Introduction
Catheter ablation is an established first-line therapy for treatment of symptomatic
supraventricular tachycardia (SVT), with high success rates and low risk of complications.
1
Coronary artery (CA) injury is a rare complication of SVT ablation and is typically
seen during radiofrequency ablation of posterior paraseptal accessory pathways inside
the coronary sinus ostium (CSO) or its branches.
2
The anterior-inferior aspect of the CSO, a site that may be targeted for atrioventricular
nodal reentrant tachycardia (AVNRT) ablation, can be near a CA.
3
Limited precordial leads displayed at high sweep speeds during standard electrophysiology
(EP) procedures coupled with the rarity of the CA injury may result in overlooking
this potential complication during AVNRT ablation.
We report a rare case of CA injury during slow pathway ablation for typical AVNRT
that manifested as spontaneous ventricular fibrillation (VF) after ablation. We also
present a brief review of literature and tips for prevention of this rare complication.
Case report
A 10-year-old male patient (weight 32.5 kg, body surface area 1.15 m2) presented with
recurrent episodes of palpitations and adenosine-sensitive narrow complex tachycardia.
After carefully evaluating pharmacological and nonpharmacological treatment options
with the family, we proceeded with an EP study and catheter ablation. The ablation
was performed by the senior author (R.M.), who is US trained and the sole pediatric
cardiac electrophysiologist at the Loma Linda University Children’s Hospital. In the
year prior to the procedure, 30 ablations in patients <12 years of age were performed
by the operator at this center. The procedure was performed under general anesthesia.
The following catheters were used for the procedure: coronary sinus: Dynamic XT, decapolar,
6F (Boston Scientific Corp, Maple Grove, MN); right atrium: Supreme Quad, JSN, 4F
(Abbott Laboratories, Abbott Park, IL); right ventricle: Supreme Quad, CRD, 4F (Abbott
Laboratories); His bundle: HIS CRD2 Supreme (Abbott Laboratories). EP study showed
evidence of dual AV nodal physiology and the patient was inducible for typical AVNRT.
A “DF” curved nonirrigated 4-mm-tip ablation catheter (Navistar EZ Steer, Biosense
Webster, Inc, Diamond Bar, CA) was advanced to the area of the rightward inferior
extension of the slow pathway under electroanatomic guidance (CARTO; Biosense Webster,
Inc) through a sheath (8F, SEPT; Abbott Laboratories).
The CSO was defined by a combination of electroanatomic mapping using the ablation
catheter, fluoroscopy, near-field atrial electrogram (usually similar or larger amplitude
than ventricular signal) and 10 Ω rises in impedance from the baseline. Ablation was
performed with a nonirrigated catheter (50 watts, temperature limit 60°C), and this
was used for all ablation lesions that are depicted in Figure 1A. Individual lesion
characteristics are outlined in Table 1. Breath-hold was utilized for all ablation
lesions to avoid respirophasic catheter movement, and there were no appreciable steam
pops with any of the lesions. Initial ablation lesions were delivered in the inferior
portion of the triangle of Koch (set 1 in Figure 1A) without inducing junctional ectopy.
After a few short test lesions in the region indicated by set 3, additional lesions
were delivered in an area that was felt to be anterior to the CSO (set 2 in Figure 1A);
these lesions were also prematurely terminated owing to impedance rises (>10 Ω) or
lack of junctional beats seen. Final ablation lesions were again delivered more anterior
to the CSO area, which resulted in junctional beats (set 3 in Figure 1A) and the endpoint
of noninducibility.
Figure 1
A: Electroanatomic views in right anterior oblique (RAO) and left lateral (LL) orientation
showing the different sets of ablation lesions delivered, and relationship to His
bundle area. The red solid arrow indicates the culprit lesion following which ST changes
were seen. The yellow dashed lines mark the anterior and posterior borders of the
triangle of Koch. The green dotted line shows the possible outline of a funnel-shaped
coronary sinus ostium, indicating that the ablation lesion could have been within
the ostium. HB = His bundle; IVC = inferior vena cava; TV = tricuspid valve. B: Ventricular
fibrillation induced by R-on-T premature ventricular contraction (yellow arrow).
Table 1
Reported cases of coronary artery injury following slow pathway ablation of atrioventricular
nodal reentrant tachycardia
Case
Authors/year
Age (years)/ sex
Ablation catheter/ sheath
Recognition
Delay in diagnosis?
