Dr. Mehdirad comments
The stepwise approach to ventricular tachycardia (VT) originating from the left ventricular
(LV) summit (LVS) described by Vyas et al. emphasizes the importance of conducting
practical yet methodical mapping of the LVS structures and achieving successful ablation
in the great cardiac vein (GCV).
1
The majority of outflow tract (OT) arrhythmias originate from the anterior and superior
septal aspects of the right ventricular (RV) OT (RVOT) with an underlying mechanism
of triggered activity secondary to cyclic adenosine monophosphate–mediated delayed
after-depolarizations.
2
However, other origins, including the LV OT (LVOT), coronary cusps (CCs), and distal
coronary sinus (CS)—especially when R/S transition occurs at V3 or earlier—have been
described.
3,4
Because of the absence of structural heart disease in OT VTs, a 12-lead electrocardiogram
(ECG) is a useful modality by which to localize the area of VT/premature ventricular
complex (PVC) origin. Although rare, OT VTs can be associated with subtle structural
abnormalities (eg, aortic sinus of a valsalva aneurysm). The presence of multiple
VT morphologies (either seen clinically or induced in the electrophysiology laboratory)
or characterization as a re-entrant mechanism should raise concern that a complex
arrhythmogenic substrate is present and a greater level of technical difficulty during
ablation is more likely to be experienced.
5
A 12-lead ECG in the case presented by Vyas et al. had the characteristics of VTs/PVCs
originating from the GCV (an inferior axis and concordant R pattern in all precordial
leads served as diagnostic markers for an LVOT origin in the surface ECG and suggested
high ablation success via the GCV).
6
Distal (DGCV) VTs/PVCs share the following ECG features: inferior axis, R pattern
in all inferior leads, QS pattern in augmented vector left (aVL) and augmented vector
right (aVR) leads, a dominant rs or rS pattern in lead I, a monophasic R or Rs pattern
in all precordial leads, and a monophasic (positive concordance), transition occurring
earlier than V1.
7
The distinct ECG characteristics of VTs originating from the DGCV can help to differentiate
VTs originating from adjacent LV endocardium sites of origin.
7
In the presence of even subtle structural abnormalities, however, a 12-lead ECG may
not be helpful for localizing the origin of VT/PVC as even subtle structural abnormalities
may impact the typical ECG characteristics of VTs in normal hearts (e.g., RVOT or
LVS).
5
As a first step, an RV versus LV origin can be inferred by an early R-wave transition.
VTs/PVCs originating from the RVOT feature a QRS transition by V4. Septal RVOT sites
(left posteromedial aspect of the RVOT) exhibit narrower and taller R-waves in inferior
leads, QRS without notching, and an S-wave in lead I.
Early QRS transition by V1–V2 and a lack of S-waves in V5–V6 are seen in the CC origin.
Left CC (LCC) VTs/PVCs frequently exhibit a W- or M-pattern shape in V1. A downward
notch in V1 has been suggested as an origin at the right CC–LCC commissure.
8
In the case presented, RVOT activation mapping was not performed as a 12-lead ECG
showed a concordant R-pattern in all precordial leads, which was a marker for an LVOT
origin. As a result, LCC was mapped first where a good early signal was not found.
In addition, the corresponding unipolar mapping signal showed an initial positive
wave.
As expected, the GCV was the next structure indicated for mapping where, intuitively
(based on 12-lead ECG characteristics), the earliest activation time was 30 ms earlier
than the surface QRS with a distinct presystolic potential where ablation was successful.
The fact that the patient was in ongoing hemodynamically stable sustained VT made
both the mapping and ablation much easier to complete.
The LVS of the heart, nicknamed the “Bermuda Triangle” (BT) by some, is an area of
the myocardium located between the following three neighboring structures: the posterior
RVOT, the LCC, and the distal CS [ie, the origin of the GCV, the anterior interventricular
vein (AIV)].
9
This epicardial area is not easily accessible; the closer the focus of the VT/PVCs
is to the center of the LVS, the more difficult it is to successfully locate the focus
from any of the LVS borders. It is important to underscore that the RVOT is anterior
and “leftward” to the aortic root.
