Title: Successful chemical ablation for intraventricular septal
ventricular tachycardia in a case with previous myocardial infarction
and stents in the left anterior descending artery stent. Alternative
approach to the septal branch.
Word count: 1888 (Full manuscript)
Authors:
Shin Hasegawa M.D. shinhasegawa721@gmail.com
Akimitsu Tanaka M.D. fallhoney9@hotmail.com
Yukihiro Uehara M.D. y.uehara0115@gmail.com
Hiroki Yabuta M.D. hi.ro.ro.children@gmail.com
Kazuo Kato M.D. Ph.D. kkato@fujita-hu.ac.jp
Affiliation:
Department of Cardiology, Nagoya Tokushukai General Hospital.
Corresponding author:
Kazuo Kato M.D.
Ph.D. kkato@fujita-hu.ac.jp
Address:
2-52, Kozoji-cho Kita, Kasugai, Aichi, Japan. 487-0016
Sources of Funding:
This research did not receive any specific grants from funding agencies
in the public, commercial, or not-for-profit sectors.
Disclosures:
None.
Data Availability Statement:
The data that support the findings of this study are available from the
corresponding author upon reasonable request.
Keywords:
ventricular tachycardia; trans-coronary ethanol ablation; previous
myocardial infarction; septal perforator; coronary computed tomography
angiography
Key clinical Message
Trans-coronary ethanol ablation for ventricular tachycardia originating
from the ventricular septum is effective, but there are cases with no
septal perforator from left anterior descending artery.
CT and angiography can reveal the optimal vessel.
Introduction
Arrhythmia-substrate-based radiofrequency (RF) catheter ablation (RFCA)
is an effective treatment for scar-related ventricular tachycardia (VT)
in patients with a previous myocardial infarction.1However, energy delivery to deep myocardial origins, such as the
ventricular septum, is challenging.
Trans-coronary ethanol ablation (TCEA) is one of an effective treatments
option for VT of deep myocardial origin, and its advantage in the
treatment of VT of septal origin has been widely reported; however, its
safety and efficacy have not yet been
established.2,3,4 This method requires the target
vessel to be in an appropriate location.5 Therefore,
TCEA becomes difficult if a stent has been implanted previously in the
culprit vessel. The following case describes a patient who developed VT
from the ventricular septum with previous myocardial infarction (MI),
which was treated with a stent implantation in the left anterior
descending branch (LAD). The VT of this patient seemed to be difficult
to treat with not only RFCA but also TCEA through the LAD. However, we
could identify the septal branch from the high lateral branch (HL), then
we could perform TCEA successfully through the HL.
We believe this would be the first case of the septal VT in which
chemical ablation of the ventricular septum could be successfully
performed even with stenting in the LAD after MI.
Case Presentation
A 64-year-old man with dyslipidemia experienced an acute myocardial
infarction in 2009 and underwent percutaneous coronary intervention
(PCI) at another hospital, where a drug-eluting stent (DES) was
implanted in the mid LAD. Subsequently, one DES was placed in the mid
right coronary artery, and two DESs were placed in the proximal left
coronary artery circumflex. DES was implanted for proximal LAD in our
hospital with an overlap with the previous stent because of unstable
angina pectoris in 2018.
In 2019, the patient visited our institution because he suddenly
developed chest pain during cycling. A 12-lead ECG showed sinus rhythm
(SR) and ventricular premature contraction (VPC) with a
right-bundle-branch-block (RBBB) waveform on the inferior axis. No de
novo lesions were observed on multidetector computed tomography and
coronary angiography (CAG), however, VT occurred occasionally in the
ward with symptoms similar to the chest pain as he felt before
admission. During VT, his vital signs were stable at 132/91 mmHg, and a
12-lead ECG showed 187 bpm with RBBB in the inferior axis. RFCA was
performed after informed consent was obtained for all procedures,
including TCEA that was approved by the review board of this institute.
The patient was heparinized at the start of the procedure, and activated
coagulation time was maintained for over 300 s. The three-dimensional
mapping system used was EnSite Precision (Abbott, St Paul, MN, USA).
Left ventricular (LV) potentials during SR were examined with the
Advisor HD grid mapping catheter (Abbott, St. Paul, MN, USA), and no
local abnormal ventricular activity (LAVA) was observed, however, a low
voltage area in the septum was observed. Programed stimulation elicited
a VT almost identical to clinical VT with earlier excitation of the
ventricular septal base. However, VT was not sustained and entrainment
pacing was not possible. The local ventricular potentials during VT from
both ventricles preceded 28 ms earlier than the body surface ECG. RF
energy was applied from the LV side, which was ineffective. The vessels
feeding the earliest VT site were examined using computed tomography
(CT) and CAG to find out the possibility of an origin from the
intramural ventricular septum. Although there was no septal perforator
from the LAD to the target region of the VT, a branch was observed from
the HL branch.
