Assessment of Risk for Ventricular Tachycardia based on Extensive Electrophysiology Simulations.

Patients that have suffered a myocardial infarction are at high risk of developing ventricular tachycardia. Patient stratification is often determined by characterization of the underlying myocardial substrate by cardiac imaging methods. In this study, we show that computer modeling of cardiac electrophysiology based on personalized fast 3D simulations can help to assess patient risk to arrhythmia. We perform a large simulation study on 21 patient digital twins and reproduce successfully the clinical outcomes. In addition, we provide the sites which are prone to sustain ventricular tachycardias, i.e, onset sites around the scar region, and validate if they colocalize with exit sites from slow conduction channels.Clinical relevance- Fast electrophysiological simulations can provide advanced patient stratification indices and predict arrhythmic susceptibility to suffer from ventricular tachycardia in patients that have suffered a myocardial infarction.

Mechanisms, time course and predictability of premature ventricular contractions cardiomyopathy-an update on its development and resolution.

Frequent premature ventricular contractions (PVCs) associated left ventricular systolic dysfunction (LVSD) is a well-known clinical scenario and numerous predictors for cardiomyopathy (CMP) development have been already thoroughly described. It may present as a "pure" form of dissynchrony-induced cardiomyopathy or it may be an aggravating component of a multifactorial structural heart disease. However, the precise risk to develop PVC-induced CMP (which would allow for tailored-patient monitoring and/or early treatment) and the degree of CMP reversibility after PVC suppression/elimination (which may permit appropriate candidate selection for therapy) are unclear. Moreover, there is limited data regarding the time course of CMP development and resolution after arrhythmia suppression. Even less known are the other components of PVC-induced CMP, such as right ventricular (RV) and atrial myopathies. This review targets to synthetize the most recent information in this regard and bring a deeper understanding of this heart failure scenario. The mechanisms, time course (both in experimental models and clinical experiences) and predictors of reverse-remodelling after arrhythmia suppression are described. The novel experience hereby presented may aid everyday clinical practice, promoting a new paradigm involving more complex, multi-level and multi-modality evaluation and possible earlier intervention at least in some patient subsets.