J A C C : C A S E R E P O R T S VO L . - , N O . - , 2 0 2 0

ª 2 0 2 0 T H E A U T H O R S . P U B L I S H E D B Y E L S E V I E R O N B E H A L F O F T H E A M E R I C A N

C O L L E G E O F C A R D I O L O G Y F OU N D A T I O N . T H I S I S A N O P E N A C C E S S A R T I C L E U N D E R

T H E C C B Y - N C - N D L I C E N S E ( h t t p : / / c r e a t i v e c o mm o n s . o r g / l i c e n s e s / b y - n c - n d / 4 . 0 / ) .

CASE REPORT

CLINICAL CASE

Ablation of Incessant PrematureVentricular Complex through RetrogradeTransvenous Ethanol Infusion

David Meier, MD,a Anna Giulia Pavon, MD,a Patrizio Pascale, MD,a,b Valérie Stolt, MD,c Antoine Delinière, MD,a

Claudia Herrera-Siklody, MD,a Olivier Muller, MD, PHD,a,b Etienne Pruvot, MDa,b

ABSTRACT

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Ethanol infusion has been used for the treatment of ventricular arrhythmia. We describe a case of ethanol infusion

through the coronary sinus venous network to treat refractory epicardial premature ventricular complexes. The prema-

ture ventricular complexes were initially successfully suppressed but recurred after resolution of the myocardial edema.

(Level of Difficulty: Intermediate.) (J Am Coll Cardiol Case Rep 2020;-:-–-) © 2020 The Authors. Published by Elsevier

on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license

(http://creativecommons.org/licenses/by-nc-nd/4.0/).

F requent premature ventricular complexes(PVC) may cause left ventricular (LV) dysfunc-tion. Treating PVCs and LV dysfunction is

especially challenging in cases of intramural andepicardial foci. Epicardial ablation is an appealingalternative but bears some potential complications(1). Transcoronary ethanol infusion has been success-fully used for ablation of arrhythmia (2), but compli-cations such as collateral myocardial damage andcomplete atrioventricular block (3) limit the use ofethanol infusion. Recently, a new technique has

EARNING OBJECTIVE

To recognize the role of alternative tech-niques in refractory cases of ventriculararrhythmia;To recognize the role of cardiac magneticresonance to monitor the effect of ablation.

N 2666-0849

m the aDepartment of Cardiology, University Hospital of Lausanne, Lausa

usanne University, Lausanne, Switzerland; and cInternal Medicine and Ca

itzerland. Dr. Herrera-Siklody is a compensated speaker for Abbott and D

y have no relationships relevant to the contents of this paper to disclose

e authors attest they are in compliance with human studies committees

tutions and Food and Drug Administration guidelines, including patient co

JACC: Case Reports author instructions page.

nuscript received October 22, 2019; revised manuscript received Decemb

emerged based on a retrograde venous ethanol infu-sion using the coronary sinus (CS) vein network.This approach has been used as an adjunct therapyfor ablation of atrial fibrillation (4,5) and for ventricu-lar tachycardia (VT) ablation in 2 short series of 7 pa-tients (6). This paper reports the case of a 24-year-oldmale patient with LV dysfunction and frequent PVCstreated with retrograde venous ethanol infusion.

PRESENTATION

A 24-year-old male patient was referred to the au-thors’ department in January 2019 for ablation ofincessant PVCs associated with LV dysfunction. Thepatient’s symptoms were marked exercise capacityreduction with no overt clinical signs of heart failure.

MEDICAL HISTORY. A high incidence of mono-morphic PVCs (30%) was first discovered in 2012.Cardiac magnetic resonance (CMR) showed no

https://doi.org/10.1016/j.jaccas.2020.01.032

nne, Switzerland; bFaculty of Biology and Medicine,

rdiology, Hôpital Intercantonal de la Broye, Payerne,

aiichi Sankyo. All other authors have reported that

.

and animal welfare regulations of the authors’ in-

nsent where appropriate. For more information, visit

er 31, 2019, accepted January 6, 2020.

