Ventricular tachycardia can occur in structurally normal hearts. It is classified based on origin, morphology, response to exercise and drugs. Non-life threatening VT is often monomorphic and originates from sites like outflow tracts and fascicles. Outflow tract VT commonly originates from the right ventricular outflow tract. Other sites include the left ventricular outflow tract and aortic cusps. Treatment includes medications, ablation, and implantable cardioverter-defibrillators for more severe cases. Life-threatening VT is often polymorphic and associated with genetic ion channel disorders like long QT syndrome.

1. VENTRICULAR TACHYCARDIA IN
STRUCTURALLY NORMAL HEART
Dr Dharam Prakash Saran

2. 10% of patients presenting with VT have no apparent
structural heart disease .
If structural heart disease is absent, the prognosis in patients
with VT and PVCs is generally very good
Inherited VT–sudden cardiac death syndromes are an
exception….
Klein LS et al Circulation 1992;85: 1666

3. Absence of structural heart disease is usually suggested if
the ECG , echocardiogram, and CAG are normal
Miles WM J Cardiovasc Electrophysiol 2001;12:536.
Structural abnormalities can be identified by MRI, even if all
other test results are normal.
In addition, focal dysautonomia in the form of localized
sympathetic denervation has been reported in patients with
VT and no other obvious structural heart disease

4. CLASSIFICATIONS
Classified with respect to the
• Origin of VT ( RV- VT vs LV -VT)
• VT morphology (LBBB vs RBBB pattern)
• Response to exercise testing
• Response to pharmacological agents (Adenosine-sensitive VT vs
Verapamil sensitive VT vs propranolol-sensitive VT)
• Behavior of VT (repetitive salvos Vs sustained)
• Morphology (Monomorphic vs Polymorphic)

6. NON–LIFE-THREATENING
(TYPICALLY MONOMORPHIC)
Classified on basis of site of origin
Most common sites are ventricular outflow tracts and left
ventricular fascicles

7. Idiopathic left VT
Left posterior fascicle
Left anterior fascicle
High septal fascicle
Others
Mitral annulus
Tricuspid annulus
Papillary muscle
Perivascular epicardial
Outflow tract VT
Right ventricular outflow- 80%
Pulmonary artery
Left ventricular outflow-10%
NON–LIFE-THREATENING (TYPICALLY MONOMORPHIC)

8. OUTFLOW TRACT VT
Idiopathic VT originate most commonly in outflow tract area
Nearly 80% of which originate from RVOT
Other outflow tract sites are rare

9. •Phenotypes are a continuum of the same focal cellular
process
• Premature ventricular complexes (PVCs)
• Nonsustained,repetitive monomorphic VT(RMVT)
• Paroxysmal, exercise-induced sustained VT
•Considerable overlap observed among three phenotypes
•Ablating one phenotype at a discrete site eliminates other
two
•Signature characteristic of sustained RVOT and LVOT is
tachycardia termination by adenosine and verapamil
PHENOTYPES

10. RVOT is bounded by
pulmonary valve
superiorly and
superior aspect of
tricuspid apparatus
inferiorly
RVOT is leftward and
anterior to LVOT
ANATOMIC CORRELATES

11. LVOT is region of LV
between anterior cusp of
mitral valve and
ventricular septum
Muscular and fibrous
parts
Large of part of right and
some part of left aortic
sinuses of Valsalva overlie
muscular LVOT
Close proximity to AV
node and His bundle -
early activation in VT

12. Non-coronary cusp
and posterior aspect of
left coronary cusp are
continuous with
fibrous aortomitral
continuity
Explain lack of VT
related to the non-
coronary cusp

13. VT from aortic sinuses of Valsalva arise from muscular
extensions of the LVOT to areas above the base of the aortic
valve cusps

14. Localization of site of
VT origin can be
predicted using QRS
morphology on surface
ECG and anatomic
relationships help to
explain shared ECG
patterns and subtle
differences

