Electrophysiological and anatomical factors determine arrhythmic risk in acute myocardial ischaemia and its modulation by sodium current availability

Figures

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  Figure 1.. Vulnerability windows for reentry (grey boxes) for different locations of ectopic stimuli (red) in acute regional transmural ischaemia (orange) caused by LAD occlusion. Ectopic stimulation applied at CI = 230–300 ms at varying locations in the ischaemic border zone (cases A–F). Reentrant mechanisms observed in the vulnerability windows are annotated below. The reentry location (italic font) refers to the pathway for retrograde propagation. F8, figure-of-eight reentry; TmR, transmural micro-reentry; MR, macro-reentry; LV, left ventricle; SEP, septum; RV, right ventricle; IZ, ischaemic zone.

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  Figure 2.. Main reentrant mechanisms observed in the ischaemia-induced reentry simulations. (a) Figure-of-eight macro-reentry, baseline ionic conditions, S2 triggered in the mid-RV at CI = 270 ms. (b) Transmural micro-reentry, baseline ionic conditions, S2 triggered in the LV/apex at CI = 250 ms. Epicardial (i) and septal view (ii). (c) Simple macro-reentry, baseline ionic conditions, S2 triggered in the septum/base at CI = 280 ms.

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  Figure 3.. Vulnerability windows for reentry (grey boxes) for different locations of ectopic stimuli (red) in acute regional transmural ischaemia (orange) caused by LAD occlusion under 50% INa block. Ectopic stimulation applied at CI = 240–355 ms at varying locations in the ischaemic BZ (cases A–F). Reentrant mechanisms observed in the vulnerability windows are annotated below. The reentry location (italic font) refers to the pathway for retrograde propagation. F8, figure-of-eight reentry; TmR, transmural micro-reentry; MR, macro-reentry; LV, left ventricle; SEP, septum; RV, right ventricle; IZ, ischaemic zone.

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  Figure 4.. Comparison of activation sequences produced by ectopics set in LV and RV under 50% INa block. (a) Activation sequence triggered by an ectopic stimulus in the LV in simulated acute myocardial ischaemia caused by LAD occlusion with 50% INa block. (a.1) Epicardial view. (a.2) Slice visualization. No reentry was produced due to bidirectional conduction block in the anterior wall (represented by a red cross). (b) Activation sequence triggered by an ectopic stimulus in the RV in simulated acute myocardial ischaemia caused by LAD occlusion with 50% INa block. (b.1) Epicardial view. (b.2) Slice visualization. Unlike the stimulus originated in LV, the ectopic stimulus in the RV caused reentry based on unidirectional conduction block (400–500 ms, red cross), and posterior reentry to the RV (570–740 ms) leading to propagation towards septum and LV (860 ms).

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  Figure 5.. Quantification of myocardial wall width annotated over the activation maps at timestamp 570 ms from figure 4b (S2 in the RV). Note that the thick-to-thin transition promotes retrograde propagation towards the RV leading to the completion of the reentry (figure 4b, 860 ms).

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  Figure 6.. Vulnerability windows for reentry (grey boxes) for different locations of ectopic stimulus in acute regional transmural ischaemia caused by LAD occlusion with diverse INa availability. Ectopic stimulus applied at CI = 240–355 ms at three S2 locations: LV free wall (a), RV base (b) and septo-basal region (c). Reentrant mechanisms observed in the vulnerability windows are annotated (bottom). The reentry location (italic font) refers to the pathway for retrograde propagation. Each S2 location triggered certain types of reentry and varying INa availability affected the occurrence of these reentrant pathways. F8, figure-of-eight reentry; TmR, transmural micro-reentry; MR, macro-reentry; LV, left ventricle; SEP, septum; RV, right ventricle; IZ, ischaemic zone.

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  Figure 7.. Simulated 12-lead ECG signal under control conditions (black dashed line), in ischaemia (light blue solid line) and ischaemia plus 50% INa block (dark blue solid line). Ischaemia leads to severe ECG changes, such as T-wave inversion in various leads (III, aVF and V1) and severe ST elevation in leads (V2–V4) in agreement with clinical data, as shown in [12]. ECG changes induced by additional 50% INa block in acute ischaemia are minor.