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j.hrcr.2018.07.018

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Accepted Manuscript
Cardioneuroablation in ictal asystole - new treatment method
Bor Antolic, MD, PhD, Veronika Rutar Gorisek, MD, PhD, Gal Granda, MD, Bogdan
Lorber, MD, Msc, Prof Matjaz Sinkovec, MD, PhD, David Zizek, MD, PhD
PII:
S2214-0271(18)30186-6
DOI:
10.1016/j.hrcr.2018.07.018
Reference:
HRCR 578
To appear in:
HeartRhythm Case Reports
Received Date: 15 June 2018
Revised Date:
26 July 2018
Accepted Date: 31 July 2018
Please cite this article as: Antolic B, Rutar Gorisek V, Granda G, Lorber B, Sinkovec M, Zizek D,
Cardioneuroablation in ictal asystole - new treatment method, HeartRhythm Case Reports (2018), doi:
10.1016/j.hrcr.2018.07.018.
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TITLE PAGE
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Title: Cardioneuroablation in ictal asystole - new treatment method
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Short title: Cardioneuroablation in ictal asystole
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Authors:
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1. Bor Antolic1, MD, PhD, email: bor.antolic@kclj.si
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2. Veronika Rutar Gorisek2, MD, PhD, email: veronika.rutargorisek@kclj.si
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3. Gal Granda, MD2, email: gal.granda@kclj.si
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4. Bogdan Lorber, MD2, Msc, email: bogdan.lorber@kclj.si
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5. Prof. Matjaz Sinkovec1, MD, PhD, email: matjaz.sinkovec@kclj.si
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6. David Zizek, MD, PhD1, email: davidzizek@yahoo.com
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1000 Ljubljana, Slovenia
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Ljubljana, Slovenia
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University Medical Center Ljubljana, Department of Neurology, Zaloska 7,
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University Medical Center Ljubljana, Department of Cardiology, Zaloska 7,
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Financial support/funding: This research did not receive any specific grant
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from funding agencies in the public, commercial, or not-for-profit sectors.
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Conflicts of interest: the authors report no conflicts of interest.
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Informed consent: informed consent was obtained from the patient before
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performing the procedure.
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Word count: 1948
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Corresponding author:
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Bor Antolic, MD, PhD
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Department of Cardiology
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University Medical Centre Ljubljana
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Zaloška 7
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1000 Ljubljana
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Slovenia
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email: bor.antolic@kclj.si
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tel: +386 1 522 2844, +386 1 522 8539, +386 41 325 796
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fax: +386 1 522 2828
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Keywords: cardioneuroablation; syncope; ictal asystole; vagal denervation;
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parasympathetic denervation
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INTRODUCTION
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We describe a case of successful parasympathetic denervation of the sinus
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node using cardioneuroablation in a patient with right temporal lobe epilepsy
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and prolonged ictal asystole. The procedure abolished seizure-induced
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bradyarrhythmia occurrence and converted patient's dramatic seizures with
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severe cerebral hypoperfusion into short focal seizures with minimal motor
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signs. To the best of our knowledge, this is the first report of successful
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cardioneuroablation procedure to potentially treat ictal asystole.
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CASE REPORT
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43-year old right-handed male patient with pharmacoresistant focal epilepsy
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was admitted to Department of Neurology for evaluation before potential
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epilepsy surgery. He had an extensive focal cortical dysplasia in the right
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temporal lobe and mild left-sided spastic hemiparesis. Seizures were resistant
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to several antiepileptic drugs, including levetiracetam and carbamazepine in
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maximal dosages he was taking before the admission. For the past five years,
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almost every seizure resulted in loss of consciousness, falls, and on several
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occasions, in traumatic injuries. During long-term video-
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electroencephalography (EEG) monitoring, the antiepileptic drugs were
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temporarily withdrawn, and nine epileptic seizures were recorded. The
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seizures manifested with ictal pouting (‘chapeau de gendarme’), right leg
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automatisms and subtle pelvic movements, dystonic left hand posturing,
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followed by unresponsiveness, upward gaze deviation and posturing
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resembling decerebration pattern. In EEG, focal ictal activity started in the
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right temporal region, quickly evolving over both hemispheres and was then
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followed by postictal EEG slowing over the right hemisphere. Unexpectedly, in
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late postictal period, we observed generalized EEG flattening and slowing,
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indicative of cerebral hypoperfusion. Simultaneously, in ECG sinus heart rate
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slowing with asystole lasting up to 25 seconds was recorded, resulting in
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patient's syncope (Figure 1, upper panel; see supplementary video).
