Propofol abolishes torsade de pointes in different models of acquired long QT syndrome

Figures

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  Figure 1. Determination of effective refractory periods (MAP = monophasic action potential).

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  Figure 2. (a) Cycle-length dependent APD90 under baseline conditions (filled rhombus) and after treatment with 50 µM (filled square), 75 µM (filled traingle) or 100 µM (filled circle) propofol. (b) Impact of propofol on effective refractory periods (ERP). (c) Concentration-dependent effect of propofol on post-repolarization refractoriness (#p < 0.05 compared to baseline conditions). (d) Box plots of the ratio of action potential duration at 90% of repolarization (APD90) and action potential duration at 50% of repolarization (APD50). A decrease in APD90/APD50 represents a rectangulation of action potential. (e) Influence of propofol treatment on repolarization heterogeneity as indicated by spatial dispersion of repolarization (#p < 0.05 compared to baseline conditions). (f) Occurrence of ventricular fibrillation (VF) tachycardia (VT) induced by programmed ventricular fibrillation.

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  Figure 3. (a,b) Cycle-length dependent APD90 and QT interval under baseline conditions (filled rhombus), after treatment with 300 µM erythromycin (filled square) and after additional infusion of 75 µM propofol (filled triangle). (c) Box plots of the ratio of APD90 to APD50. (d) Impact of erythromycin and propofol on spatial dispersion of repolarization (#p < 0.05 compared to baseline conditions; *p < 0.05 compared to sole erythromycin infusion). (e) Occurrence of torsade de pointes under baseline conditions, with erythromycin and with the combination of erythromycin and propofol (#p < 0.05 compared to baseline conditions; *p < 0.05 compared to sole erythromycin treatment).

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  Figure 4. (a,b) Cycle-length dependent APD90 and QT interval under baseline conditions (filled rhombus), after treatment with 5 µM ondansetron (filled square) and after additional infusion of 75 µM propofol (filled triangle). (c) Box plots of the ratio of APD90 to APD50 (#p < 0.05 compared to baseline conditions) (d) Influence of ondansetron and propofol on spatial dispersion of repolarization (#p < 0.05 compared to baseline conditions; *p < 0.05 compared to sole ondansetron administration). (e) Occurrence of torsade de pointes under baseline conditions, with ondansetron and with the combination of ondansetron and propofol (#p < 0.05 compared to baseline conditions; *p < 0.05 compared to sole ondansetron treatment).

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  Figure 5. (a) Representative example of early afterdepolarizations induced by erythromycin (MAP = monophasic action potential). (b) Spontaneously occurring polymorphic ventricular tachycardia resembling torsade de pointes after ondansetron treatment.

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  Figure 6. Illustrative example of action potential and ECG tracings under baseline conditions (a) and after administration of erythromycin (b) in spontaneously beating bradycardic hearts under hypokalemic conditions. With erythromycin, action potentials are substantially prolonged and triangulated. Of note, spatial dispersion of repolarization (as determined by the duration differences between MAP 5 and MAP 3 in (b)) is amplified. (MAP = monophasic action potential).