In the hyperadrenergic state of VT storm where shocks are psychologically and physiologically traumatizing, suppression of sympathetic outflow from the organ level of the heart up to higher braincenters plays a significant role in reducing the propensity for VT recurrence. The autonomic nervous system continuously receives input from the heart (afferent signaling), integrates them, and sends efferent signals to modify or maintain cardiac function and arrhythmogenesis. Spinal anesthesia with thoracic epidural infusion of bupivicaine and surgical removal of the sympathetic chain including the stellate ganglion has been shown to decrease recurrences of VT. Excess sympathetic outflow with catecholamine release can be modified with catheter-based renal denervation. The insights provided from animal experiments and in patients that are refractory to conventional therapy have significantly improved our working understanding of the heart as an end organ in the autonomic nervous system.

Epicardial mapping and ablation via a percutaneous subxiphoid technique has been instrumental in improving the working understanding of complex myocardial scars in various arrhythmogenic substrates. Endocardial ablation alone may not be sufficient in patients with ischemic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy, and Chagas disease to prevent recurrent ventricular tachycardia. Multiple observational studies have demonstrated greater freedom from recurrence with adjunctive epicardial ablation compared with endocardial ablation alone. While epicardial ablation is performed predominantly at tertiary referral centers, knowledge of the technical approach, clinical indications, and potential complications is imperative to maximizing clinical success and patient safety. In 1996, Sosa and colleagues modified the pericardiocentesis technique to enable percutaneous access to the pericardial space for mapping and catheter ablation of ventricular tachycardia.1 Originally developed for patients with epicardial scarring due to chagasic cardiomyopathy and patients with ischemic cardiomyopathy refractory to endocardial ablationm,2,3 this approach has since become an essential part of the armamentarium for the treatment of ventricular tachycardia. Myocardial scars are three-dimensionally complex with varying degrees of transmurality, and the ability to map and ablate the epicardial surface has contributed to a greater understanding of scar-related VT in postinfarction cardiomyopathy and nonischemic substrates including idiopathic dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy, and chagasic cardiomyopathy. In this review, we highlight the percutaneous approach and discuss clinical indications and potential complications.

Advances in the treatment of myocardial infarction (MI) have improved survival after ischemic cardiac injury. Post-infarct structural and functional remodeling results in electrophysiologic substrates at risk for monomorphic ventricular tachycardia (MMVT). Characterization of this substrate using a variety of clinical and investigative tools has improved our understanding of MMVT circuits, and has accelerated the development of device and catheter-based therapies aimed at identification and elimination of this arrhythmia. This review will discuss the central role of the ischemic heart disease substrate in the development MMVT. Electrophysiologic characterization of the post-infarct myocardium using bipolar electrogram amplitudes to delineate scar border zones will be reviewed. Functional electrogram determinants of reentrant circuits such as isolated late potentials will be discussed. Strategies for catheter ablation of reentrant ventricular tachycardia, including structural and functional targets will also be examined, as will the role of the epicardial mapping and ablation in the management of recurrent MMVT.

We describe a scar-related reentrant ventricular tachycardia circuit with a proximal segment in an endocardial basal septal scar and an exit in a region of slow conduction in a non-overlapping region of epicardial basal lateral scar. The 12-lead EKG demonstrates criteria for a basal lateral epicardial VT, however the same morphology could be produced with a longer stim-latency with pace mapping or VT induction from the endocardial septal region of scar. A significant segment of myocardium demonstrated no endocardial or epicardial scar on electroanatomic mapping, suggesting the presence of a mid-myocardial isthmus. Further evidence was provided by assessment of unipolar settings. The epicardial VT that initially appeared to originate from the basal lateral epicardial region, was successfully treated with radiofrequency ablation of the lateral aspect of the endocardial septal scar.