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Immediate surgical treatment of epilepsy was not feasible and also,
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considering the extensive nature of the presumed epileptogenic lesion,
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chances of favourable epilepsy surgery outcome were estimated to be low.
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The cardiology team was consulted. Since asystole after the seizure onset
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was suggestive of an increased direct vagal stimulation of the cardiac
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conduction system we decided to try cardioneuroablation as an alternative to
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permanent pacemaker implantation.
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After patient’s consent, the cardioneuroablation procedure was performed
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using mild sedation with midazolam and additional fentanyl boluses. Mapping
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and ablations were performed using a 3,5 mm irrigated tip catheter (Navistar
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Thermocool SmartTouch, Biosense Webster, Diamond Bar, CA, USA). Initially,
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three-dimensional virtual anatomy of the right (RA) and left atrium (LA) was
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created using CARTO 3 fast anatomical mapping system (Biosense Webster,
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Diamond Bar, CA, USA), facilitated by intracardiac echocardiography
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(AcuNav, Siemens Medical Solutions, USA). Tagging the phrenic nerve
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capture points on the lateral RA allowed us to map the nerve course (Figure
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2). Afterwards, the electrogram fractionations indicative of epicardial ganglia
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presence1 were mapped and tagged in the anatomic areas where epicardial
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parasympathetic ganglia for sinus and AV node innervation are located
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(anteriorly and superiorly to the right superior pulmonary vein (RSPV) and
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anteriorly to the right inferior pulmonary vein in LA). These locations
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correspond to locations on the posterior septal side of the RA, where
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fractionated electrograms were also mapped and tagged. Multiple ablations
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(power control, 25W in RA, 30W in LA, target contact force 10-30 g, duration
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up to 40s, temperature limit 43 °C, total RF time 1 544s) were performed in
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target areas from both the LA and RA with care taken to avoid ablations in the
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proximity of the mapped course of the phrenic nerve. We aimed to achieve
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local electrogram attenuation and ablation index (Biosense Webster, Diamond
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Bar, CA, USA) of 350 to 500. During initial ablations anteriorly to the RSPV
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increase in heart rate was noticed indicating parasympathetic denervation of
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the sinus node. Later ablations more inferiorly along the posterior interatrial
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septum from the LA and RA were anatomically guided. After no additional
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increase in heart rate was achieved with further ablations and target
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anatomical area were sufficiently densely ablated the procedure was
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terminated. Atropine test (3mg of atropine sulphate given intravenously; dose
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calculated as 0,04mg/kg body weight, maximal dose 3mg) at the end of
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procedure resulted in only 7% sinus rate increase (from 117 bpm to 125 bpm),
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which according to published data2 suggests successful denervation of the
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sinus node. The procedure duration was 200 min, fluoroscopy time was 6,8
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min (dose-area product - DAP 560 µGym2).
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To evaluate the impact of cardioneuroablation on bradyarrhythmia occurrence
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an implantable loop recorder (ILR; Reveal Linq, Medtronic) was implanted.
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The patient resumed antiepileptic drugs and was released from the hospital.
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One month after the procedure, patient had a seizure without loss of
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consciousness, reporting only lightheadedness and stiffness of his left arm.
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Interrogation of ILR showed no bradyarrhythmias at the time of the seizure.
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The patient was then readmitted for follow-up video-EEG monitoring and the
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antiepileptic drugs were again withdrawn. Five seizures were recorded. All of
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the recorded seizures ended with a short postictal EEG slowing over the right
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hemisphere, followed by rapid restoration of normal background activity
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(Figure 1, lower panel). There were no bradyarrhythmias recorded during the
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seizures. He is still under evaluation for epilepsy surgery, but at present, his
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seizures have a minor impact on his quality of life. During 6 months follow-up
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period the patient reported no syncope and there were no bradyarrhythmias
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recorded by the ILR.
