Epicardial catheter ablation for ventricular tachycardia in heparinized patients.

AIMS: In patients undergoing epicardial catheter ablation of ventricular tachycardia (VT), current guidelines recommend obtaining pericardial access prior to heparinization to minimize bleeding complications. Consequently, access is obtained before endocardial mapping (leading to unnecessary punctures) or during an additional procedure. We present our experience of obtaining pericardial access during the index procedure in heparinized patients. METHODS AND RESULTS: Patients undergoing catheter ablation of VT in whom pericardial access was performed after heparinization were included. Clinical and procedural data and complications were recorded. Electrocardiograms (ECGs) were analysed for published criteria suggesting an epicardial ablation target and compared with patients (matched for substrate) undergoing successful endocardial ablation. Seventeen patients (13 males, age 58 ± 16 years, 8 (47%) ischaemic) were evaluated. Pericardial access was achieved in 16 (94%), including 2 patients with prior epicardial ablation. The mean activated clotting time was 273 ± 36 s. No bleeding complications occurred. In three patients, inadvertent puncture of the right ventricle caused no adverse consequences. An epicardial ablation target was found in nine of which three (33%) had ECG criteria, suggesting an epicardial circuit. In comparison 5 of 17 patients undergoing successful endocardial ablation had at least one ECG criterion suggesting an epicardial ablation target. CONCLUSION: Obtaining pericardial access for epicardial catheter ablation for VT appears to be safe in heparinized patients. Electrocardiogram criteria suggesting an epicardial ablation target lack the sensitivity and specificity accurately to predict which patients might need epicardial ablation. Performing pericardial access in heparinized patients therefore may reduce unnecessary punctures and reduce the number of additional procedures in some patients.

Analyses of the redistribution of work following cardiac resynchronisation therapy in a patient specific model.

Regulation of regional work is essential for efficient cardiac function. In patients with heart failure and electrical dysfunction such as left branch bundle block regional work is often depressed in the septum. Following cardiac resynchronisation therapy (CRT) this heterogeneous distribution of work can be rebalanced by altering the pattern of electrical activation. To investigate the changes in regional work in these patients and the mechanisms underpinning the improved function following CRT we have developed a personalised computational model. Simulations of electromechanical cardiac function in the model estimate the regional stress, strain and work pre- and post-CRT. These simulations predict that the increase in observed work performed by the septum following CRT is not due to an increase in the volume of myocardial tissue recruited during contraction but rather that the volume of recruited myocardium remains the same and the average peak work rate per unit volume increases. These increases in the peak average rate of work is is attributed to slower and more effective contraction in the septum, as opposed to a change in active tension. Model results predict that this improved septal work rate following CRT is a result of resistance to septal contraction provided by the LV free wall. This resistance results in septal shortening over a longer period which, in turn, allows the septum to contract while generating higher levels of active tension to produce a higher work rate.

Coupled personalization of cardiac electrophysiology models for prediction of ischaemic ventricular tachycardia.

In order to translate the important progress in cardiac electrophysiology modelling of the last decades into clinical applications, there is a requirement to make macroscopic models that can be used for the planning and performance of the clinical procedures. This requires model personalization, i.e. estimation of patient-specific model parameters and computations compatible with clinical constraints. Simplified macroscopic models can allow a rapid estimation of the tissue conductivity, but are often unreliable to predict arrhythmias. Conversely, complex biophysical models are more complete and have mechanisms of arrhythmogenesis and arrhythmia sustainibility, but are computationally expensive and their predictions at the organ scale still have to be validated. We present a coupled personalization framework that combines the power of the two kinds of models while keeping the computational complexity tractable. A simple eikonal model is used to estimate the conductivity parameters, which are then used to set the parameters of a biophysical model, the Mitchell-Schaeffer (MS) model. Additional parameters related to action potential duration restitution curves for the tissue are further estimated for the MS model. This framework is applied to a clinical dataset derived from a hybrid X-ray/magnetic resonance imaging and non-contact mapping procedure on a patient with heart failure. This personalized MS model is then used to perform an in silico simulation of a ventricular tachycardia (VT) stimulation protocol to predict the induction of VT. This proof of concept opens up possibilities of using VT induction modelling in order to both assess the risk of VT for a given patient and also to plan a potential subsequent radio-frequency ablation strategy to treat VT.