15. LBBB and inferior axis
Right sided origin-
LBBB pattern with
transition from a small
r-wave to a large R-
wave at V3 to V4
OT site - inferior axis
RVOT VT

16. RVOT VT
Approximately 60% to 80% of idiopathic VTs arise from the
RVOT
More common in females
3rd to 5th decade of life
Two predominant clinical forms
• Nonsustained repetitive monomorphic VT (RMVT), alternating
with periods of sinus rhythm
• Paroxysmal exercise-induced sustained VT

17. CLINICAL FEATURES
Most patients present with palpitations
50% develop dizziness
Minority (10%) present with syncope.
Symptoms are related to frequent PVCs or NSVT.
Less commonly, paroxysmal sustained VT is precipitated by
exercise or emotional stress.
The clinical course is benign and prognosis is excellent
Sudden cardiac death is rare
Spontaneous remission of the VT occurs in 5% to 20%.

18. ECG IN RVOT VT
Sinus Rhythm- Usually normal. Up to 10% can have
complete or incomplete RBBB
Repetitive monomorphic VT
• frequent PVCs, couplets, and salvos of nonsustained VT,
• interrupted by brief periods of NSR
Paroxysmal exercise induced VT
• sustained episodes of VT precipitated by exercise or
emotional stress
Rate is frequently rapid but can be highly variable.

19. RMVT

20. SUSTAINED RVOT VT

21. RVOT LOCALIZATION:
FREE WALL VS SEPTAL
• QRS duration ≥ 140 msec
• QRS notching in inferior leads
• Lead V3 R/S ratio ≥ 1

22. RVOT LOCALIZATION
LEAD I: ANTERIOR(LEFT) VS POSTERIOR(RIGHT)

24. AMBULATORY
MONITORING
Ventricular ectopy typically occurs at a critical range of heart rates
A positive correlation between the sinus rate preceding the VT and
the VT duration
VT occurs in clusters
Most prevalent on waking and during the morning and later afternoon
hours.
 VT is extremely sensitive to autonomic influences, resulting in poor
day to day reproducibility

25. VT ARISING FROM THE PULMONARY ARTERY
(PAVT)
Thought to be from remnants of embryonic muscle sleeves that
have been noted in amphibian and mammalian outflow tract
Timmermans C, Circulation 2003;108:1960

26. •Larger R-wave amplitude in inferior leads
•Ratio of the Q-wave amplitude in avL/avR was larger in the
PA group

27. Atriofascicular fibers (Mahaim fibers)
AVRT using Rt-sided accessory pathway
VT after repair of TOF
ARVD
DIFFERENTIAL
DIAGNOSIS OF RVOT VT

28. LVOT VT
LBBB morphology with inferior
axis with small R-waves in V1
and early precordial transition
(R/S ≥ 1 by V2 or V3), QS or rS
in L I or
RBBB morphology with inferior
axis and presence of S-wave in
V6
Q wave amplitude in aVL is
typically more than or equal to
aVR,

29. For LVOT VT,
• Absence of an S wave in leads V5 or V6 suggests a
supravalvular location,
• Presence of such waves indicates an infravalvular location

30. AORTIC CUSP VT
Origin from the aortic cusp is strongly suggested by
• Longer duration and greater amplitude of the R wave in leads
V1 and V2
• (R/QRS duration more than 50% and R/S amplitude more
than 30%) as compared with VT originating from the RVOT
because the aortic valve lies to the right and posterior to the
RVOT

31. Depending on site of
origin from right or left
coronary cusp-LBBB or
RBBB morphology
AORTIC CUSP VT
LBBB morphology with transition by V3, tall
R waves in the inferior leads, and an s
wave in lead I suggest the VPC from left
coronary cusp.

