Role of Scar and Border Zone Geometry on the Genesis and Maintenance of Re-Entrant Ventricular Tachycardia in Patients With Previous Myocardial Infarction

Abstract

In patients with healed myocardial infarction, the left ventricular ejection fraction is characterized by low sensitivity and specificity in the prediction of future malignant arrhythmias. Thus, there is the need for new parameters in daily practice to perform arrhythmic risk stratification. The aim of this study is to identify some features of proarrhythmic geometric configurations of scars and border zones (BZ), by means of numerical simulations based on left ventricular models derived from post myocardial infarction patients. Two patients with similar clinical characteristics were included in this study. Both patients exhibited left ventricular scars characterized by subendo- and subepicardial BZ and a transmural BZ isthmus. The scar of patient #1 was significantly larger than that of patient #2, whereas the transmural BZ isthmus and the subdendo- and subepicardial BZs of patient #2 were thicker than those of patient #1. Patient #1 was positive at electrophysiologic testing, whereas patient #2 was negative. Based on the cardiac magnetic resonance (CMR) data, we developed a geometric model of the left ventricles of the two patients, taking into account the position, extent, and topological features of scars and BZ. The numerical simulations were based on the anisotropic monodomain model of electrocardiology. In the model of patient #1, sustained ventricular tachycardia (VT) was inducible by an S2 stimulus delivered at any of the six stimulation sites considered, while in the model of patient #2 we were not able to induce sustained VT. In the model of patient #1, making the subendo- and subepicardial BZs as thick as those of patient #2 did not affect the inducibility and maintenance of VT. On the other hand, in the model of patient #2, making the subendo- and subepicardial BZs as thin as those of patient #1 yielded sustained VT. In conclusion, the results show that the numerical simulations have an effective predictive capability in discriminating patients at high arrhythmic risk. The extent of the infarct scar and the presence of transmural BZ isthmuses and thin subendo- and subepicardial BZs promote sustained VT.

Keywords: cardiac re-entry; infarct border zone; monodomain model; monomorphic ventricular tachycardia; myocardial infarction.

Figure 1

Cardiovascular magnetic resonance (CMR) short-axis slices of the basal, mid, and apical segment of patients #1 and #2.

Figure 2

CMR short-axis slices (left) of interest of patients #1 and #2 and the resulting ventricular segmentation (right) into non-infarcted myocardium (blue), border zone (gray), and scar (white).

Figure 3

Geometric models of the left ventricles of the two patients: healthy tissue (blue), border zone (BZ) tissue (yellow), scar tissue (red). From the transmural view, one can appreciate the transmural BZ isthmuses of the two patients.

Figure 4

Schematic representation of stimulation sites.

Figure 5

Patient #1. M1 stimulation. (A–P) Transmembrane potential snapshots (t = 395–975 ms) on the epicardial surface and on a transmural section. t = 0 corresponds to the S1 stimulus. The S2 stimulus is applied at t = 350 ms.

Figure 6

Patient #1. M1 stimulation. (A–P) Transmembrane potential snapshots (t = 1,000–1,575 ms) on the epicardial surface and on a transmural section. t = 0 corresponds to the S1 stimulus. The S2 stimulus is applied at t = 350 ms. The colorbar is the same as in Figure 5.

Figure 7

Patient #1. A2 stimulation. (A–P) Transmembrane potential snapshots (t = 450–900 ms) on the epicardial surface and on a transmural section. t = 0 corresponds to the S1 stimulus. The S2 stimulus is applied at t = 350 ms. The colorbar is the same as in Figure 5.

Figure 8

Patient #1. A2 stimulation. (A–P) Transmembrane potential snapshots (t = 925–1550 ms) on the epicardial surface and on a transmural section. t = 0 corresponds to the S1 stimulus. The S2 stimulus is applied at t = 350 ms. The colorbar is the same as in Figure 5.

Figure 9

Patient #1. Epicardial activation time distributions of S2 and first reentrant excitation sequences for M1 (A) and A2 (B) stimulations. Below each panel is reported the minimum, maximum, and isochrones step in ms of the displayed map.

Figure 10

Patient #1. (A–F) Transmembrane potential waveforms in the six stimulation cases, computed from an epicardial size located in the BZ, at the exit of the transmural isthmus.

Figure 11

Patient #2. M2 stimulation. (A–P) Transmembrane potential snapshots (t = 350–1,150 ms) on the epicardial surface. t = 0 corresponds to the S3 stimulus. The S4 stimulus is applied at t = 300 ms. The colorbar is the same as in Figure 5.

Figure 12

Patient #2. M2 stimulation. (A–P) Transmembrane potential snapshots (t = 350–1,100 ms) on a transmural section. t = 0 corresponds to the S3 stimulus. The S4 stimulus is applied at t = 300 ms. The colorbar is the same as in Figure 5.

Figure 13

Modifications of patient #2. (A–C) Transmembrane potential waveforms in the three modified configurations, computed from an epicardial size located in the BZ, at the exit of the transmural isthmus. M1 stimulation.

Figure 14

Patient #1. Reentry of types A and B. (A–H) Transmembrane potential snapshots on transmural sections across the central isthmus (First row) and across the apical isthmus (Second row). t = 0 corresponds to the S1 stimulus. The S2 stimulus is applied at t = 350 ms. First row: Reentry of type A related to M1 stimulation. Second row: Reentry of type B related to M2 stimulation.