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\begin{document}

\title{Don't Forget the Sinuses: an important site for some infarct-related VT}



\author[1]{Gregory E. Supple}%
\affil[1]{University of Pennsylvania}%


\vspace{-1em}



  
  \date{May 19, 2024}


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\selectlanguage{english}
\begin{abstract}
The aortic sinuses of Valsalva are an important ablation site in
non-ischemic substrates and in patients with idiopathic ventricular
arrhythmias. Siontis and colleagues have demonstrated that these sites
should also be considered for ablation in patients with infarct-related
inferior axis VT. Low voltage in the aortic sinuses of Valsalva or in
the sub-aortic region should prompt further evaluation of these regions
for ablation.%
\end{abstract}%



\sloppy


Title:

Don't Forget the Sinuses: an important site for some infarct-related VT

Author Name:

Gregory E. Supple, MD

Author Affiliations:

University of Pennsylvania Perelman School of Medicine, Philadelphia, PA

Corresponding author:

Gregory E. Supple, MD

Corresponding author contact information:

Email: gregory.supple@pennmedicine.upenn.edu

Phone: 215-615-3811

Fax: 215-662-2879

Address: Founders 9

3400 Spruce St.

Philadelphia, PA 19104

Funding: none

Disclosures: none

Subject terms:

VT ablation, aortic sinuses of Valsalva, ischemic cardiomyopathy

Keywords:

VT ablation, aortic sinuses of Valsalva, ischemic cardiomyopathy, aortic
cusps, ventricular tachycardia

Abstract:

The aortic sinuses of Valsalva are an important ablation site in
non-ischemic substrates and in patients with idiopathic ventricular
arrhythmias. Siontis and colleagues have demonstrated that these sites
should also be considered for ablation in patients with infarct-related
inferior axis VT. Low voltage in the aortic sinuses of Valsalva or in
the sub-aortic region should prompt further evaluation of these regions
for ablation.

Catheter ablation of ventricular tachycardia from the aortic sinuses of
Valsalva (SoV) has been performed for about 20 years. It has been
recognized as an important site to access both idiopathic ventricular
arrhythmias (VA) from the region of the outflow tracts and LV
summit\textsuperscript{1-3}, as well as myocardial substrate for
reentrant VA in patients with dilated non-ischemic cardiomyopathy (NICM)
and scarring in the basal septum and peri-aortic and mitral valve
regions\textsuperscript{4}. From within the aortic cusps, we may be
accessing myocardial extensions to the valvular
plane\textsuperscript{5}, or the adjacent myocardial tissue of the LV
ostium\textsuperscript{6}. While it is important to avoid injury to the
ostia of the coronary arteries and aortic cusps, we have learned that
ablation of the myocardial tissue can be performed safely through the
valve tissue without resulting in valvular dysfunction, and when the
ablation is performed in areas in close proximity to the myocardium,
this is typically a safe distance from the coronary arteries to avoid
damage---either in the base of the cusp, well below the ostium; or
higher in the commissures or junction of the cusps.

Ablation of idiopathic VA and non-ischemic substrate from within the SoV
has expanded over the years as we have learned to safely perform
ablation within these regions, supported by electroanatomic mapping and
intracardiac echocardiography to better visualize and understand the
relevant anatomy being targeted. While the sinuses have become a common
site of evaluation and ablation for idiopathic and non-ischemic
substrates, it has not previously been identified as a common site for
ablation of ventricular tachycardia in patients with infarct-related
ventricular tachycardia (VT). In this issue of the \emph{Journal of
Cardiovascular Electrophysiology} , Siontis and colleagues report on the
findings of a cohort of patients with ischemic cardiomyopathy and VT
ablated from the sinuses of Valsalva, comparing them to a cohort of
patients with idiopathic VT ablated from the sinuses as well as patients
with ischemic VT without VT originating from the
sinuses\textsuperscript{7}. This cohort represented patients from a
single referral center for VT ablation: 13 patients were identified
based on successful ablation of ventricular tachycardia from an aortic
sinus of Valsalva, from a series of 217 consecutive patients with
post-infarction VT undergoing ablation at their center between 2006 to
2018. These 13 patients were compared to two cohorts of randomly
selection patients with 1. idiopathic ventricular arrhythmias and 2.
infarct related VT without ablation performed in the sinuses of
Valsalva.

The study identified several notable findings. First, when compared to
their reference cohort of infarct-related VT ablation patients, the
patients with VT ablated from the SoV were more likely to present as
repeat ablation, suggesting that this important substrate may have been
missed during an initial VT ablation. During these procedures, these
patients also had a lower number of induced VTs which is unsurprising if
more of them were repeat ablations.