32. RVOT VT Vs aortic cusp VT
R wave duration and R/S wave
amplitude ratio in leads V1
and V2 were greater in
tachycardias originating from
cusp compared with RVOT
Precordial lead transition
earlier in cusp VT occurring
before lead V3

33. Proximity of RCC to RVOT- ECG based differentiating algorithms
may not be consistently accurate
Must be based on the earliest intracardiac activation or on pace
mapping

34. ELECTROPHYSIOLOGIC
MECHANISM
Outflow tract VT is due to triggered activity
Secondary to cyclic AMP mediated DAD
Example-Exertion results in increased cyclic AMP due to beta
receptor stimulation
Release of calcium from sarcoplasmic reticulum and DAD
Mutations in signal transduction pathways involving cAMP
may be etiology for VT in some patients
Tachycardia may terminate with Valsalva maneuvers,
adenosine, BB or CCB

35. CLINICAL FEATURES
20 and 40 years,Slight female preponderance
May be asymptomatic but often present with palpitations,
chest pain, dyspnea, presyncope and even syncope
Occur more frequently with exertion or emotional stress
Circadian variation- peaks at 7 AM and between 5 and 6 PM
Women-symptoms related to changes in hormonal status
Truly idiopathic OTVT is benign
Small percentage of patients with very frequent VT –TCM
Rare reports of cardiac arrest and PMVT

36. TREATMENT
May respond acutely to carotid sinus massage, Valsalva
maneuvers or intravenous adenosine or verapamil
Long-term oral therapy with either BB or CCB
Nonresponders (33%)- class I or III antiarrhythmic agents

37. RFA
When medical therapy is ineffective or not tolerated
High success rate (>80%)
Ablation of epicardial or aortic sinuses of Valsalva sites is
highly effective
Technically challenging and carries higher risks -proximity to
coronary arteries

38. Tachycardia localization
12-lead ECG
Intracardiac activation
Pace mapping

39. PACE MAPPING
Useful because typically site of origin is focal and because
underlying tissue is normal
Performed with a low output
Result in a small discrete area of depolarization
Mapping performed at site of origin of clinical arrhythmia,
ECG should mimic clinical arrhythmia perfectly (12/12,
including notches)

40. Predictors for successful ablation
Single VT morphology
Accurate pace maps

41. Some tachycardias arise from epicardium, necessitate
ablation from great cardiac vein or epicardium itself using
pericardial puncture technique
Coronary angiography is performed before ablation on
epicardium or in aortic sinus

42. Complications during outflow tract VT ablation are rare
RBBB (1%)
Cardiac perforation
Damage to the coronary artery (LAD) - cusp region ablation
Overall recurrence rate is approximately 10%

43. IDIOPATHIC LEFT VT
Three varieties
left posterior fascicular VT -RBBB and LAD (90%)
left anterior fascicular VT -RBBB and RAD
high septal fascicular VT -relatively narrow QRS and normal axis

44. CHARACTERISTIC FEATURES
• Induction with atrial pacing;
• RBBB morphology with left axis deviation;
• Occurrence in patients without structural heart disease.
• Termination by verapamil.

45. CLINICAL FEATURES
• Between the ages of 15 to 40 years
• More commonly affects male.
• Symptoms include palpitations, fatigue, dyspnea, dizziness, and
presyncope
• Syncope and sudden death very rare
• Most of the episodes occur at rest
• Can be triggered by exercise and emotional stress.
• Tachycardia-induced cardiomyopathy has been described
• Spontaneous remission may occur with time

46. MECHANISM: THEORIES
• Microreentry circuit in the territory of the left posterior fascicle (LPF)
• Circuit is confined to the Purkinje system, which is insulated from
the underlying ventricular myocardium.
• False tendons or fibromuscular bands that extend from the
posteroinferior LV to the basal septum have also been implicated in
the anatomical substrate

47. ECG FEATURES
The resting ECG is usually normal.
Symmetrical, inferolateral T wave inversion can be present
after VT termination.
During VT -RBBB with left anterior fascicular (LAF) block
or, less commonly (5% to 10%), LPF block pattern
 R/S ratio >1 in V1 and V2
 Upper septal fasicular VT presents as RBBB, narrow QRS
complex and a normal frontal axis.