Ablation of cavotricuspid ishtmus flutter and atrial tachycardia in a complex substrate has never been reported using remote navigation via superior approach. Venous access was obtained via right internal jugular for ablation and left subclavian for duodecapolar catheter placement into the coronary sinus. In a posttransplant patient presenting with both regular and irregular tachycardia, both cavotricuspid isthmus flutter in the donor and atrial tachycardia in the recipient was mapped using a two catheter approach. Successful ablation of typical atrial flutter and anastomotic block was achieved. This is the first report of successful ablation of cavotricuspid isthmus flutter and posttransplant atrial tachycardia using magnetic navigation via superior approach. Using only two catheters, this approach is logical and feasible in complex substrates with interrupted inferior venous access.

We describe a scar-related reentrant ventricular tachycardia circuit with a proximal segment in an endocardial basal septal scar and an exit in a region of slow conduction in a non-overlapping region of epicardial basal lateral scar. The 12-lead EKG demonstrates criteria for a basal lateral epicardial VT, however the same morphology could be produced with a longer stim-latency with pace mapping or VT induction from the endocardial septal region of scar. A significant segment of myocardium demonstrated no endocardial or epicardial scar on electroanatomic mapping, suggesting the presence of a mid-myocardial isthmus. Further evidence was provided by assessment of unipolar settings. The epicardial VT that initially appeared to originate from the basal lateral epicardial region, was successfully treated with radiofrequency ablation of the lateral aspect of the endocardial septal scar.

Advances in the treatment of myocardial infarction (MI) have improved survival after ischemic cardiac injury. Post-infarct structural and functional remodeling results in electrophysiologic substrates at risk for monomorphic ventricular tachycardia (MMVT). Characterization of this substrate using a variety of clinical and investigative tools has improved our understanding of MMVT circuits, and has accelerated the development of device and catheter-based therapies aimed at identification and elimination of this arrhythmia. This review will discuss the central role of the ischemic heart disease substrate in the development MMVT. Electrophysiologic characterization of the post-infarct myocardium using bipolar electrogram amplitudes to delineate scar border zones will be reviewed. Functional electrogram determinants of reentrant circuits such as isolated late potentials will be discussed. Strategies for catheter ablation of reentrant ventricular tachycardia, including structural and functional targets will also be examined, as will the role of the epicardial mapping and ablation in the management of recurrent MMVT.

We review the pharmacologic, interventional and device programming treatment options for patients with implantable cardioverter-defibrillators who present with acute heart failure and implantable cardioverter-defibrillator shocks.

Background

The precise localization of the site of origin of a premature ventricular contractions (PVC) prior to ablation would facilitate the planning and execution of the electrophysiological procedure. Current electrocardiographic imaging (ECGI) techniques require body surface maps, a costly and complex procedure, that requires as many as 256 leads to localize the PVC origin. We developed and tested a novel myocardial activation based ECGI technique utilizing the readily available 12-lead ECG to localize the PVC origin.

Methods

The major components of the 12-lead ECGI method are: the source model, proximity effect and spatial orientation, volume conductor, and patient specific model of the heart, lungs, and thorax as derived from magnetic resonance imaging (MRI). For the PVC origin localization, the fastest route algorithm is used on patient specific models created by newly developed morphing software. PVC localization by the 12-lead ECGI was correlated to the site of successful ablation.

Results

Seven patients that underwent electrophysiological mapping and ablation of PVCs were studied. All patients (7/7) had accurate prediction of the PVC origin. However in two patients, no specific MRI was used for localization that resulted in an incorrect switch between the RV free wall and septum of the RVOT. With patient-specific models, these latter two cases would likely be localized correctly.

Conclusions

This feasibility study of a novel myocardial activation-based ECGI using only the standard 12-lead ECG shows promise to localize the origin of PVC. This ECGI method yields activation estimates of isochrones on both ventricles from which the PVC origin location is derived. This method has the capability to localize the PVC from any part of the ventricular endocardium, intra-myocardium or epicardium.