Melphalan, CTX, 4-hydroperoxycyclophosphamide, cyclophosphamide, Ifosfamide. |
15.5% | cardiomyocyte contractions, mitochondrial abnormalities, ER stress and apoptosis, ROS, and inflammation, inducing cellular sodium, calcium, potassium, ATP content, the lysosome injury | Eskilsson et al., 1988; Petrella et al., 1989; Menard et al., 1991; Tomkowski et al., 2004; Pfister et al., 2006; Richards et al., 2006; Kilickap et al., 2007; Tilleman et al., 2009; Zellos et al., 2009; Liu et al., 2015 | |
| HER2/Neu receptor blockers | Etaracizumab, trastuzumab. | 19.9% | oxidative stress, apoptosis, ErbB2-ErbB4 signaling | Kupari et al., 1990; Quezado et al., 1993 | |
| Antimetabolites | 5-Fluorouracil, leucovorin. | 2.6% | the DNA synthesis, coronary spasm, myocardial ischaemia | de Forni et al., 1992; Perez-Verdia et al., 2005 | |
| Antimicrotubule agents | Paclitaxel, Docetaxel, Gemcitabine, gemcitabinevinorelbine |
9.4% | block cell division, coronary flow and left ventricular systolic pressure | Slamon et al., 1987; Keefe et al., 1993; Meydan et al., 2005 | |
| Histone deacetylase inhibitors | Depsipeptide, Belinostat. |
4.6% | No report | Bryan-Brown, 1932; Brouty-Boye et al., 1995; Alloatti et al., 1998 | |
| Antiestrogens | tamoxifen | No report | No report | Ueda et al., 1994b | |
| Proteosome inhibitors | Lenalidomide, lidomide, bortezomib. |
the cellular proliferation, apoptosis | Weber et al., 2003 | ||
| Immunotherapy | Interleukin-2, TNF-α, MIF, | 6.0% | proinflammatory cytokines, calcium homeostasis, inflammation, falling ICa, L amplitudes, and activating c-Src kinases | Thompson et al., 1994; White et al., 1994; Issac et al., 2007; Fildes et al., 2009; Rao et al., 2009; Pérez Persona et al., 2011; Guo et al., 2012a,b | |
| Radiotherapy | No report | myocardial fibrosis | Haudek et al., 2007; Lee et al., 2007 | ||
| Postoperation | 10%-20% | CRP and IL-6 increased, increased K+ outward current, and shortened action potentials | Chung et al., 2001; Craig et al., 2001; Aviles et al., 2003; Gaudino et al., 2003; Anselmi et al., 2009; Heerdt et al., 2012; Alifano et al., 2014 |
AF, atrial fibrillation; CTX, cyclophosphamide; TNF-α, tumor necrosis factor-α; ER stress, endoplasmic reticular stress; Cx43/45, connexin 43/45; BTK, bruton kinase; TEC, tec protein tyrosine kinase; HDAC, hydroxamic acid histone deacetylase; MIF, macrophage migration inhibitory factor.