49. Upper septal form of LV VT
• Narrow QRS duration (100 msec)
• R/S transition between V3 and V4 on the ECG during VT
• Precordial QRS similar to sinus rythm

50. Long-term prognosis is very good
Patients who have incessant tachycardia may develop a
tachycardia related cardiomyopathy
Intravenous verapamil is effective in acutely terminating VT
Mild to moderate symptoms oral –verapamil
BB and class I and III antiarrhythmic agents useful in some
Medical therapy is often ineffective in patients who have
severe symptoms

51. ANNULAR VENTRICULAR TACHYCARDIAS
VTs arising from the mitral or tricuspid annulus account for between
4% and 7% of idiopathic VTs
Most often, they are of the repetitive monomorphic type
Behave similarly to outflow tract VT, both in prognosis and in drug
response
Are amenable to ablation

52. ANNULAR VT
Based on the chamber of origin this can be classified as :
• 1. VT arising from the mitral annulus (MAVT)
• 2. VT rising from the tricuspid annulus

53. Mechanism : appears to be triggered activity based on the response
to adenosine, verapamil, and the pacing maneuvers

54. MITRAL ANNULAR VT
RBBB pattern (transition in V1 or V2), S-wave in V6, and
monophasic R or Rs in leads V2-V6.
They further classified MAVT into three categories depending
on the site of origin:
1. Anterolateral (AL) MAVT (58%)
2. Posterior (Pos) MAVT (11%)
3. Posteroseptal (PS) MAVT (31%)

56. TRICUSPID ANNULAR VT
7% of the idiopathic VTs
Preferentially seen to originate from the septal region (78%)
than the free wall (22%)
Septal VT
• Commonly arise from anteroseptal region (72%)
• Early transition in precordial leads (V3)
• Narrower QRS complexes
• Qs in lead V1
• Absence of “notching” in the inferior leads

57. IDIOPATHIC PROPRANOLOL-
SENSITIVE VT (IPVT)
Usually occurs by fifth decade of life
Can arise from LV or RV
Morphology may be monomorphic or polymorphic
Not inducible with programmed stimulation
Isoproterenol infusion usually induces
Beta-blockers are effective in terminating tachycardia.

58. TREATMENT OF IPVT
BBs
Effective in acute situations
Insufficient information available regarding long-term
management.
Survivors of sudden cardiac death may receive ICD

60. REFERENCES
•Braunwald 9th edition
•Hurst 13th edition
•Ventricular tachycardia in structurally normal hearts:RECOGNITION AND
MANAGEMENT,P NATHANI supplement of JAPI • april 2007 • vol. 55
•Ventricular tachycardia in the absence of structural heart disease
komandoor srivathsan, md, IPEJ (issn 0972-6292), 5(2): 106-121 (2005)
•Ventricular arrhythmias in the absence of structural heart disease eric n.
Prystowsky, md, Vol. 59, no. 20, 2012 issn 0735-1097 jacc

61. T
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THANK YOU

62. LIFE-THREATENING
(TYPICALLY POLYMORPHIC VT)
Rare
Generally occurs with genetic ion channel disorders
Unlike monomorphic VT associated with SCD
Abnormalities exist at molecular level

63. Genetic syndromes
Long QT
Brugada Syndrome
CPVT
Short QT
LIFE-THREATENING
(TYPICALLY POLYMORPHIC VT)

64. LONG QT SYNDROME
Corrected QT interval 440 ms in men and 460 ms in women
with or without morphological abnormalities of the T waves
Decrease in outward potassium currents or increase in
inward sodium currents
Prolongs repolarization phase of cardiac action potential
Result in prolongation of QT interval
Predisposition to EAD and torsade de pointes VT

