Key result
Cyclophosphamide exposure decreases maximum capture rate in stem cell-derived cardiomyocytes by ~25%.
Why the study?
The cellular-level mechanisms of cyclophosphamide side effects at low doses (< 100 mg/kg) remain unclear.
Effect estimate: 25% ± 7% decrease
Cyclophosphamide induces arrhythmogenic conduction changes in human iPSC-derived cardiomyocytes through alpha-actinin disruption rather than ion channel effects.
Hypothesis-generating for cyclophosphamide cardiotoxicity mechanisms; should not change clinical practice.
Cyclophosphamide (CP) is an anticancer drug, an alkylating agent. Cardiotoxicity of CP is associated with one of its metabolites, acrolein, and clinical cardiotoxicity manifestations are described for cases of taking CP in high doses. Nevertheless, modern arrhythmogenicity prediction assays in vitro include evaluation of beat rhythm and rate as well as suppression of cardiac late markers after acute exposure to CP, but not its metabolites. The mechanism of CP side effects when taken at low doses (i.e., < 100 mg/kg), especially at the cellular level, remains unclear. In this study conduction properties and cytoskeleton structure of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) obtained from a healthy donor under CP were evaluated. Arrhythmogenicity testing including characterization of 3 values: conduction velocity, maximum capture rate (MCR) measurements and number of occasions of re-entry on a standard linear obstacle was conducted and revealed MCR decrease of 25% ± 7% under CP. Also, conductivity area reduced by 34 ± 15%. No effect of CP on voltage-gated ion channels was found. Conduction changes (MCR and conductivity area decrease) are caused by exposure time-dependent alpha-actinin disruption detected both in hiPSC-CMs and neonatal ventricular cardiomyocytes in vitro. Deviation from the external stimulus frequency and appearance of non-conductive areas in cardiac tissue under CP is potentially arrhythmogenic and could develop arrhythmic effects in vivo.
No takes yet. Share an insight, caveat, or question.
Podgurskaya et al. (2021) studied Cardiotoxicity. Cyclophosphamide vs. Tyrode's solution (control) was evaluated on Maximum capture rate (MCR) (25% ± 7% decrease). Cyclophosphamide exposure decreased the maximum capture rate of human induced pluripotent stem cell-derived cardiomyocytes by 25% ± 7% and reduced the conductivity area by 34 ± 15%.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: