Emerging evidence for a mechanistic link between low-frequency oscillation of ventricular repolarization measured from the electrocardiogram T-wave vector and arrhythmia

Figures

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  Figure 1. Recording of ECG T-wave vector measures of ventricular repolarization (PRD). Upper panel: ECGs are recorded using the X, Y, Z configuration. (Middle) T waves are converted into polar vector angles. Two successive T-wave vectors are shown projected onto virtual spheres. The angle between successive vectors is taken as a measure of repolarization stability. Lower panel: Plot of vector angle over time showing pronounced regular peaks with a frequency of about 0.1 Hz, i.e. 1 per 10 s. From Rizas et al.2 with permission.

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  Figure 2. Low-frequency oscillations of the ECG T-wave vector and ventricular APD. Low-frequency ECG T-wave oscillations in a post-MI survivor (left) and a non-survivor (right) showing higher amplitude oscillations in the non-survivor. From Rizas et al.2 with permission.

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  Figure 3. Recording of activation-recovery intervals (APD). (A) Upper panel: Unipolar electrogram recorded from the LV lead of an ICD device in a patient. Dots represent dv/dt min of the QRS and dv/dt max of the T wave. The interval between them defines the ARI widely used as a surrogate for APD. Lower panel: Beat-by-beat plot of ARI showing oscillatory pattern at a frequency of about 15–20 s, 0.05 Hz within the LF range. (B) Activation recovery interval provides an established measure of APD.

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  Figure 4. Beat-to-beat plot of left ventricular ARIs as a surrogate for APD showing oscillations in the low-frequency range at ∼0.05 Hz (upper trace) and 0.1 Hz (lower trace). Corresponding power spectral densities (PSD) are shown to the right of each trace.

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  Figure 5. Left panel: Illustration of the timing of two currents thought to play a key role in generation oscillations of the ventricular action potential in humans. The inward L-type calcium current (ICaL) occurs early during phases 0, 1, and 2 and the outward potassium current (IKs) occurs later during phases 2 and 3. Right panel: The overall effect of ICaL is APD prolongation and the effect of IKs is APD shortening.

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  Figure 6. (A) Time course of normalized phosphorylation levels for the slow delayed rectifier potassium IKs current (fIKs, blue) and L-type ICaL current following constant beta-adrenergic stimulation. (B) Normalized peak current values for IKs,(blue) and ICaL current (red) following prolonged beta-adrenergic stimulation. (C) Systolic levels of free cytosolic calcium (Cai, blue) and calcium bound to troponin (Ca Trop, red) following prolonged phasic and mechanical stretch. (D) Current through all stretch-activated channels (ISAC, blue) and through K+-selective stretch-activated channels (ISACK, red) following prolonged mechanical stretch.

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  Figure 7. Simulated ventricular action potentials during beta-adrenergic stimulation (BAS). (A) Healthy myocardium during constant BAS, (B) Healthy myocardium during phasic BAS and stretch, (C) Myocardium with diseased conditions (simulated by addition of reduced repolarization reserve and calcium overload) during constant BAS, (D) Diseased conditions during phasic BAS and stretch. In C early afterdepolarizations are seen but no arrhythmia occurred. In D early afterdepolarizations and triggered activity are evident (see text).