Key result
Computational models link larger infarct scars with transmural isthmuses and thin border zones to sustained VT.
Why the study?
In patients with healed myocardial infarction, left ventricular ejection fraction has low sensitivity and specificity for predicting malignant arrhythmias, creating a need for new arrhythmic risk stratification parameters.
Do specific geometric configurations of scars and border zones (such as thin subendo- and subepicardial BZs) promote the genesis and maintenance of re-entrant ventricular tachycardia in post-myocardial infarction patients?
Do specific geometric configurations of scars and border zones (such as thin subendo- and subepicardial BZs) promote the genesis and maintenance of re-entrant ventricular tachycardia in post-myocardial infarction patients?
Numerical simulations based on CMR data suggest that the extent of infarct scar and the presence of transmural border zone isthmuses with thin subendo- and subepicardial border zones promote sustained ventricular tachycardia.
Answers are grounded in this paper and cite their sources.
Does not support geometry-guided VT risk stratification clinically; hypothesis-generating for scar features and requires prospective validation.
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.
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Gionti et al. (2022) studied Previous Myocardial Infarction (n=2). Patient-specific computational modeling of left ventricle was evaluated on Inducibility of sustained ventricular tachycardia. Patient-specific computational modeling demonstrated that larger infarct scars with transmural border zone isthmuses and thin subendo- and subepicardial border zones promote sustained VT.
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