Prolongation of The Activation Time in Ischemic Myocardium is Associated with J-wave Generation in ECG and Ventricular Fibrillation

Figures

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  Figure 1. Positioning of intramural leads in the ventricles. (A) A schematic presentation of a typical location of the electrodes in relation to ventricular walls, cavities and ischemic regions on a cross-section. (B) A photograph of outside appearance of the explanted heart with electrodes in place after Evans blue infusion. See input (on the LV) and output (on the RV) points of three electrode-bearing threads. (C) A photograph of the ventricular cross-section with electrode-bearing thread (white arrows) in place coming through the LV and RV cavities and free walls. Dye-impregnated areas identify for the perfused (nonischemic) regions and a dye-free septum and adjacent free walls show the ischemic regions (black arrows). LV, left ventricle; RV, right ventricle.

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  Figure 2. Regional differences in LAT prolongation at 5 min of LAD occlusion. (A) Representative unipolar electrograms recorded in the same animal demonstrating different behavior during coronary occlusion. IVS base demonstrates ischemic changes with activation delay. See dramatic R-wave prolongation and loss of q-wave at 5-min point. Middle part of IVS demonstrates ST-segment elevation without significant activation delay, whereas nonischemic LV apex shows no changes. (B) LAT medians (lines), interquartile range (boxes), mean (crosses) and limits (error bars) in different myocardial regions at baseline and 5 min after LAD occlusion. (C) Maximal observed LATs irrespective of lead localization at baseline and 5 min after LAD occlusion.

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  Figure 3. Dynamics of local activation times (LATs) during coronary occlusion in different parts of LV (panel A), IVS (panel B), RV (panel C) and maximal LAT throughout all intramyocardial leads (panel D). Apex, Middle and Base designate different portions of the corresponding chamber walls on an apicobasal axis. *p < 0,05 vs baseline; #p < 0,05 vs 5 min time-point. LV, left ventricular; RV, right ventricular; IVS, interventricular septum; Max LAT, maximal local activation time, n = 14.

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  Figure 4. Time evolution of local activation times (blue markers, panel A) determined in the left ventricular subendocardium and left precordial ECG (“V5”, panel B). See the association between the activation delay and J-wave development (arrows).

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  Figure 5. ROC curve analysis of association between maximal local activation times and J-wave development (A), or VF episode (B).

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  Figure 6. Schematic relationship between the range of maximal LAT and ECG morphology according to the statistical analysis of J-wave and VF associations with LAT. Representative ECGs (limb lead III) in the right column were recorded in the same animal at baseline and at 20th and 40th minutes of occlusion. Sp – specificity.