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Ventricular
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Tachyarrhythmias
AmoleOjo, SinanTankut, TravisPrinzi,
andDavidT.Huang
Abstract
Ventricular tachyarrhythmias (VTAs) remain a signicant contributor to the morbidity and mortality of cardiology patients
population. Additionally, the incidence of VTAs are increasing
in our ICD population resulting in shocks that can have a detrimental impact on quality of life. Medications alone have limited efcacy on VTAs, and can be poorly tolerated due to their
side effects. The ever increasing burden and complexity of
these VTAs call for novel invasive approaches for denitive
treatment. Standard approaches to VT ablation such as entrainment and activation mapping remain crucial to identify the
critical isthmus as a target ablation site. However, in the past
decade there have been many advancements in pre- procedural
imaging, mapping technologies, and approaches to substrate
based ablation. Developments in techniques to epicardial ablations also allow for better procedural outcomes. Mechanical
circulatory support can now be utilized among tenuous patients
and allows for safer and more precise ablations. There are also
9
A. Ojo (*) · S. Tankut · T. Prinzi · D. T. Huang
University of Rochester Medical Center, Rochester, NY, USA
e-mail: Amole_Ojo@urmc.Rochester.edu
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
D. T. Huang et al. (eds.), Cardiac Electrophysiology in Clinical
Practice, In Clinical Practice,
https://doi.org/10.1007/978-3-031-41479-4_9
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non-invasive treatments for refractory VTAs not responsive to
medical therapy or amenable to catheter ablation. In this chapter, we review the different mechanisms of VTAs, medical
treatments, advancements in mapping technologies and
approaches to catheter ablation, and discuss non-invasive treatments for VTAs.
Keywords
Ventricular tachyarrhthmia · Ventricular tachycardia ·
Ventricular brillation · Electroanatomic mapping · Activation
mapping · Entrainment mapping · Catheter ablation · Epicardial
access · Substrate modication · Cardiac radioablation
A. Ojo et al.
Introduction
Ventricular tachyarrhythmias can present with a wide variety of
symptoms, including sudden cardiac death. There are several
causes of sustained arrhythmias that originate from the ventricles
and can have varying prognosis and therapy needs to be tailored
accordingly. Understanding critical aspects of ventricular arrhythmias such as initiating mechanisms, proper risk stratication and
response to medical and ablation therapies is critical in the proper
treatment of the patients with these conditions.
How Do Arrhythmias Start?
Electrical impulse normally travels through the heart chambers
in a very organized and uniform manner. However, disturbances
in how electrical signals are initiated or how they propagate
through the cardiac chamber can lead to the onset of arrhythmias. In general, there are three mechanisms of how arrhythmias
start. A common arrhythmia mechanism is impulse reentry.
Tissues may intrinsically exhibit multiple pathways (as in dual
atrioventricular nodal physiology, see “Chap. 3, SVT”) or
develop multiple pathways in the healing process (as in scars
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post myocardial infarction) through which the electrical signal
may travel. If these paths are associated with different conduction velocities and correspondingly different refractory periods,
the electrical signals can circle around in an “endless loop”
through these circuit paths. Conditions suitable for reentry
require the slower conducting pathway to have a shorter refractory period and the faster conducting pathway to have a longer
refractory period. Most ventricular tachycardias (VT), though
certainly not all, related to post myocardial infarction substrate
or cardiomyopathy are due to impulse reentry. Monomorphic
VT is often due to stable and xed circuits of reentry whereas
polymorphic VT can be due to unstable and meandering or even
multiple circuits of reentry. Another mechanism for arrhythmia
onset is due to triggered activity. Increased intracellular calcium
concentration due to heightened adrenergic stimulation (such as
exercise), initiates a cascade of reaction through activation of
stimulatory G proteins resulting in enhanced calcium entry
through the cellular calcium channels and calcium induced calcium release in the sarcoplasmic reticulum. This increase in the
intracellular calcium then may activate the sodium calcium
exchanger leading to abnormal sodium entry into the cell which
may trigger depolarization of the heart cell resulting in premature beats or even tachycardia [1]. Forms of normal heart idiopathic ventricular tachycardia associated with exercise, such as
one originating right ventricular outow tract, are often resulting from triggered activity. A third mechanism for arrhythmogenesis is enhanced automaticity, where cardiac muscle tissue
develops spontaneous electrical activity through abnormal depolarization during phase 4 of the action potential. These arrhythmias are usually referred as “automatic” tachycardia. Some
examples of these include variants of tachycardia related to diseased tissue where the baseline membrane potential may be
unstable. Typically, sources of tachycardia that are focal are due
to either triggered activity or enhanced automaticity.
The management of ventricular arrhythmias is thus complex
and quite variable, with this variance discussed in the following
segments. Our initial focus will be scar mediated VT (VT with an
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abnormal left ventricular ejection fraction [LVEF]) followed by
idiopathic PVC’s and less frequent forms of idiopathic ventricular
tachycardia (VT with a normal LVEF).
A. Ojo et al.
Electrocardiographic Evaluation ofVentricular
Arrhythmias
The rst and most important diagnostic tool remains the 12 lead
electrocardiogram during a wide QRS complex tachycardia.
Often the type of cardiomyopathy, location of scarring, and VT
exit can be estimated from the appearance of the tachycardia.