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DISCUSSION
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Seizure-induced asystole, or ictal asystole, is caused by spread of ictal activity
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to loci where it intervenes with central autonomic networks which can result in
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direct vagal stimulation of the cardiac conduction system. This rare, but
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devastating condition is a feature of focal, most commonly temporal and
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mesial frontal lobe epilepsy involving insula, cingulate gyrus and other parts of
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central autonomic network.3-6 It is estimated that only 0.27% of epileptic
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patients suffer from the condition, which is hypothesized as one of many
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potential mechanisms of sudden unexpected death in epilepsy (SUDEP).7-10
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Several approaches are proposed to treat ictal asystole, including adjustment
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of antiepileptic drugs, epilepsy surgery for medically refractory patients, and
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only recently permanent pacemaker implantation.8 However, despite the
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technological development of implantable electronic cardiac devices,
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complication incidence in modern pacing therapy is still substantial. Although
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most adverse events occur in the early postimplantation period (lead-related),
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complications rates during long-term follow-up are not scarce, ranging from
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7.5% to almost 10% of the patients.11,12
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Pachon et al.13 first described cardioneuroablation in 2005 as a new treatment
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modality for neurocardiogenic syncope, functional sinus node dysfunction and
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functional atrioventricular block. The technique is based on radiofrequency
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ablation of main epicardial parasympathetic ganglia in the heart. With this
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procedure partial parasympathetic denervation of the sinus and/or AV node is
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achieved and consequently the adverse parasympathetic influence on the
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heart diminished. Long term follow-up2 of patients undergoing
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cardioneuroablation procedure for cardioinhibitory neurocardiogenic syncope
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showed very promising results, with only 3 patients out of 43 experienced
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recurrent syncope. In addition, post procedure 24-hour Holter ECGs and
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stress tests showed no major abnormalities except mildly elevated basal heart
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rate.
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Although cardioneuroablation procedure considerably diminished patient’s
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seizure presentation longer follow-up and close monitoring of the patient is
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required to detect possible recurrence of bradyarrhythmias and worsening of
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seizures. Consequently, pharmacoresistant epilepsy merits constant
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evaluation for potential surgical treatment.
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CONCLUSIONS
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Cardioneuroablation might represent a new treatment modality in select
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pharmacoresistant patients with ictal asystole. In addition, with this treatment
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option permanent pacemaker implantation could be avoided and device-
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related complications prevented. Further research is warranted to evaluate
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this treatment option.
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References
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1. Lellouche N, Buch E, Celigoj A, Siegerman C, Cesario D, De Diego C,
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Mahajan A, Boyle NG, Wiener I, Garfinkel A, Shivkumar K. Functional
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characterization of atrial electrograms in sinus rhythm delineates sites
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of parasympathetic innervation in patients with paroxysmal atrial
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fibrillation. J Am Coll Cardiol. 2007;50:1324-1331. doi:
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10.1016/j.jacc.2007.03.069
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2. Pachon JC, Pachon EI, Cunha Pachon MZ, Lobo TJ, Pachon JC,
Santillana TG. Catheter ablation of severe neurally meditated reflex
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(neurocardiogenic or vasovagal) syncope: cardioneuroablation long-
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term results. Europace. 2011;13:1231-1242. doi:
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3. Schuele SU, Bermeo AC, Alexopoulos AV, Locatelli ER, Burgess RC,
Dinner DS, Foldvary-Schaefer N. Video-electrographic and clinical
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features in patients with ictal asystole. Neurology. 2007;69:434-441.
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doi: 10.1212/01.wnl.0000266595.77885.7f
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4. Ghearing GR, Munger TM, Jaffe AS, Benarroch EE, Britton JW.
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Clinical cues for detecting ictal asystole. Clin Auton Res. 2007;17:221-
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5. Rocamora R, Kurthen M, Lickfett L, Von Oertzen J, Elger CE. Cardiac
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asystole in epilepsy: clinical and neurophysiologic features. Epilepsia.
