Ventricular tachycardia are difficult to understand. it is classified in to two types. 1. VT in structurally normal heart, 2. VT in heart with structural diseases. I have tried to simplify the VT in structurally normal heart, which may be helpful to many students and learners.

1. VENTRICULAR TACHYCARDIA
IN
STRUCTURALLY NORMAL HEART
Dr. Pruthvi Puwar
DNB Cardiology
Vijaya Hospital Chennai

2. WIDE COMPLEX TACHYCARDIA
 Definition
 Importance of History
 Clinical examination
 ECG features

3. DEFINITION
Wide QRS complex tachycardia is a rhythm with a rate of more than
100 b/m and QRS duration of more than 120 ms
VT (80%)
SVT (20%)

4.  VT-
 Non-sustained VT: three or more ventricular beats with a maximal
duration of 30 seconds.
 Sustained VT: a VT of more than 30 seconds duration (or less if
treated by electrocardioversion within 30 seconds).
 Monomorphic VT: all ventricular beats have the same configuration.
 Polymorphic VT: the ventricular beats have a changing configuration.
The RR interval is 180-600 ms
 Biphasic VT: a ventricular tachycardia with a QRS complex that
alternates from beat to beat.
 SVT- a tachycardia dependent on participation of structure at
or above bundle of His
 LBBB morphology- QRS > 12 msec. with prominent negative
deflection in V1
 RBBB morphology- QRS > 12 msec. with prominent positive
deflection in V1.

5. POINTS IN HISTORY DIAGNOSIS
H/O MI VT
H/O CHF VT
H/O ANGINA VT
Recurrent episodes SVT
Duration of illness >3 years SVT
Minimally symptomatic events including
palpitations and light headedness without
syncope
SVT
Each has a
PPV of 95%

6. PHYSICAL EXAMINATION
 Signs of AV dissociation favours VT
- varying intensity of S1
- variation of systolic BP
- hypotension
 Termination of WCT with maneuvers ~
carotid,vasalva,adenosine favours SVT

7. BRUGADA CRITERIA

8. OTHER ECG FINDINGS FAVOUR VT
 North - west QRS axis deviation i.e superior and rightward
minus 90 degree to 180 degree
 Negative or positive concordance of QRS complex in all
precordial leads
 AV dissociaton : Fusion beats, capture beats
 In LBBB, QRS duration >160 ms
 In RBBB,QRS duration > 140 ms
 Previous ECG show MI

9. RABBIT EAR IN RBBB PATTERN

10. POSITIVE CONCORDANCE

11. FUSION & CAPTURE BEATS
ECG strip shows series of ectopic beats (a run of Vtach; the ectopic rhythm)
followed by capture beats (normal configuration; the sinus rhythm) and then a
gradual merging of the capture beats into the ectopic beats.

12. New aVR algorithm
 Vereckei et al;Heart Rhythm 2008
 483 WCT (351 VT, 112 SVT, 20 preexcited tachycardia)
analysed
 Greater sensitivity for VT diagnosis than Brugada
algorithm(96.5% vs 89.2%, P .001)
 Greater specificity for diagnosing SVT compared with Brugad
criteria
András Vereckei, MD et al Heart Rhythm, Vol 5, No 1, January 2008

13. AVR ALGORITHM

14. If the distance traveled on the Y axis in the initial
40ms of the QRS complex is smaller than that
traveled in the terminal 40ms of the QRS complex, a
VT is much more likely

15. ULTRASIMPLE BRUGADA CRITERION: RW TO PEAK
TIME (RWPT)
 In 2010 Joseph Brugada et al. published a new
criterion to differentiate VT from SVT in wide
complex tachycardias: the R wave peak time in
Lead II [4].
 They suggest measuring the duration of onset of
the QRS to the first change in polarity (either nadir
Q or peak R) in lead II. If the RWPT is ≥ 50ms the
likelihood of a VT very high (positive likelihood ratio
34.8).

17. VT IN STRUCTURALLY NORMAL HEART:
 Idiopathic Ventricular tachycardia
 10% patients with VT
 Structural heart disease can be ruled out if - ECG,
ECHO and CAG are normal
 However , MRI can detect RVOT origin VT despite all
modalities being normal
 SPECT – single photon emission CT

18. IDIOPATHIC VT
 Subclassified based on several criterias: mechanism,
location, response to therapy
 OUTFLOW TRACT TACHYCARDIAS
 IDIOPATHIC LEFT VTs (ILVT)
 AUTOMATIC VTs

19.  RVOT VT (80-90% of VT)
 ILVT (idiopathic LV outflow tract)
 IPVT (idiopathic propranolol sensitive VT)
 CPVT (catecholaminergic polymorphic VT)
 Brugada Syndrome
 Long QT syndrome
VT IN STRUCTURALLY NORMAL HEART:
Inherited Ion-channelopathies
Taken from Supplement of JAPI , 2007