Second, the QRS morphology of the VT in the study group was frequently
different compared to the classic morphologies that have been described
to localize site of origin of idiopathic VT ablated from the sinuses of
Valsalva. This is likely due to a combination of factors: in the setting
of significant substrate, the VT isthmus is frequently a significant
distance from the exit, thereby generating a morphology that would be
predicted to be remote from the aortic cusps. Additionally, just as
significant scarring and substrate alters the normal sinus QRS
morphology, VT morphology can similarly be affected. These unexpected
morphologies may help explain why the SoV represent an underassessed
substrate in infarct-related VT patients. The morphologies of these VTs
are provided in the first figure in the article, and the authors suggest
based on their findings that with any inferior axis VT, mapping in the
SoV should be considered even when the precordial transition is later
than would be typically expected.

Third, some of these patients had infarct scar that was contiguous with
the subaortic valve region, but some had an isolated scar in this
region. Their second figure demonstrates an example of each type.
Similarly, while the median bipolar voltage in the SoV in patients with
idiopathic VA was 1.06 mV, in the infarct patients the median voltage
was 0.33 mV. While normal bipolar voltage range in the SoV has not been
previously reported in large series, these data suggest that while
normal may be lower than the standard \textgreater{}1.5 mV bipolar
voltage noted in normal ventricular myocardium, patients with scar or
substrate adjacent to the SoV still result in lower voltage than would
be seen in healthy patients.

An important question that remains to be answered is if the VT substrate
in these study patients is related to an infarct, or if this represents
a mixed cardiomyopathy with non-ischemic substrate responsible for these
VTs. Reports on the incidence of combined non-ischemic and ischemic
cardiomyopathy substrate are variable. A prior study from our center
identified 1.2\% (9 of 732) patients with prior infarction who had
non-ischemic substrate and VTs at the time of ablation. All these
patients had VT from basal peri-valvular substrate, however only 4 of
the 9 were from the LV outflow tract or SoV\textsuperscript{8}. In
distinction, some prior MRI imaging work has identified up to 19\%
prevalence of a nonischemic scar pattern in patients who had ischemic
cardiomyopathy\textsuperscript{9}. MRI and late gadolinium
enhancement-based series have previously been conducted to differentiate
between ischemic cardiomyopathy and NICM, and these studies have
reported up to 13\% prevalence of subendocardial and/or transmural scar
pattern in patients without coronary artery stenosis that was
indistinguishable from patients with CAD\textsuperscript{10,11}.
Alternatively, some patients with CAD may have mid-wall late gadolinium
enhancement consistent with NICM\textsuperscript{9,11}. Other studies
monitoring for development of ischemic disease in NICM identified 4\% of
139 patients over three years who developed MI or ischemic disease
requiring revascularization. These mixed results highlight the
challenges in understanding and identifying when patients may have both
ischemic and non-ischemic substrate responsible for ventricular
tachycardia.

In this study, the authors point out that the SoVs are known to have
vasculature (conus artery branches to the right SoV and early septal
perforators for the left) which may result in extension of infarction to
these regions, particularly when it is contiguous with other infarction
territory. Conversely, in patients with peri-annular substrate that is
distinct from the infarct scar, this may be more likely non-ischemic.
Unipolar voltage mapping in such cases may help determine if there are
more prominent abnormalities compared to bipolar mapping, which is often
suggestive of mid-myocardial scar (Figure 1).

Regardless of the cause of the substrate, Siontis and colleagues are to
be commended for this work which highlights an entity that may be
underrecognized for a small subset of patients with ischemic VT
undergoing ablation. While it is relatively straightforward to sample
voltage and pace from the SoV during ablation with retrograde aortic
access, this is more challenging if a transseptal approach is utilized.
Nonetheless, low voltage in the SoV or inferior axis VTs in ischemic
cardiomyopathy patients should prompt the electrophysiologist to
consider if ablation is warranted in the SoV. Pattern recognition of VT
morphology and substrate location often helps guide a VT ablation, and
this information should be added to the patterns we are watching for in
the electrophysiology lab.

Figure 1: Top, a patient with non-ischemic substrate and a small basal
septal bipolar scar (A), with much more prominent and diffuse unipolar
voltage abnormality of the entire LV septum (B); Bottom, a patient with
septal myocardial infarction and a unipolar voltage abnormality (C) that
closely mirrors the bipolar scar (D).\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

References

\begin{enumerate}
\tightlist
\item
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  tachycardia originating from the aortic sinus cusp:
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\item
  Kanagaratnam L, Tomassoni G, Schweikert R, et al. Ventricular
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\item
  Yamada T, McElderry HT, Doppalapudi H, et al. Idiopathic ventricular
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\item
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\item
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\item
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\item
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\item
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\item
  Soriano CJ, Ridocci F, Estornell J, et al. Noninvasive diagnosis of
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\item
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\end{enumerate}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-1/Figure-1}

\end{center}
\end{figure}

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