Currently, several approaches to ablate VTs/PVCs originating from the LVS/BT through
the RVOT (anteroseptal/posteroseptal) exist, including via the LCC, the LV myocardium
just beneath the LCC, the distal CS (GCV, AIV), the septal perforator vein, and a
percutaneous subxiphoid epicardial approach. Although these anatomical structures
are electrophysiologically accessible, there is a small area of the myocardium adjacent
to all of them that is not accessible. If ablation from conventional and commonly
approached structures (ie, RVOT, LCC, GCV) fails, then the percutaneous subxiphoid
epicardial approach may be considered as the next option. Although ablation through
the left atrial appendage where the ablation electrode is directed toward the left
LVS/BT may be considered, due to a high risk for perforation inherent with ablation
from the left atrial appendage, only rare case reports on this approach have been
published.
10
In addition to intramural thrombosis and cardiac tamponade, as the LVS is an area
surrounded by the left anterior descending (LAD) artery, the first septal perforating
branch, and the left circumflex artery, the most serious complication involved with
the ablation procedure is coronary artery injury. Integration of three-dimensional
electroanatomical mapping with coronary angiography during an LVS ablation procedure
is a new method with which real-time visualization of cardiac structures can be achieved.
11
Ali Mehdirad, md (ali.mehdirad@va.gov)1
1Chief of Medicine, Carl Vinson VA Medical Center, Dublin, GA, USA
Dr. Mehdirad reports no conflicts of interest for the published content.
References
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Dr. Hutchinson discusses
Vyas et al. report the case of a 57-year-old man with episodes of symptomatic wide
complex tachycardia (WCT) who underwent catheter ablation.
1
The approach to this patient should begin with a close examination of the spontaneous
WCT morphology to generate a differential diagnosis. This includes aberrant supraventricular
tachycardia, pre-excited tachycardia, and ventricular tachycardia (VT). In this case,
we have a right-bundle, right-inferior-axis tachycardia with precordial concordance.
Close examination of the patient’s sinus rhythm ECG (not shown in the case report)
is necessary to confirm the presence of baseline conduction abnormalities or ventricular
pre-excitation. The wide atypical right branch bundle block (RBBB) pattern shown would
be an unusual pattern of aberration. Given the appearance of this patient’s WCT, one
would anticipate early ventricular activation at the superior lateral mitral annulus.
Anterogradely conducting accessory pathways in this anatomical location may often
produce subtle degrees of pre-excitation due to competition with ventricular activation
over the His–Purkinje system. If there is any question regarding the presence of pre-excitation,
bedside vagal maneuvers or the administration of adenosine can readily unmask accessory
pathway conduction. There is clear evidence of 1:1 atrioventricular (AV) association
during the tachycardia presented in the upper panel of Vyas et al.’s
Figure 1
. The report is unclear whether this specific tracing was recorded during spontaneous
tachycardia or (as I suspect) during atrial overdrive pacing of tachycardia. In any
event, the demonstration of QRS fusion with atrial overdrive pacing during WCT strongly
suggests VT as the mechanism (see Vyas et al.’s
Figure 1
, lower panel). The VT mechanism may be focal or reentrant and tachycardias involving
the His–Purkinje system (eg, fascicular reentry) should be considered.
Although the morphology of this patient’s VT can certainly be present in normal hearts,
it should also raise the specter of an occult arrhythmogenic cardiomyopathy. Further
diagnostic testing may identify occult cardiomyopathic processes, particularly in
patients with sustained VT. A prior study performed cardiovascular magnetic resonance
(CMR) imaging in 46 consecutive patients presenting with presumed idiopathic ventricular
arrhythmias and reported structural abnormalities in 41% of patients with tachycardias
originating in the LV as compared with in 5% of patients with tachycardias originating
from the RV.
2
The presence of an arrhythmogenic cardiomyopathy poses important issues for ablation
planning in addition to its potential implications for subsequent sudden death risk
stratification. A prior study used CMR imaging to characterize substrate pattern in
19 patients with nonischemic LV cardiomyopathy and observed predominant inferior and
lateral involvement in 47% of cases.