FIGUR

The PV

focus o

ventric

ABBR EV I A T I ON S

AND ACRONYMS

CMR = cardiac magnetic

resonance

CS = coronary sinus

LGE = late gadolinium

enhancement

LV = left ventricle

MVO = microvascular

obstruction

NSVT = nonsustained

ventricular tachycardia

PVC = premature ventricular

complex

VT = ventricular tachycardia

Meier et al. J A C C : C A S E R E P O R T S , V O L . - , N O . - , 2 0 2 0

Ablation of PVC Using Ethanol Infusion - 2 0 2 0 :- –-

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structural anomaly and normal LV functionand the absence of fibrosis. Treatments withbeta-blockers and amiodarone were unsuc-cessful. In 2013, the first retroaortic ablationattempt was unsuccessful, resulting in a lowlocal prematurity, raising the suspicion of anepicardial focus.

INVESTIGATIONS

Repeated CMR performed in May 2018revealed LV dilation and reduced LV ejectionfraction (40%). Electrocardiography (ECG)showed PVCs with a morphology that sug-gested an origin from the mid-lateral LV wall(Figure 1). The patient was then referred to

the authors’ center for a new endocardial attemptthrough transseptal access, with additional retrogradevenous ethanol infusion in case of repeated failure.

MANAGEMENT

With the patient under general anesthesia, adecapolar catheter (Decanav, Biosense Webster,Irvine, California) was advanced into the CS. Anablation catheter (SmartTouch SF, BiosenseWebster) was inserted into the LV using a trans-septal access. The site of earliest endocardial acti-vation during the PVC was at best at 0 ms comparedto the QRS onset and localized at the junction

E 1 12-Lead ECG of the PVC

C displays a complete RBBB morphology in V1, suggestive of an LV

n the LV lateral wall, and the pseudo-delta wave in V1 suggests a

le; PVC ¼ premature ventricular complex; RBBB ¼ right bundle b

between the mid and basal thirds of the infero-lateral LV. The endocardial approach failed despiteprolonged ablation with significant force and powerapplication (20 g, 40 W, with impedance monitoringshowing a significant drop). The CS and 2 lateralside branches directed toward the arrhythmic focuswere reconstructed using the ablation catheter(Figure 2A). The anterolateral vein appeared to drainthe site of PVC origin as shown by both selectivecontrast infusion (Figure 2B) and 5�C saline infusionthat briefly suppressed the PVCs (Figure 3). Onemilliliter of 96% ethanol injected through the abla-tion catheter triggered a nonsustained VT thatperfectly matched the morphology of the clinicalPVC followed by its disappearance (Figure 4, toppanel). However, the PVCs resumed within minutes.A coronary guiding catheter (Voda Left, SciMed,Durham, North Carolina) was advanced into the CSallowing the insertion of 2 guidewires (Sion blue,Asahi, Tokyo, Japan) into a downstream vein(Figure 2C). A 1.5-mm balloon (Sprinter Legend,Medtronic, Dublin, Ireland) was then inflated for 5minutes to prevent backflow during the infusion of1 ml of ethanol (Figure 2D). A nonsustained VToccurred again, followed by PVC terminationwithout procedural recurrence. Monitoring of thepatient on the ward showed an initial high inci-dence of PVCs and nonsustained VTs, followed bygradual disappearance with lengthening coupling

origin. The QS pattern in V5 and V6, and in aVL and D1 localizes the

n epicardial focus (see inset). ECG ¼ electrocardiography; LV ¼ left

ranch block.

FIGURE 2 Fluoroscopic and Electroanatomical Mapping Views of the CS Cannulation

(A) Anteroposterior combined fluoroscopic and electroanatomical mapping views show the ablation catheter (blue arrow) in the target vein of

the CS (transparent green). The site of earliest endocardial activation is encircled in red. (B) Anteroposterior fluoroscopic view of the

angiogram of the target CS vein (red arrow) performed through the ablation catheter (blue arrow). (C) Two guidewires (red arrow) were

inserted through a guide catheter (blue arrow). (D) Myocardial staining (circle) after ethanol infusion. CS ¼ coronary sinus.