Multiple algorithms have been developed and studied for the electrocardiographic diagnosis of VT including the Brugada criteria
[2] and various individual lead (Lead II, AVR) [3, 4] analysis techniques all with good specicity and sensitivity for the identication of VT in distinction from supraventricular tachyarrhythmias
(SVT) with aberrancy. All these algorithms take advantage of the
initial forces of activation to distinguish VT from SVT.Tachycardia
of ventricular origin depolarized the myocardial muscles by cellto-cell contact and thus will have slower forces of activation represented by delayed or fragmented portions early in the QRS
signals. On the other hand, during SVT, even with aberrancy, the
heart muscles are activated via engaging the specialized conduction tissues and are generally associated with a more smooth and
rapid initial QRS signals. Of note, all of these algorithms are qualied and should be used with caution in patients with manifest
preexcitation (i.e., Wolff-Parkingson-White syndrome) or on antiarrhythmic medical therapy. Updated morphology criteria developed in recent years have more elegant and simplied algorithm
to decipher whether a wide complex tachycardia may be VT or
SVT with aberrancy. Inspecting the morphology of the initial
QRS signals in lead aVR can be used to suggest ventricular origin
of a wide complex tachycardia. As illustrated in Fig. 9.1, QRS
with slow or notched initial forces as well as those with unusual
axis all suggest a diagnosis of VT rather than SVT.Similarly, if
the duration of the QRS signal from the beginning of the onset to
the peak of the R wave in lead II measures to be greater or equal
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Fig. 9.1 Algorithm to determine VT vs. SVT with aberrancy as described by
Brugada etal. [2]
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to 50msec, then VT can be diagnosed with better than 95% condence (Figs.9.1, 9.2 and 9.3).
Once diagnosis is made that the arrhythmia is VT, the next step
is to determine the activation vector of the ventricle. As a simplistic
starting point, the bundle branch block appearance of the QRS
complex indicates the culprit chamber where the VT is originating
from. A left bundle branch block appearance indicates an RV or
septal LV VT while a right bundle branch appearance indicates an
LV VT origin. Taking this approach a step further, using the right
sided leads (V1, AVR), inferior leads (II/III/AVF), lateral leads (1/
AVL) and apical leads (V5/V6) one can identify where the VT is
coming from (negative QS vector) and going towards (positive RS
vector). Generally, biphasic QRS vectors mean that the origin is
somewhere in the middle of that individual vector, i.e. a biphasic
QRS vector in 1 and V1 likely indicate that the origin/exit site of
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A. Ojo et al.
Fig. 9.2 Algorithm to determine VT vs. SVT with aberrancy by criteria
developed in lead aVR [3]
the VT is in the septum and not on the right (RV, Q wave in V1) or
left (posterior LV, Q wave in 1). This approach is primarily useful
in reentrant VT’s and idiopathic PVC’s.
A close examination of the resting 12 lead ECG can also provide signicant clues as to the underlying process and likely culprit areas of myocardial scarring. The presence of Q waves in the
distribution of a coronary artery should indicate the presence of
scarring that will often play a critical role in sustaining
VT.Fragmentation (extra notching) of the surface QRS complex
in a similar distribution to a major coronary vessel and Q waves
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a
a
a
Fig. 9.3 Algorithm to determine VT vs. SVT by measuring the duration of
onset of QRS to the peak of R wave lead II (a - 12 lead ECG; b - lead II).
Signals measuring >50msec (top two panels) suggest VT whereas <50ms
suggest SVT with aberrancy [4]
b
b
b
often can provide a more sensitive indicator of myocardial scarring and may indicate the presence of epicardial scarring in that
region. There are also ECG criterias to help differentiate endocardial versus epicardial VT. The maximum deection index is a
ratio from the beginning of the QRS to the maximum deection
point to the total width of the QRS.If the ratio is ≥0.55, idiopathic
left ventricular VT was likely to be epicardial in origin [5]. Other
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A. Ojo et al.
published morphology criteria include q wave in lead I (QWLI)
and no q waves in inferior leads and interval criteria: pseudo-delta
wave ≥34ms, intrinsicoid deection time≥85ms, and shortest
RS complex ≥121ms.
For idiopathic VT’s such as RVOT and LVOT VT, the
appearance should be consistent with an outow origin (inferior axis, i.e., positive in the inferior leads II/III/AVF) with an
earlier precordial transition (V3 or less) indicating an LV origin and a later transition (V3 or later) indicating an RV origin.
Transition at V3 could represent either LV or RV origin. V2
transition ratio can help to distinguish LVOT origin from
RVOT origin in patients with lead V3 precordial transition. V2
transition ratio is calculated by computing the percentage
R-wave during VT (R/R +S)(VT) divided by the percentage
R-wave in sinus rhythm (R/R+S)(SR). In a study by Betensky
etal., a V(2) transition ratio≥0.60 predicted an LVOT origin
with 91% accuracy while a PVC precordial transition occurring later than the sinus rhythm transition excluded an LVOT
origin with 100% accuracy [6]. RV1-V3 transition ratio is
another criterion that can be used to distinguish LVOT from
RVOT origin in patients with lead V3 precordial transition.
RV1- V3 is dened as (RV1 + RV2 + RV3) PVC /
(RV1 + RV2 + RV3) SR (sinus rhythm). In the study by
Efremidis etal., a cut-off value of ≥0.9 predicting LVOT origin with 94% sensitivity and 73% specicity [7]. Idiopathic
VT utilizing the conduction system (bundle branch and fasicular reentry VT’s) are quite uncommon but do have characteristic features that should set them aside from VT associated with
structural heart disease. The VT is generally slower with a
typical bundle branch or fasicular block appearance during
tachycardia that is usually very similar to the appearance of the
baseline QRS complex at rest. Bundle branch and fasicular
reentry are usually associated with baseline conduction disease, including bundle branch block of either right or left and
prolonged AV or PR interval, with the absence of such on a
resting 12 lead ECG making them very unlikely to be the
mechanism for the VT.
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