3
Epicardial ablation was required to eliminate VT in five of the eight patients with
inferior and lateral substrate patterns. Pacemapping from the basal superior LV epicardium
produces an initial Q-wave in limb lead 1 and, thus, the presence of this finding
during spontaneous VT may suggest the need for a nonendocardial ablation approach.
4
Appropriate patient education is also essential for cases in which epicardial mapping
may be required.
One should approach the mapping of ventricular arrhythmias in a manner that facilitates
sampling of all potentially relevant areas. Presuming that this patient has idiopathic
VT, it seems to be originating near the superior lateral mitral valve annulus. Thus,
we should anticipate accessing the aortic sinuses, the LV endocardium, and the epicardium
via both the coronary venous system and, if needed, via a pericardial-access approach.
Dedicated arterial access is required for aortic root mapping and can often facilitate
easier access to the superior and lateral aspects of the mitral annulus than when
using a transseptal approach. One should place a multipolar catheter into the distal
CS, ideally with the distal poles located within the great cardiac vein. For summit
PVCs with a left bundle morphology, mapping of the AIV may be required. Using smaller
diagnostic catheters may facilitate sampling of these distal regions. Given the possibility
of arrhythmias involving the Purkinje system, placing a dedicated catheter in the
His position may be useful. Standard patient-related and perioperative considerations
for pericardial access should also be considered.
As discussed already, the presence of a QS complex in lead 1 of the spontaneous WCT
is not commonly seen with endocardial pacemaps from this region; thus, we should anticipate
the earliest activation to occur closer to the epicardium. As such, it is not surprising
that activation times obtained from the left CS and the LV endocardium were not presystolic
in this case. The LVS encompasses a triangular section of the LV epicardium subtended
by the LAD coronary artery septally and the circumflex coronary artery basally. The
summit is divided by the course of the coronary veins into inaccessible and accessible
regions. The latter is more relevant for the current patient given the ECG morphology.
5
The general approach in summit arrhythmias is to find the safest proximate site to
the target. This requires understanding the relevant anatomical relationships vis-à-vis
the coronary vasculature. Adopting the multipolar CS catheter to bracket the earliest
annular region is extremely useful. Failure to pass the multipolar catheter distally
is usually due to a tight Vieussens valve, which can be overcome with a dedicated
long introducer and guidewire. The information provided by the CS recordings is essential
to have in these cases and time spent to gather such is well worth the effort. Occasionally,
the coronary vein may provide an excellent ablation target on the basis of activation
and pacemapping, thus obviating the need for endocardial access at all. The current
case presentation highlights the electrogram characteristics that suggest proximity
of the CS recording site to the VT site of origin. Note the steep QS complex on the
local unipolar electrogram and the presence of a consistent early sharp potential
on the bipolar channel that precedes the unipolar onset. Whether this is a local CS
muscular potential is debatable. It would be nice to have seen a pacemap from the
earliest CS site; however, an imperfect match would not necessarily predict ablation
failure. Coronary angiography is essential to determine their proximity of the desired
CS ablation site. Ablation within the CS is challenging due to rapid impedance drops
that limit conventional energy titration schema. When CS ablation is not possible
due to the proximity to the coronary arteries, specific ECG criteria may predict success
with a percutaneous epicardial approach.
6
When the activation and pacemapping within the CS are less perfect, then sampling
of the LV endocardium is completed. The CS catheter provides an excellent fluoroscopic
or electroanatomical reference to begin targeted endocardial mapping. When the CS
and LV endocardium exhibit similar activation times, this often suggests an intramural
focus and ablation ideally should be initiated in the endocardium. In these cases,
the use of longer lesions with unipolar ablation is often necessary to suppress the
arrhythmia. The use of simultaneous unipolar or bipolar ablation in this region can
be considered in refractory cases; however, data supporting safety and efficacy are
limited at present.
7
Alcohol instillation is another consideration; however, its’ use is better studied
in arrhythmias originating within the septum in which small branches can be subselected
to limit collateral damage.
8
Overall, this case highlights the importance of using a systematic approach in evaluating
WCTs. One should consider pursuing adjunctive diagnostic testing in evaluating occult
cardiomyopathic processes as their presence may increase the level of procedural complexity.