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intervals over the next 24 hours, until completedisappearance (Figure 4, middle and bottom panels).A CMR performed 48 hours after the procedureshowed late gadolinium enhancement (LGE)affecting 4 segments at the junction between thebasal and median thirds of the LV lateral wall withsmall areas of microvascular obstruction (Figure 5A).At 3 months, a new CMR showed slight improve-ment of LV ejection fraction (from 32% right afterthe ablation to 40% to 45%) and marked reductionof the LGE from 4 to 2 segments with a sub-endocardial distribution involving 50% of themyocardial thickness (Figure 5B, arrow). Neverthe-less, the referring cardiologist reported PVC recur-rence, although at a lower incidence, 4 weeks afterablation.

DISCUSSION

This case reports the ablation of PVCs by usingretrograde CS ethanol infusion with acute suppres-sion followed by recurrence after 4 weeks. Thisapproach offers the advantage of feasibility using thesame femoral venous access rather than the trans-septal approach, allowing the operator to reach theepicardium without the need for a dry pericardialpuncture and its potential complications. Three ob-servations can be drawn.1)Arrhythmic focus loca l i zat ion . With regard toethanol toxicity, it is highly recommended that thetarget myocardium be targeted precisely. Cold salineinjection is confirmed as an effective tool that can beused to map the myocardium to be ablated (7).

FIGURE 3 Effect of Cold Saline on PVC

Transient suppression of PVCs by cold saline infusion into the target vein. Abbreviation as in Figure 1.

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Interestingly, venous mapping with contrast and sa-line injection did not require specific guiding cathe-ters but were performed using the ablation catheter.2)Ethanol vo lume. Here, 2 ml of ethanol was used.The optimal dose remains to be determined, given thelimited experience reported so far (6). This issue isimportant because an excessive volume of ethanolmay cause collateral myocardial damage, whereas aninsufficient dose may favor PVC recurrence. Based onthe PVC recurrence and on the CMR lesion assess-ment reported here, one or more repeated injectionsare most probably warranted in such cases as pro-posed by others, who tended to repeat the 1-ml in-jection (up to 4 ml) (6).3)CMR is usefu l to moni tor ab lat ion damagesand myocard ia l recovery . Even if the spatial andtemporal resolution of CMR does not allow precisedifferentiation between the effect of the endocardialand epicardial ablation, the epicardial ablation, theextended edema associated with PVC disappearance

2 days after the current procedure speaks for a com-bined effect of both approaches.

Residual LGE seen at 1 month spanning 2 thirdsof the myocardium toward the epicardium corre-lates well with the site of the endocardial approach,whereas the reappearance of viable epicardial tissueafter edema resolution, in parallel with PVC recur-rence, militates for an insufficient epicardial abla-tion. Interestingly, the first CMR performed beforethe current procedure did not show LGE at the siteof the first ablation attempt in 2013.

Treatment of the present case bears some limita-tions, such as the lack of definite proof that the focuswas indeed epicardial, which might have beenconfirmed and successfully ablated based on adetailed epicardial mapping using a dry pericardialpuncture. Alternatively, a more focused identificationof the target site could be obtained through detailedelectrical mapping of the CS network using dedicatedunipolar guidewires.

FIGURE 4 PVC Evolution after the Ablation

(Top) Nonsustained VT reproducing the clinical PVC morphology after ethanol infusion. (Middle) Evolution of PVC count during monitoring. Numbers indicate

PVC incidence per 2-h periods. (Bottom) Progressive lengthening of PVC coupling intervals after ablation. (A) extract from the original PVC before ablation.

(B) Telemetry strip during the first 12 h. (C) Telemetry strip 24 h after the ablation. Abbreviations are as in Figure 1.