An angiographic catheter (6F SPB 3.75, ASAHI Intec, Tokyo, Japan) was
cannulated into the left coronary artery from the radial artery, and a
guidewire (0.014-inch Sionblue for coronary angioplasty, ASAHI Intec)
was used to inflate the balloon catheter (15-mm length Emerge
over-the-wire with a 1.25-mm nominal diameter for angioplasty, Boston,
MA, USA) at the target branch. Immediately after injection of the
contrast medium through over-the-wire lumen, the VPC disappeared, and VT
was no longer observed. We ensured that the injection of ice-cold saline
would not affect AV conduction after confirming the absence of shunting
and then injected 3 ml of dehydrated ethanol (98%) twice at 1 ml per
minute. The procedure was completed after it was determined that neither
VPCs nor VTs were induced. The patient was discharged after implanted
defibrillator, which revealed that there was no VT recurrence for the
next two years.
Discussion
Despite showing the RBBB morphology in this case, the earliest
activation sites were located at both of the RV base and the LV base,
suggesting that the VT might be originated from the ventricular septal
base. TCEA has been one of the alternative approaches for ventricular
arrhythmias (VA) originated from deep septal origin that can be hardly
treated by endocardial or epicardial RFCA6.7, most of
which has been performed in the septal branch diverging from the LAD.
However, in our case, two stents were placed in the LAD after PCI, and
there might not be an appropriate septal perforator for TCEA, but it
branched from the HL. But frequency of septal branching from other than
the LAD. Millar et al . reported a VT case associated with
nonischemic cardiomyopathy treated with ethanol injection into septal
branches from vessels other than the LAD,9 and the
frequency is reported as 10.0-14.7%.8 TCEA may be
feasible even in cases of deep septal-originated VAs with stents in the
LAD after PCI, if the culprit area would be fed by other artery from
other vessels as we could experience in this case. We had better search
for an optimal vessel using CT or CAG to achieve successful TCEA even in
case implanted stent to the culprit site.10
Further large clinical trials are needed to assess the success rate and
safety of chemical ablation in post-stenting VT cases.
However, this report has the following limitations. First, LV and RV
potentials were evaluated only in SR, and all of LAVAs in the LV and RV
were recorded in SR. Other arrhythmogenic insight may have obtained if
the ventricular activation sequence map would be obtained under right or
left ventricular pacing. Second, the contrast injection alone could
abolish the VPC, suggesting that the perfusion area might be culprit. We
chose the coated guidewire for its better lubricity and cross ability,
which unfortunately spoiled detecting the local information. If we would
use uncoated wire so as to record local potentials, we could obtain
further evidence for the culprit site.
Conclusion
TCEA might be effective in patients with VT originated from deep septal
lesions associated with previous MI with a stent implantation in the
LAD, if there are other septal feeding arteries to the VT origin than
the LAD. Detailed evaluation of the coronary arteries using CT and CAG
would be crucial for such patients requiring VT therapy originating from
deep septal origin.
Acknowledgments:
None.
Author contributions:
Shin Hasegawa performed the conception, design, and data collection.
Yukihiro Uehara, Akimitsu Tanaka, and Kazuo Kato collected the data.
References:
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Alkhouli M,
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Figure legends:
Figure 1:
(A) Left: 12-lead ECG during sinus rhythm (SR). right: 12-lead ECG
during ventricular tachycardia (VT). The patient had sustained
monomorphic VT with a right bundle branch block and wide QRS on the
inferior axis.
(B) Observation of the left ventricular (LV) endocardium with HD grid
during VT showed the earliest potentials at the base of the LV septum.
(C) During SR, the HD grid showed a low voltage area at the mid of the
LV septal endocardium.
Figure 2:
(A) Irrigation catheter placed in the left ventricle, and HD grid placed
in the right ventricle during ventricular tachycardia (VT).
(B) The earliest VT potentials were almost the same during the use of
the irrigation catheter and HD grid.
(C) Pacing stimulation was performed at the earliest VT site from the
left and right ventricles, and the morphology was more similar to VT in
the left ventricle.
(D) The RF energy was delivered in the left ventricular septal
endocardium during VT.
Figure 3:
Coronary computed tomography (CT; volume rendering) showing stents
implanted in the left coronary artery, Two stents were implanted in the
left anterior descending branch (LAD) in 2009 (a) and 2018 (b), and also
two stents were implanted in the left coronary artery circumflex (c,d).
(B) No vessels returns to the base of the ventricular septum from LAD
(red asterisk).
(C) Coronary CT shows the HL branch (yellow star) and LAD. The septal
perforator (white arrow) is seen at the base of the ventricular septum.
(D) Ethanol injection into the septal perforator. A guiding catheter was
canulated into the left coronary artery, and selective contrast was
performed on the septal perforator (white arrow) branching from the HL
branch (yellow star) with a microcatheter.
(E) The contrasts did not shunt (black arrow).
(F) Ventricular premature contractions were observed before ethanol
administration but were suppressed after ethanol administration.