Key result
Exposure to p-Cresylsulfate prolonged the cardiomyocyte action potential duration and sped up the re-entrant wave in vitro and in computer simulations, suggesting a role in cardiac arrhythmias.
Why the study?
Does p-Cresylsulfate (PCS) alter electrophysiological properties such as action potential duration in cardiomyocytes?
Does p-Cresylsulfate (PCS) alter electrophysiological properties such as action potential duration in cardiomyocytes?
The protein-bound uremic toxin p-cresylsulfate prolongs cardiomyocyte action potential duration and speeds up re-entrant waves, suggesting a mechanism for ventricular arrhythmias in uremia.
PCS-induced APD prolongation may promote ventricular arrhythmias in CKD; in vitro data leave open its clinical relevance pending in vivo confirmation.
BACKGROUND: experiments and computer simulation. METHODS: with increasing concentrations of PCS. Electrophysiological studies and mathematical computer simulations were performed. RESULTS: induced by PCS prolonged the action potential duration (APD) and sped up the re-entrant wave, which is known to be a trigger mechanism for lethal ventricular arrhythmias. CONCLUSIONS: current activity, which increased the cardiomyocyte APD. This was observed both in vitro and in the computer O'Hara-Rudy dynamic human ventricular model. These findings suggest that PCS may play a key role in the development of cardiac arrhythmias.
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Tsai et al. (2019) studied Cardiac arrhythmias. p-Cresylsulfate (PCS) was evaluated on Action potential duration (APD) and re-entrant wave speed. Exposure to p-Cresylsulfate prolonged the cardiomyocyte action potential duration and sped up the re-entrant wave in vitro and in computer simulations, suggesting a role in cardiac arrhythmias.
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