Selective autonomic stimulation of the AV node fat pad to control rapid post-operative atrial arrhythmias.

Junctional ectopic tachycardia (JET) and atrial fibrillation (AF) occur in patients recovering from open-heart surgery (OHS). Pharmacologic treatment is used for the control of post-operative atrial arrhythmias (POAA), but is associated with side effects. There is a need for a reversible, modulated solution to rate control. We propose a non-pharmacologic technique that can modulate AV nodal conduction in a selective fashion. Ten mongrel dogs underwent OHS. Stimulation of the anterior right (AR) and inferior right (IR) fat pad (FP) was done using a 7-pole electrode. The IR was more effective in slowing the ventricular rate (VR) to AF (52 +/- 20 vs. 15 +/- 10%, p = 0.003) and JET (12 +/- 7 vs. 0 +/- 0%, p = 0.02). Selective site stimulation within a FP region could augment the effect of stimulation during AF (57 +/- 20% (maximum effect) vs. 0 +/- 0% (minimum effect), p<0.001). FP stimulation at increasing stimulation voltage (SV) demonstrated a voltage-dependent effect (8 +/- 14% (low V) vs. 63 +/- 17 (high V) %, p<0.001). In summary, AV node fat pad stimulation had a selective effect on the AV node by decreasing AV nodal conduction, with little effect on atrial activity.

Autofluorescence hyperspectral imaging of radiofrequency ablation lesions in porcine cardiac tissue.

Radiofrequency ablation (RFA) is a widely used treatment for atrial fibrillation, the most common cardiac arrhythmia. Here, we explore autofluorescence hyperspectral imaging (aHSI) as a method to visualize RFA lesions and interlesional gaps in the highly collagenous left atrium. RFA lesions made on the endocardial surface of freshly excised porcine left atrial tissue were illuminated by UV light (365 nm), and hyperspectral datacubes were acquired over the visible range (420-720 nm). Linear unmixing was used to delineate RFA lesions from surrounding tissue, and lesion diameters derived from unmixed component images were quantitatively compared to gross pathology. RFA caused two consistent changes in the autofluorescence emission profile: a decrease at wavelengths below 490 nm (ascribed to a loss of endogenous NADH) and an increase at wavelengths above 490 nm (ascribed to increased scattering). These spectral changes enabled high resolution, in situ delineation of RFA lesion boundaries without the need for additional staining or exogenous markers. Our results confirm the feasibility of using aHSI to visualize RFA lesions at clinically relevant locations. If integrated into a percutaneous visualization catheter, aHSI would enable widefield optical surgical guidance during RFA procedures and could improve patient outcome by reducing atrial fibrillation recurrence.

Seeing the Invisible: Revealing Atrial Ablation Lesions Using Hyperspectral Imaging Approach.

BACKGROUND: Currently, there are limited means for high-resolution monitoring of tissue injury during radiofrequency ablation procedures. OBJECTIVE: To develop the next generation of visualization catheters that can reveal irreversible atrial muscle damage caused by ablation and identify viability gaps between the lesions. METHODS: Radiofrequency lesions were placed on the endocardial surfaces of excised human and bovine atria and left ventricles of blood perfused rat hearts. Tissue was illuminated with 365nm light and a series of images were acquired from individual spectral bands within 420-720nm range. By extracting spectral profiles of individual pixels and spectral unmixing, the relative contribution of ablated and unablated spectra to each pixel was then displayed. Results of spectral unmixing were compared to lesion pathology. RESULTS: RF ablation caused significant changes in the tissue autofluorescence profile. The magnitude of these spectral changes in human left atrium was relatively small (< 10% of peak fluorescence value), yet highly significant. Spectral unmixing of hyperspectral datasets enabled high spatial resolution, in-situ delineation of radiofrequency lesion boundaries without the need for exogenous markers. Lesion dimensions derived from hyperspectral imaging approach strongly correlated with histological outcomes. Presence of blood within the myocardium decreased the amplitude of the autofluorescence spectra while having minimal effect on their overall shapes. As a result, the ability of hyperspectral imaging to delineate ablation lesions in vivo was not affected. CONCLUSIONS: Hyperspectral imaging greatly increases the contrast between ablated and unablated tissue enabling visualization of viability gaps at clinically relevant locations. Data supports the possibility for developing percutaneous hyperspectral catheters for high-resolution ablation guidance.