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2003;44:179-185. doi: 10.1046/j.1528-1157.2003.15101.x
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monitoring. Seizure. 2011;20:167-172. doi:
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10.1016/j.seizure.2010.11.017
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7. Velagapudi P, Turagam M, Laurence T, Kocheril A. Cardiac
arrhythmias and sudden unexpected death in epilepsy (SUDEP).
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Pacing Clin Electrophysiol. 2012;35:363-370. doi: 10.1111/j.1540-
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8. Wittekind SG, Lie O, Hubbard S, Viswanathan MN. Ictal asystole: an
indication for pacemaker implantation and emerging cause of sudden
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9. Nashef L, Hindocha N, Makoff A. Risk factors in sudden death in
epilepsy (SUDEP): the quest for mechanisms. Epilepsia. 2007;48:859871. doi: 10.1111/j.1528-1167.2007.01082.x
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10. Scorza FA, Arida RM, Cysneiros RM, Terra VC, Sonoda EY, de
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Albuquerque M, Cavalheiro EA. The brain-heart connection:
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implications for understanding sudden unexpected death in epilepsy.
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Cardiol J. 2009;16:394-399.
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11. Ellenbogen KA, Hellkamp AS, Wilkoff BL, Camunãs JL, Love JC,
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Hadjis TA, Lee KL, Lamas GA. Complications arising after implantation
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of DDD pacemakers: the MOST experience. Am J Cardiol.
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2003;92:740-741. doi:10.1016/S0002-9149(03)00844-0
12. Udo EO, Zuithoff NP, van Hemel NM, de Cock CC, Hendriks T,
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Doevendans PA, Moons KG. Incidence and predictors of short- and
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long-term complications in pacemaker therapy: the FOLLOWPACE
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study. Heart Rhythm. 2012;9:728-735. doi:
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10.1016/j.hrthm.2011.12.014
13. Pachon JC, Pachon EI, Pachon JC, Lobo TJ, Pachon MZ, Vargas RN,
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Jatene AD. "Cardioneuroablation"--new treatment for neurocardiogenic
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syncope, functional AV block and sinus dysfunction using catheter RF-
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ablation. Europace. 2005;7:1-13. doi: 10.1016/j.eupc.2004.10.003
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Figure 1
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Electroencephalography (EEG) and electrocardiography (ECG) changes
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occurring 35 seconds after the start of the seizure before (upper panel A) and
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after (lower panel B) cardioneuroablation procedure. A) Before the procedure,
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single-channel ECG demonstrated sinus rhythm slowing followed by asystole
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(23 seconds) and then slow return to normal sinus rhythm. In postictal EEG
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with slow activity over right hemisphere, the cerebral hypoperfusion resulted
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in generalized slow activity, followed by a 'flat' EEG (22 seconds) and then
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generalized slow activity. B) After the procedure, single-channel ECG
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demonstrated normal sinus rhythm. In EEG, postictal slow activity over right
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hemisphere abruptly returned to normal background activity.
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Figure 2
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A posterolateral view of three-dimensional constructed virtual anatomy of the
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left and right atrium. Red dots designate radiofrequency ablation lesions on
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the interatrial septum. Violet dots show the phrenic nerve course.
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LA left atrium, LIPV left inferior pulmonary vein, LSPV let superior pulmonary
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vein, RA right atrium, RIPV right inferior pulmonary vein, RSPV right superior
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pulmonary vein, SVC superior vena cava
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Key teaching points
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Seizure-induced (ictal) asystole is caused by direct vagal stimulation of the
cardiac conduction system. It is estimated that only 0.27% of epileptic patients
suffer from the condition, which is hypothesized as one of many potential
•
RI
PT
mechanisms of sudden unexpected death in epilepsy.
Several approaches are proposed to treat ictal asystole, including adjustment
of antiepileptic drugs, epilepsy surgery, and only recently permanent
Cardioneuroablation – parasympathetic denervation of the sinus node - might
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represent a new treatment option in select patients with ictal asystole. In
addition, with this treatment option permanent pacemaker implantation could
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be avoided and device-related complications prevented.
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pacemaker implantation.
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