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Finally, hypo-osmolar irrigation of the ablationcatheter could have been used as it hasbeen shown, first in animal models and then inhumans (8, 9), to allow deeper penetration ofablation energy into the muscle, which seems very

promising when targeting intramural or epicardialfocus.FOLLOW-UP. A combined attempt using retrogradevenous infusion and the percutaneous epicardialapproach through pericardial puncture was

FIGURE 5 CMR Views of the Ablation Zone

(A) T1-weighted inversion-recovery gradient echo sequence shows diffuse and transmural LGE on the lateral wall (red square) with a small

area of MVO (yellow arrow) 48 h after ablation. (B) T1-weighted inversion-recovery gradient echo sequence of the same slice shows

reduction in the extension of the subendocardial LGE (red arrow) and reappearance of a thin rim of viable epicardial tissue (green arrow) at

3 months. LGE ¼ late gadolinium enhancement; LV ¼ left ventricle; MVO ¼ microvascular obstruction.

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programmed, but the patient did not show up tofollow-up visits.

CONCLUSIONS

Retrograde venous infusion of ethanol seemstechnically feasible for refractory cases of PVC/VT. To optimize efficacy-to-damage ratio, localepicardial mapping may be achieved using

dedicated unipolar mapping guide wires. Theoptimal volume of ethanol needs to be determinedas well.

ADDRESS FOR CORRESPONDENCE: Prof. EtiennePruvot, Department of Cardiology, Arrhythmia Unit,University Hospital of Lausanne (CHUV), 46, Rue duBugnon, 1011 Lausanne, Switzerland. E-mail: etienne.pruvot@chuv.ch.

RE F E RENCE S

1. Lim HS, Sacher F, Cochet H, et al. Safety andprevention of complications during percutaneousepicardial access for the ablation of cardiac ar-rhythmias. Heart Rhythm 2014;11:1658–65.

2. Gabus V, Jeanrenaud X, Eeckhout E, Pruvot E.Transcoronary ethanol for incessant epicardial ven-tricular tachycardia. Heart Rhythm 2014;11:143–5.

3. Kumar S, Tedrow UB, Stevenson WG. Adjunctiveinterventional techniques when percutaneouscatheter ablation for drug refractory ventriculararrhythmias fail: a contemporary review. CircArrhythm Electrophysiol 2017;10:e003676.

4. Liu CM, Lo LW, Lin YJ, et al. Long-term efficacyand safety of adjunctive ethanol infusion into thevein of Marshall during catheter ablation for

nonparoxysmal atrial fibrillation. J CardiovascElectrophysiol 2019;30:1215–28.

5. Valderrabano M, Liu X, Sasaridis C, Sidhu J,Little S, Khoury DS. ethanol infusion in the veinof Marshall: adjunctive effects during ablation ofatrial fibrillation. Heart Rhythm 2009;6:1552–8.

6. Kreidieh B, Rodriguez-Manero M, et al. Retro-grade coronary venous ethanol infusion for abla-tion of refractory ventricular tachycardia. CircArrhythm Electrophysiol 2016;9.

7. Brugada P, de Swart H, Smeets JL, Bar FW,Wellens HJ. Termination of tachycardias by inter-rupting blood flow to the arrhythmogenic area.Am J Cardiol 1988;62:387–92.

8. Nguyen DT, Gerstenfeld EP, Tzou WS, et al.Radiofrequency ablation using an open irrigatedelectrode cooled with half-normal saline. J AmColl Cardiol EP 2017;3:1103–10.

9. Nguyen DT, Tzou WS, Sandhu A, Gianni C,Anter E, Tung R, et al. Prospective multicenterexperience with cooled radiofrequency ablationusing high impedance irrigant to target deepmyocardial substrate refractory to standard abla-tion. J Am Coll Cardiol EP 2018;4:1176–85.

KEY WORDS ablation, ethanol, prematureventricular complexes, retrograde infusion,ventricular arrhythmia