Arrhythmias originating from the LV summit pose significant ablation challenges due
to the anatomical complexity and proximity to critical structures inherent with this
location. CS mapping is of critical importance in targeting summit arrhythmias as
it can provide activation and pacemapping data from an epicardial location and, in
selected cases, an attractive site for ablation.
Mathew D. Hutchinson, md, facc, fhrs (mathewhutchinson@shc.arizona.edu)1
1Sarver Heart Center, University of Arizona College of Medicine Tucson, Tucson, AZ,
USA
Dr. Hutchinson reports no conflicts of interest for the published content.
References
1.
Vyas
A
Lokhandwala
Y
Mahajan
A
Which way to the summit
J Innov Cardiac Rhythm Manage
2020
11
12
4313
4316
10.19102/icrm.2020.1101201
2.
Nucifora
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Dr. Gerstenfeld explains
Vyas et al. present an interesting case of a 57-year-old male with sustained idiopathic
VT originating from the region of the LVS, treated successfully with catheter ablation.
1
The patient presented with monomorphic VT requiring electrical cardioversion. Echocardiogram
and coronary angiogram findings were normal, suggesting the VT was idiopathic (ie,
not associated with scar or structural heart disease). Sustained monomorphic VT from
the LVS in a structurally normal heart is uncommon. Depending on the availability
of more advanced imaging modalities, one might consider performing CMR imaging with
delayed enhancement (DE-MRI) in such a patient. Subtle scarring not detected by echocardiography
might be detected by DE-MRI and could portend a worse prognosis. We don’t have an
example of a sinus rhythm 12-lead ECG or chest X-ray in this case; both would be important
to examine. Any evidence of conduction disease and/or hilar adenopathy could also
suggest a diagnosis of cardiac sarcoidosis, which would merit a cardiac positron-emission
tomography (PET) scan to identify active inflammation. While unlikely, the treatment
of cardiac sarcoidosis would be quite different from that for idiopathic VT.
In this case, the authors proceeded to perform catheter ablation without first trying
antiarrhythmic therapy. I think that this approach is perfectly reasonable. Electrophysiologic
study has the advantage of aiding in the diagnosis by excluding scar with voltage
mapping and potentially curing the VT in a young man with an apparently normal heart
and is considered guideline-directed first-line therapy.
2
The 12-lead ECG in this case has a morphology that is clearly VT, with a monophasic
R in V1, positive concordance across the precordium, and a QS pattern in lead I. There
is also an interesting cycle-length/morphology QRS alternans, which can sometimes
occur at rapid ventricular rates. The morphology clearly places the VT exit at the
superior mitral annular region and the QS in lead I should raise the suspicion of
an epicardial exit. This region at the superior aspect of the LV septum has been termed
the LV “summit” and can pose unique challenges for catheter ablation. The LVS is defined
as the superior most aspect of the LV septum, bounded by the bifurcation of the LAD
and circumflex coronary arteries (Figure 1). The LVS contains an inferior and lateral
portion that is often accessible by catheter ablation from the LV endocardium together
with a superior “inaccessible” portion that is more challenging to reach and which
may require more advanced approaches.
When approaching an LVS VT, we will typically start with a CS venogram and then position
a small multipolar microcatheter out the distal great coronary vein (GCV) into the
AIV to facilitate detailed mapping (Figure 2). Although these branches are often too
small in caliber to allow an ablation catheter to enter, they do allow one to approach
adjacent structures for catheter ablation, which may be efficacious. Examination of
the 12-lead ECG is also helpful. Abularach et al.
3
found that, when the aVL/aVR q-wave ratio was less than 1.45, the PVC/VT could often
be ablated from the left sinus of Valsalva as opposed to the GCV. In this case, the
aVL/aVR ratio (while difficult to measure on paper) appears to be greater than 1.45,
suggesting that ablation from the GCV might be necessary.
The authors appropriately began mapping in the left sinus of Valsalva (LSV) and found
a bipolar electrogram that is only slightly pre-QRS, with a small r-wave on the unipolar
recording suggesting exit from a site deep or adjacent to the catheter tip. The ablation
catheter tip in the authors’
Figure 2
appears to show the ablation catheter in the aortic root, interpreted as the left
sinus of Valsalva. In their Figure 3, the authors advance a 7-French ablation catheter
out of the GCV, where they find an earlier signal and QS unipolar signal that results
in successful ablation.