Angiographic finding
Treatment
1
Blaufox et al/ 2004
2.5/ male
Unknown
ST elevation during reinduction post ablation
Yes
80% stenosis of the right posterolateral branch
Intracoronary nitroglycerinIntravenous nitroglycerin, heparin, and solumedrolStenosis
<50% in 48 hours, resolved in 12 months
2
Garabelli et al/ 2015
17/ male
Magnetic navigation catheter / SRO sheath
ST elevation after catheter fell to middle cardiac vein
No
100% stenosis of right posterolateral branch
Percutaneous coronary intervention with bare metal stent
Following this, isoproterenol (10 mcg intravenous bolus) was administered, and testing
was repeated with abolition of AH jump. Approximately 4 minutes after isoproterenol
administration, the patient developed spontaneous VF from an R-on-T premature ventricular
contraction (Figure 1B), requiring defibrillation. This rather unusual finding raised
suspicion for CA injury, and review of the surface 12-lead electrocardiogram (EGC)
at a 25 mm/s sweep speed showed precordial ST-segment depression (Figure 2A, red arrows)
with subtle elevation in the inferior leads (Figure 2A, red arrowheads) after 1 of
the ablation lesions (Figure 1A, red arrows). The 12-lead ECG during the entire ablation
lesion as well as a plot of biophysical parameters during this ablation lesion are
shown in Supplemental Figure S1; there was a gradual increase in impedance of >10
Ω, after which ablation was terminated. These subtle ECG changes post ablation were
not evident on 200 mm/s sweep speed that is used during EP study and ablation (Figure 2B
and C). Emergent coronary angiography was performed with a JR4 guide catheter, which
revealed complete occlusion of the right posterolateral branch of the right CA (Figure 3A
and D). Intracoronary nitroglycerin and verapamil were administered through the guide
catheter, without improvement in appearance or flow. Percutaneous transluminal coronary
angioplasty (PTCA) was performed, which resulted in flow restoration. However, there
was residual stenosis followed by complete reocclusion resulting in ST changes and
another episode of VF requiring defibrillation. Repeat PTCA was attempted, with administration
of additional vasodilators; however, the vessel continued to occlude, suggesting extrinsic
compression from myocardial edema or direct thermal injury to the artery. Coronary
stenting was performed with a Xience Alpine 2.25/15 drug eluting stent (Abbott Laboratories),
with successful resolution of ST changes and TIMI 3 flow with good myocardial blush
(Figure 3B and E).
Figure 2
A: Electrocardiogram at low sweep speed (25 mm/s) showing worsening ST changes during
ablation, including ST depression (red arrows) in the precordial leads and subtle
ST elevation (red arrowheads) in the inferior leads. These changes (highlighted area
with white arrow) were less apparent on the higher sweep speed with limited precordial
leads (B) when compared to the ST segment prior to ablation (C).
Figure 3
Left anterior oblique 60° (A–C) and right anterior oblique 30° (D–F) fluoroscopic
images showing coronary occlusion (A and D, yellow arrows), restoration of flow post
percutaneous coronary intervention (B and E), and manual overlay of ablation lesions
from electroanatomic map on fluoroscopic image using ablation catheter as a reference
(C and F, occlusion site: yellow arrow; culprit lesion: white arrow; red dots: ablation
lesions; purple dot: reference for catheter tip on electroanatomic map to allow manual
overlay).
The patient was placed on weight-based dual antiplatelet therapy with aspirin and
clopidogrel. Echocardiogram performed on the following day showed preserved left ventricular
ejection fraction without wall motion abnormalities. The patient has remained arrhythmia
free 1 year after the procedure and the clopidogrel was discontinued without further
events.
Since the center did not have software that automatically combines fluoroscopic images
with electroanatomic maps, we planned to perform a manual overlay after the procedure
was completed to understand the relationship between the ablation lesion and the site
of occlusion. For this purpose, after the initial diagnostic angiogram, while awaiting
the interventional cardiologist, the ablation catheter was placed close to the occlusion
site using both right and left anterior oblique views on fluoroscopy to use as a reference.
Manual overlay was performed using PowerPoint (Microsoft Office; Microsoft Corp, Redmond,
WA) at a later stage in an attempt to show the relationship between the site of occlusion
and the culprit lesion (Figure 3C and F). The exact distance between these 2 sites,
however, could not be determined owing to limitations with performing a manual overlay
of electroanatomic maps on fluoroscopic images.
Discussion
We report a rare case of CA injury after slow pathway modification that was initially
missed owing to low clinical suspicion for this complication and limited precordial
leads displayed at high sweep speeds, as is routinely done during EP procedures. Spontaneous
VF seen after ablation prompted us to evaluate for this possibility, and the patient
was successfully managed with PTCA and stenting of the right posterolateral branch.
CA injury during SVT ablation is typically seen when targeting posteroparaseptal pathways
that are within the coronary sinus, including the middle cardiac vein.