Nonpharmacologic control of postoperative supraventricular arrhythmias using AV nodal fat pad stimulation in a young animal open heart surgical model.

BACKGROUND: Supraventricular arrhythmias (junctional ectopic tachycardia [JET] and atrial tachyarrhythmias) frequently complicate recovery from open heart surgery in children and can be difficult to manage. Medical treatment of JET can result in significant morbidity. Our goal was to develop a nonpharmacological approach using autonomic stimulation of selective fat pad (FP) regions of the heart in a young canine model of open heart surgery to control 2 common postoperative supraventricular arrhythmias. METHODS AND RESULTS: Eight mongrel dogs, varying in age from 5 to 8 months and weighting 22±4 kg, underwent open heart surgery replicating a nontransannular approach to tetralogy of Fallot repair. Neural stimulation of the right inferior FP was used to control the ventricular response to supraventricular arrhythmias. Right inferior FP stimulation decreased baseline AV nodal conduction without altering sinus cycle length. AV node Wenckebach cycle length prolonged from 270±33 to 352±89 ms, P=0.02. Atrial fibrillation occurred in 7 animals, simulating a rapid atrial tachyarrhythmias. FP stimulation slowed the ventricular response rate from 166±58 to 63±29 beats per minute, P<0.001. Postoperative JET occurred in 7 dogs. FP stimulation slowed the ventricular rate during postoperative JET from 148±31 to 106±32 beats per minute, P<0.001, and restored sinus rhythm in 7/7 dogs. CONCLUSIONS: Right inferior FP stimulation had a selective effect on the AV node, and slowed the ventricular rate during postoperative JET and atrial tachyarrhythmias in our young canine open heart surgery model. FP stimulation may be a useful new technique for managing children with JET and atrial tachyarrhythmias.

Newly created animal model of human postoperative junctional ectopic tachycardia.

OBJECTIVE: Junctional ectopic tachycardia complicates the postoperative recovery from open heart surgery in children. The reported risk factors include younger age, prolonged cardiopulmonary bypass times, and administration of inotropic agents. Junctional ectopic tachycardia occurs early after open heart surgery, in the setting of relative postoperative sinus node dysfunction, and exhibits QRS morphology consistent with an origin from the atrioventricular node or proximal conduction system. Our goal was to develop a reproducible animal model for postoperative junctional ectopic tachycardia. METHODS: Eleven pigs, aged 2 to 4 months, underwent open heart surgery after induction of general anesthesia. Electrodes were sewn to the left atrium and right ventricle. RESULTS: Sinus node dysfunction was created using clamp crushing without or with radiofrequency ablation (successful in 1 of 5 pigs) or sinus node removal (successful in 4 of 4). After prolonged cardiopulmonary bypass (>120 minutes) alone and with isoproterenol infusion, no spontaneous junctional ectopic tachycardia developed. Junctional ectopic tachycardia or fascicular tachycardia could be initiated after either slow atrioventricular nodal pathway ablation and/or digoxin administration. Junctional ectopic tachycardia occurred in 8 of 9 pigs (mean ventricular rate, 171 ± 32 bpm), and fascicular tachycardia occurred in 9 of 9 pigs (mean ventricular rate, 187 ± 39 bpm). His and right bundle recordings confirmed the conduction system origin. CONCLUSIONS: Experimental junctional ectopic tachycardia or fascicular tachycardia can occur in the intraoperative setting of sinus node dysfunction, prolonged cardiopulmonary bypass, and enhanced conduction system automaticity. Conduction system automaticity occurred after either physical injury (ablation or tricuspid valve stretch) or measures to augment the transient inward current of the conduction system (isoproterenol and digoxin). This animal model can serve as the basis to assess new treatments of postoperative junctional ectopic tachycardia.