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.

Ablation of the vanishing PVC, facilitated by quantitative morphology-matching software.

BACKGROUND: Ablation of cardiac arrhythmias in children and teenagers often necessitates the use of anesthesia, which can suppress ventricular arrhythmias (VAs), making it difficult to map the site of origin using activation time (AT). Pace mapping, a technique employed to assist with VA origin localization, depends on subjective comparison of paced and targeted QRS morphology. We assessed the utility of a quantitative approach to paced QRS to VA morphology matching using the PaSo software (Carto 3, Biosense Webster), to localize the VA site of origin. METHODS: Twenty-four patients underwent 26 procedures for frequent VAs, 29 for targeted VA. If AT mapping was precluded due to infrequent VA, pace mapping was executed using the PaSo software, after regionalization based on targeted VA QRS morphology. RESULTS: Subjects were aged 1-32 (mean 14 ± 6) years; 10 were male. Heart disease was present in six patients. PVC frequency prior to onset of anesthesia was 15 ± 16/min, decreasing to 0-1 PVC/min in 17 cases prior to ablation. Arrhythmia localization was performed by AT mapping + PaSo (12) or PaSo only (17). Pace mapping exhibited an intraventricular gradient of percent QRS morphology match. Highest achieved QRS match averaged 96 ± 2%. Successful ablation (> 1-month follow-up) was achieved in 24/29 targeted VAs, 11/12 ablated using AT and pace mapping, and 13/17 VA ablated using pace mapping only, P  =  0.29. CONCLUSIONS: (1) Spontaneous VA frequency was markedly reduced following anesthesia, despite catecholamine administration. (2) Notwithstanding the ability to perform AT mapping, successful ablation can still be performed using pace mapping only, facilitated by the PaSo software.

Radiofrequency catheter ablation of intractable ventricular tachycardia in an infant following arterial switch operation.

A full-term male neonate presented with cyanosis upon delivery and was subsequently diagnosed with d-transposition of the great arteries, ventricular septal defect, and restrictive atrial septal defect. Following initiation of intravenous prostaglandins and balloon atrial septostomy, an arterial switch operation was performed on day 3 of life. The postoperative course was complicated by intractable ventricular tachycardia that was refractory to lidocaine, amiodarone, esmolol, fosphenytoin, and mexiletine drug therapy. Ventricular tachycardia was suppressed with overdrive atrial pacing but recurred upon discontinuation. Seven weeks postoperatively, radiofrequency catheter ablation was performed due to hemodynamically compromising persistent ventricular tachycardia refractory to medical therapy. The ventricular tachycardia was localized to the inferior-lateral right ventricular outlet septum. The procedure was successful without complications or recurrence. Antiarrhythmics were discontinued after the ablation procedure. Seven days after the ablation, a different, slower fascicular rhythm was noted to compete with the infant's sinus rhythm. This was consistent with the preablation amiodarone having reached subtherapeutic levels given its very long half-life. The patient was restarted on oral beta blockers and amiodarone. The patient was subsequently discharged home in predominantly sinus rhythm with intermittent fascicular rhythm.

Cryoablation and angiographic evidence of a concealed right atrial appendage to right ventricle accessory pathway in an infant.

We report a case of successful cryoablation of a concealed accessory pathway from the right atrial appendage to the right ventricle in an infant. A 4-month-old female who had previously undergone successful ablation of a left-sided accessory pathway was taken to the electrophysiology lab due to recurrent supraventricular tachycardia. While in this second supraventricular tachycardia, we found earliest atrial activation in the distal right atrial appendage. Angiography confirmed a connection between right atrial appendage and the right ventricle. Cryoablation at this location promptly terminated the supraventricular tachycardia. Following ablation, there were no further inducible arrhythmias and ventriculo-atrial dissociation was appreciated.

Long-term follow-up of children and adolescents diagnosed with hypertrophic cardiomyopathy: risk factors for adverse arrhythmic events.

Our aim was to identify prognostic factors for an arrhythmic event (AE) in children with hypertrophic cardiomyopathy (HCM) without a previous AE. One hundred thirty-one nonconsecutive patients (≤ 20 years) with HCM but no previous AE were evaluated at the NIH Clinical Center from 1980 to 2001. At a median follow-up of 6.4 years, 22 patients experienced an AE [sudden death (SD) (n = 12), resuscitated cardiac arrest (n = 3), clinical sustained ventricular tachycardia (VT) (n = 2), and implantable cardiac defibrillator discharge (n = 5)], resulting in a 2% annual AE rate. Baseline factors that were most predictive in univariate risk analysis included ventricular septal thickness (ST) (P = 0.01), VT induction by programmed ventricular stimulation (PVS) (P = 0.01), age (P = 0.05), and presyncope/syncope (P = 0.05). In multivariate analysis, ST, age, presyncope/syncope, and PVS were not independently predictive of risk for an AE. However, the 5-year event rates for AE was 15% (95% CI: 5-23%) if ST ≥ 20 mm, 19% (95% CI: 6-31%) when age ≥ 13 years and ST ≥ 20 mm were combined together, and 23% (95% CI: 3-39%) when PVS and ST ≥ 20 mm were combined together. Of the various risk factors that were considered in our pediatric HCM cohort, ST and inducible VT were the most significant univariate predictors of risk for an AE. More traditional risk factors identified in older patients (family history of SD, VT on Holter, and exercise-induced hypotension) were not predictive of an AE in patients age under 21 years.

Painful sweating.

OBJECTIVE: The authors report a case of spontaneous and gustatory facial pain and sweating. METHODS: The patient had frequent episodes of pain, sweating, and flushing bilaterally in the hairless skin of the ophthalmic and maxillary distributions of the trigeminal nerve. Gustatory stimuli (e.g., orange juice, pickled onions) reliably evoked episodes, but episodes also frequently came on spontaneously. The problem had begun during adolescence, about the time of topical treatment and then electrocauteries for facial warts. The patient reported benefit from tricyclic antidepressants, guanethidine, and trospium chloride (an anti-cholinergic quaternary amine used in Europe for urinary urgency). There was no pain or excessive sweating in other body areas, nor pain with exercise. RESULTS: Administration of edrophonium IV evoked pain and sweating, and ganglion blockade by IV trimethaphan eliminated pain and sweating and markedly attenuated responses to edrophonium. Trospium chloride also prevented edrophonium-induced pain and sweating. Bicycle exercise produced the same increment in forehead humidity as in a spontaneous episode but did not evoke pain. Tyramine infusion did not bring on pain or sweating, whereas iontophoretic acetylcholine administration to one cheek evoked pain and sweating bilaterally. Topical glycopyrrolate cream eliminated spontaneous, gustatory, and edrophonium-induced episodes. CONCLUSIONS: The findings indicate that facial pain and sweating can result from occupation of muscarinic cholinergic receptors after acetylcholine release from local nerves. The authors propose that after destruction of cutaneous nerves, aberrant regenerant sprouting innervates sweat glands, producing gustatory sweating as in auriculotemporal syndrome (Frey syndrome), and innervates nociceptors, producing pain.