Several aspects of this case are worthy of discussion. Whenever possible, we always
prefer ablation from the aortic sinus over the GCV because of (1) the ability to deliver
higher power and (2) greater distance from the epicardial coronary arteries. Certainly,
the ECG and activation in the LSV suggest that ablation may not be effective in this
case. However, the use of intracardiac echocardiography, when available, can facilitate
confirmation of location and mapping in the aortic sinuses, which often need to be
extensively mapped as a separate cardiac chamber. If activation in the GCV and LSV
are similar or even if the GCV is slightly earlier than the LSV, we would usually
start with ablation in the LSV for the reasons stated. If ineffective, mapping of
adjacent sites in the LV or RV endocardium using the earliest electrode on the multipolar
microcatheter as a guide is undertaken, which may yield an effective site for ablation.
If none of these sites are suitable, then manipulation of the ablation catheter into
the GCV is reasonable. A CS venogram can help to determine the various branches and
whether they will accommodate a radiofrequency ablation catheter or not. Irrigated
ablation is almost always required in the GCV given its small caliber. Vyas et al.
describe using a 7-French irrigated ablation catheter, which is an advantage in their
particular case as the smallest irrigated ablation catheter available in the United
States is on an 8-French shaft, which may not allow mapping into small venous branches.
As the authors have noted, it is imperative to perform coronary angiography before
ablating in the GCV, as the coronary veins often run in parallel with the arterial
system. This is illustrated in the authors’ Figure 3, which demonstrates the catheter
tip quite close to the LAD coronary artery. The authors ablated with 20 W of power
in this location, which exemplifies the power limitations that exist when ablating
inside a small vein due to low blood flow. Sometimes, manually increasing the catheter
irrigation rate can permit higher delivered power. Would I have ablated at this location?
It is always difficult to ascertain catheter location on still images as compared
to examining moving cine views from multiple angles during a live case. Typically,
the catheter tip should be located greater than 5 mm from a coronary artery to avoid
injury, although this distance is somewhat empiric. In this case, I would certainly
have heightened concern. Assuming the catheter tip electrode is 4 mm in diameter,
it appears that it may be within 5 mm of a very proximal LAD and the tip is pointed
directly at the artery, which will maximize heating. Damage to this artery could have
catastrophic complications. If ablation were to be undertaken, I would certainly ask
for an interventional colleague to be standing by with images of the artery taken
before and after each ablation. In the end, one must weigh the benefits of successful
ablation against the risk of complications. In this patient who presented with sustained
monomorphic VT, an aggressive approach is certainly warranted. However, I would explore
all feasible LV locations, as described above, before ablating at this location. Epicardial
access has also been described for mapping and ablating LVOT arrhythmias, particularly
since the exit of this VT appears epicardial by ECG. We typically try to avoid routine
epicardial access in LVOT arrhythmias because of proximity to the coronary arteries
and a thick layer of epicardial fat in this location, which often precludes adequate
heating of the myocardium. Nevertheless, epicardial mapping can sometimes add to success
in this location. Other options that can be considered are use of a half-normal saline
irrigant from the earliest site in the LV endocardium to improve the lesion depth,
4
coronary wire mapping/ablation via the LAD,
5
or cryocatheter ablation in the GCV (which may be safer because the warm blood protects
the LAD in this context).
I congratulate the authors for their successful ablation of a difficult arrhythmia.
Such cases emphasize the importance of understanding the complex anatomy of the LVS
the biophysics of ablation, and the expertise of multipolar venous mapping.
Edward P Gerstenfeld, md (Edward.Gerstenfeld@ucsf.edu)1
1Section of Cardiac Electrophysiology, Department of Medicine, University of California,
San Francisco, CA, USA
Dr. Gerstenfeld reports no conflicts of interest for the published content.
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A
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A
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MEJ
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B
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KM
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Nguyen
DT
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A
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5.
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J
Diaz
JC
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