2
However, other ablations are also commonly performed in close vicinity to coronary
vessels, and although a 5 mm safety distance is advisable during epicardial ablation,
multiple endocardial target sites violate this rule. Examples include cavotricuspid
isthmus and posterior right ventricular outflow tract ablation, where the right CA
and the left main CA can be close to the ablation site, respectively. The anterior-inferior
aspect of the CSO is yet another site commonly targeted for AVNRT ablation, and can
also be in close proximity (±2 m) to the posterolateral branch of the right CA with
right-dominant coronary circulation and left circumflex artery with left-dominant
coronary circulation.
3
Upon systematic review of literature, we identified 2 reported cases of CA stenosis
during ablation of AVNRT (Table 1).
4
,
5
One of these was a 2.5-year-old patient with a body weight of 15 kg, and the other
was a patient who underwent inadvertent ablation within the middle cardiac vein. To
the best of our knowledge, this is the first case of CA injury in an older, larger
child (weight 32 kg) where the ablation lesion appeared to be outside of the CSO,
as evidenced by electrogram characteristics (small atrial with large ventricular electrogram),
electroanatomic map defining the CSO, and impedance measurements (no significant increase
in baseline impedance at the site while creating the electroanatomic map). The possibility
of the ablation lesion being within a “funnel-shaped” CSO cannot be ruled out, as
high-density electroanatomic mapping as well as venography were not performed.
Acute CA occlusion after ablation may be due to several mechanisms, which include
coronary vasospasm, extrinsic compression from surrounding edema, spontaneous plaque
rupture or arterial dissection, and direct thermal injury to the artery causing arterial
wall edema and inflammation.
6
,
7
A delayed response has also been described, with the development of intimal hyperplasia
following medial necrosis and loss of intimal and elastic tissue.
8
In this young patient without coronary atherosclerotic disease, neither intracoronary
nitroglycerin nor verapamil relieved the occlusion, and the artery reoccluded shortly
after PTCA. The mechanism for occlusion was likely direct thermal injury, and flow
could only be restored after a stent scaffold. The apparent distance between the ablation
lesion and the site of occlusion could be related to the inability to perform a perfect
manual overlay of electroanatomic maps on fluoroscopic images (due to x-ray tube rotation,
different scales, cardiac cycle gating, or lack of high-density coronary sinus mapping)
in addition to proximal extension of radiofrequency energy–related thermal injury
and external compression from tissue edema.
The true os of the coronary sinus can be difficult to define with the usual techniques
used during ablation procedures (electroanatomic mapping, impedance changes, fluoroscopy,
and electrogram characteristics). At the time of ablation, it was felt that electroanatomic
mapping performed to define the CSO was sufficient. However, it is possible that more
detailed mapping would have revealed that the culprit ablation lesion was within a
“funnel-shaped” CSO (Figure 1A; dotted green line indicates possible outline of funnel-shaped
CS os), which has been described by CS venography.
9
This type of os would potentially not have the same impedance change and signal characteristics
as a non-funnel-shaped CSO, and could mislead electrophysiologists into thinking that
the catheter tip is outside the coronary sinus. Use of multielectrode catheters for
high-density mapping (instead of using an ablation catheter only) and coronary sinus
venography can be used to better delineate the true os in select cases; up-front CA
angiography prior to ablation should be considered only if ablation is being performed
at the CSO. If the distance between the CA and the slow pathway ablation site is <5
mm, an alternative ablation site should be chosen, or cryoenergy should be used. Lower
power (for, eg, 30 or 40 watts) can be considered in pediatric patients, especially
if the weight is <25 kg.
10
Incorporation of additional limb and precordial ECG leads in the standard intracardiac
electrogram page during ablation could help identify ST changes earlier at faster
sweep speeds. A review of 12-lead ECG at 25 mm/s sweep speed when ablation is performed
close to the CSO area is also a reasonable strategy to avoid any delay in diagnosis
of this potential complication.
Conclusion
In conclusion, we report a rare case of CA injury that occurred during ablation of
typical AVNRT manifesting as VF during isoproterenol testing after ablation. Knowledge
of regional anatomy is important to implement during routine ablations, and rapid
recognition of this complication can allow for life-saving intervention.
Key Teaching Points
•
The posterolateral branch of the right or left coronary artery can have a close relationship
to the coronary sinus ostium, and can be potentially damaged during slow pathway ablation
for atrioventricular nodal reentrant tachycardia.
•
Electrocardiographic ST-segment changes can be missed with limited precordial leads
displayed at a high sweep speed during typical electrophysiology study and ablation
procedures.
•
It is important to define the extent and morphology of the coronary sinus ostium with
high-density electroanatomic mapping, and in select cases venography, prior to performing
ablation.
•
In cases where potential target sites for ablation appear to be close to the coronary
sinus ostium, coronary angiography should be considered, especially in pediatric patients.