65. Twelve different genes described
LQT1, LQT2, and LQT3 account for 90%
LQT1 and LQT2 -mutations of KCNQ1 and KCNH2 genes that
encode subunits of IKs and Ikr potassium channels,
respectively
LQT3 -mutations of SCN5A gene that encode subunits of INa
sodium channels
Approximately 25% not have identifiable gene mutations

66. Mean age of symptom onset is 12 years
Present with syncope, seizures, or cardiac arrest.
Clinical presentation and ECG repolarization (ST-T) patterns
have been correlated to genotype

67. LQT1 -often have broad-based T waves and frequently
experience events during physical activity (especially
swimming).
LQT2- T-wave is often notched in multiple leads.
Triggers for LQT2 include startling auditory stimuli (e.g., from
an alarm clock) and emotional upset.
LQT3- often demonstrate long ST segments
Most LQT3 events occur at rest or sleep.

69. MANAGEMENT
Avoid trigger events and medications prolong QT interval
Risk stratification schemes based on degree of QT
prolongation, genotype, and sex
Corrected QT interval exceeding 500 ms poses a high risk for
cardiac events
Patients who have LQT2 and LQT3 may be at higher risk for
SCD compared with patients who have LQT1

70. BB are indicated for all patients with syncope and for
asymptomatic patients with significant QT prolongation
Role of BB in asymptomatic patients with normal or mildly
prolonged QT intervals remains uncertain.
BB are highly effective in LQT1, but less effective in other
LQTS
Role of BBs in LQT3 is not established.
Because LQT3 is a minority of all LQTS,symptomatic patients
who have not undergone genotyping should receive BBs

71. ICD are indicated for secondary prevention of cardiac arrest
and for patients with recurrent syncope despite BB therapy
Less defined therapies
Gene-specific therapy with mexiletine , flecainide , or
ranolazine for some LQT3 patients
PPI for bradycardia-dependent torsade depointes
Surgical left cardiac sympathetic denervation for recurrent
arrhythmias resistant to BB therapy
Catheter ablation of triggering PVCs-abolish recurrent VT/VF

72. BRUGADA SYNDROME
Characterized by coving ST-segment elevation in V1 to V3
2 mm in 2 of these 3 leads are diagnostic
Complete or incomplete RBBB pattern
Pattern can be spontaneously present or provoked by
sodium-channel– blocking agents such as
ajmaline,flecainide, or procainamide
Typical ECG pattern can be transient and may only be
detected during long-term ECG monitoring.

73. CLINICAL PRESENTATION
Syncope or cardiac arrest
Predominantly in men in third and fourth decade
Also been linked to SCD in young men in Southeast Asia and
has several local names,including Lai Tai (“died during
sleep”) in Thailand
Prone to atrial fibrillation and sinus node dysfunction

74. ELECTROPHYSIOLOGY
STUDY
Induction of VAs has inconsistent predictive value
Fragmented QRS interval -predict poor prognosis

75. TREATMENT
No well-validated preventive medical therapy
Patients who don’t have cardiac arrest risk stratified on the
basis of spontaneous ECG pattern and syncope
Lowdose quinidine may be used to treat frequent VAs in
patients who already have an ICD
Quinidine and isoproterenol may be useful in patients having
VT storms
Catheter ablation of triggering PVCs and ablation of RV
outflow epicardial musculature successful in abolishing
recurrent VT/VF in a small number of patients

76. ICD
ICD are effective in preventing SCD and are indicated for
cardiac arrest survivors
Major management dilemma arises in decision to place
prophylactically an ICD based on patient’s perceived risk of
SCD

77. Patients with spontaneous ECG pattern and syncope are at
high risk and ICD insertion is generally recommended for
primary prophylaxis
Asymptomatic patients with spontaneous ECG pattern are at
intermediate risk, and their best therapeutic options may
need to be individualized
Asymptomatic patients without spontaneous ECG pattern are
at low risk and may be followed up clinically
Family history of SCD and specific genotypes do not predict
events

78. 7 different genes involved
SCN5A gene mutations (BrS1) - loss of function of cardiac
sodium channel (NaV 1.5) account for majority of genotyped
cases
Typical Brugada syndrome ECG pattern- a positive genotype
is obtained only in 13%
BrS1 and LQT3 share SCN5A mutations
Overlapping phenotypes of Brugada syndrome and LQT3
have been reported

79. Disorder of myocardial
calcium homeostasis
Clinically manifested
as exertional syncope
and SCD due to
exercise induced VT
Often polymorphic or
bidirectional
CATECHOLAMINERGIC PMVT.

