Blood potassium concentration ([K+]) influences the electrocardiogram (ECG), particularly T-wave morphology. We developed a new method to quantify [K+] from T-wave analysis and tested its clinical applicability on data from dialysis patients, in whom [K+] varies significantly during the therapy. To elucidate the mechanism linking [K+] and T-wave, we also analysed data from long QT syndrome type 2 (LQT2) patients, testing the hypothesis that our method would have underestimated [K+] in these patients. Moreover, a computational model was used to explore the physiological processes underlying our estimator at the cellular level. We analysed 12-lead ECGs from 45 haemodialysis and 12 LQT2 patients. T-wave amplitude and downslope were calculated from the first two eigenleads. The T-wave slope-to-amplitude ratio (TS/A) was used as starting point for an ECG-based [K+] estimate (KECG). Leave-one-out cross-validation was performed. Agreement between KECG and reference [K+] from blood samples was promising (error: −0.09 ± 0.59 mM, absolute error: 0.46 ± 0.39 mM). The analysis on LQT2 patients, also supported by the outcome of computational analysis, reinforces our interpretation that, at the cellular level, delayed-rectifier potassium current is a main contributor of KECG correlation to blood [K+]. Following a comprehensive validation, this method could be effectively applied to monitor patients at risk for hyper/hypokalemia.
Patients suffering from renal failure often develop cardiac disturbances. In order to give a mathematical description of the effects of uremia on cardiac cellular excitability, the Ten Tusscher's model (2006) of human ventricular myocyte has been modified to incorporate the known effects of uremia on several ionic currents. The model was applied to study the effects of uremia and of the dialysis therapy on action potential duration (APD) and its restitution in response to the S1-S2 protocol. An altered transient repolarization and a shorter APD were found in the uremic myocyte. The APD restitution was also affected by uremia. At the end of dialysis, action potentials obtained after short diastolic intervals were characterized by the absence of the plateau phase. This could contribute to electrical inhomogeneity and explain the increase of arrhythmia occurrence often clinically observed in the last stage of the dialysis session.
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