80. Autosomal dominant form involves mutation of cardiac
ryanodine receptor (RyR2 gene) in approximately 50% of
patients
Autosomal recessive form, accounting for only 3% to 5% of
genotyped cases-mutations of calsequestrin 2 gene (CASQ2)

81. Ryanodine receptor spans membrane of sarcoplasmic
reticulum and releases calcium triggered by calcium entry
into cell through L-type calcium channels
Calsequestrin is a protein that sequestrates calcium ions
within the sarcoplasmic reticulum
RyR2 and CASQ2 mutations cause intracellular calcium
overload and DAD -basis of arrhythmogenesis

82. Resting ECG is unremarkable
Typical VT patterns are reproducible with exercise or
catecholamine infusion
VAs typically appear during sinus tachycardia rates of 120
beats/min to 130 beats/min, with progressive frequency of
PVCs followed by bursts of polymorphic or bidirectional VT
Mean age for presentation with syncope is 7.8 4 years
Electrophysiology study is not helpful in risk stratification

83. Mainstay of medical management is BB therapy
46% may have recurrent events while receiving therapy
CCB may have limited effectiveness as adjunctive therapy
Flecainide blocks RyR2 receptor and shows promise as a
medical therapy

84. ICD insertion is appropriate for patients who had cardiac
arrest and with life-threatening VA despite maximal medical
therapy
Recurrent ICD shocks may occur and an initial shock with its
accompanying pain and anxiety may trigger further VAs
Surgical left cardiac sympathetic denervation -resistant
cases

85. SHORT QT SYNDROME
Rare disorder
characterized by short QT intervals of 300 to 320 ms.
Diagnostic criteria involving corrected QT interval, clinical
history, and genotyping
Syndrome is associated with SCD and atrial fibrillation
Patients may present early in childhood

86. Mutations leading to gain of function of 3 genes encoding
for repolarizing potassium currents (IKr, IKs, and IK1)

87. ICD implantation for secondary and primary prevention
Preliminary observations suggest quinidine might be useful

89. REFERENCES
•Braunwald 9th edition
•Hurst 13th edition
•Ventricular tachycardia in structurally normal hearts:RECOGNITION AND
MANAGEMENT,P NATHANI supplement of JAPI • april 2007 • vol. 55
•Ventricular tachycardia in the absence of structural heart disease
komandoor srivathsan, md, IPEJ (issn 0972-6292), 5(2): 106-121 (2005)
•Ventricular arrhythmias in the absence of structural heart disease eric n.
Prystowsky, md, Vol. 59, no. 20, 2012 issn 0735-1097 jacc

90. T
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91. MITRAL ANNULAR VT
ECG of ventricular complexes originating from mitral annulus
may show significant slurring of QRS complex onset resembling
a delta-wave
Regardless of where along circumference of mitral annulus VT
originates ECG shows RBBB pattern across precordium and an
S wave in lead V6.
More lateral site- more likely is the presence of S wave in lead I
and of notching in inferior leads
In contrast with other mitral annular sites, posterior focus will
have superior axis.

92. PVCs or VT also originate from RVOT along region of
tricuspid annulus
Most common site is para-Hisian
Characteristic ECG findings are
Inscription of an R wave in lead I and Avl
Relatively small R wave in inferior leads
QS wave in V1
Precordial transition in V2 to V4
Sites of successful ablation record an atrial and a
ventricular potential
TRICUSPID ANNULAR VT