20. OUTFLOW TRACT TACHYCARDIA
 Account for most cases (80-90%)
 Outflow tract encompases RV region between pulm &
tricuspid valves; AND basal left ventricle (including
LVOT, aortic cusps)
 Most commonly presenting as VPCs, Monomorphic
nonsustained VT
 Sustained VT less common
 Ppt: Exercise, emotional stress, exercise testing,
menstrual cycles in female

21.  DAD mediated triggered activity
 Typically mediated by intracellular calcium overload
through increased intracellular cAMP
 This explains Sensitivity to beta-blockers, CCBs
MECHANISM
Lerman et al, Circulation 1995, 92

22. RVOT VT:
 RV monomorphic extrasystoles are considered benign
 This may progress to ARVD or RVOT VT, with MRI
evidence of functional/anatomical abnormality
 ECG: LBB morphology, inferior Axis, QRS transition in
V3/V4
 Common in females of 30-50 yr age
 Palpitation, presyncope, syncope (less common)
 Exercise or emotional stress
 Sudden death is rare

23.  Two phenotypic forms:
 Non-sustained repetitive monomorphic VT
 Paroxysmal exercise induced sustained VT
 Classification based on site of origin:
 Originating from pulmonary artery
 RV-end outflow tract
RVOT VT:

24. 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
RVOT VT

25. RVOT region can be divided
into nine regions
Anterior sites demonstrate
Q wave (Q or qR) in lead I
and QS in lead aVL
Posterior sites demonstrate
R wave in lead I and early
precordial transition (R> S in
V3)
Between anterior and
posterior locations typically
demonstrate a multiphasic
QRS morphology in lead I
JADONATH AND COLLEAGUES

26. Differentiation of septal
from free wall RVOT VT
RVOT VTs originating from
septum - taller,narrower
monophasic R waves in
inferior leads
Free wall RVOT VT-
typically broader QRS
(>140ms) and R wave
notching in inferior leads
Later transition in
precordial leads (>V4)
DIXIT AND COLLEAGUES

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

28. ECG during VT
shows
S wave in lead I
R-wave transition
in lead V1or
V2(Earlier precordial
transition zone)
More rightward
axes
Taller R waves in
inferior leads
LVOT VT –
- CLINICALLY SAME LIKE RVOT VT
- MECHANISM ALSO SAME
S wave in LI and R-wave transition in V1 suggest LVOT VT.
R:S amplitude ratio of 30% and R:QRS duration ratio of 50%
Presence of an S wave in leads V5 and V6 suggests an infravalvular
origin of the tachycardia.

29. May originate from supravalvular or
infravalvular endocardial region of
coronary cusp of aortic valve
Distinction is important –RF ablation
LVOT VT

30. 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
Absence of an S wave in V5 or
V6 -specificity of 88% for cusp
VT compared with RVOT VT
OUYANG AND COLLEAGUES

31. TREATMENT
• Usually benign course
• Good prognosis
1. May respond acutely to carotid sinus massage, Valsalva
maneuvers or intravenous adenosine or verapamil
2. Long-term oral therapy with either BB or CCB
3. Non-responders (33%)- class I or III antiarrhythmic
agents

32. RFA
1. When medical therapy is ineffective or not tolerated
2. High success rate (>80%)
3. Ablation of epicardial or aortic sinuses sites is highly
effective
4. Technically challenging and carries higher risks -
proximity to coronary arteries
5. Recurrence 10%

33. 15 to 40 years
More in men (60%)
Most occur at rest
Usually paroxysmal
Incessant forms
leading to TCM are
described
IDIOPATHIC LEFT VT

34. Re-entrant mechanism
Lower turnaround point is
toward the apex
Retrograde limb is formed
by Purkinje network
ELECTROPHYSIOLOGIC
MECHANISM

35. Baseline 12-lead ECG is normal in most patients
Exit near the area of the left posterior fascicle
RBBB + left superior frontal plane axis
Relatively narrow QRS duration (<140 msec)
RS interval <80 msec
Exit near the area of the left anterior fascicle
RBBB+ right frontal plane axis

36. 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

37. RFA
Associated with significant symptoms or who are intolerant
or resistant to medical therapy
Post ablation: 10% chances of recurrence (either ILVT or
RVOT-VT) of different morphology
Requires re-ablation

38. AUTOMATIC VENTRICULAR TACHYCARDIA
IPVT: PROPRANOLOL SENSITIVE
 A form of IVLT
 <50 yr, often ppt by exercise
 Can arise from anywhere within heart
 Unresponsive to Verapamil
 Beta blockers very effective in terminating VT
 Chances of SCD
 ICD recommended in survivors

39. AHA/ESC GUIDELINES RECOMMENDATIONS
FOR TREATMENT:
 Class IC: catheter ablation useful in drug refractory
and symptomatic pts or in pts who are intolerant to
longterm drug therapy
 Class IIa:
1. EP study reasonable for diagnosis in suspected outflow tract VT
(LOA: B)
2. BB/CCB can be useful for symptomatic VT arising from RVOT
(LOA: C)
3. ICD – can be effective therapy for sustained VT who are
receiving chronic drug therapy & who have reasonable
expected survival for more than 1yr (LOA:C)

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

41. Genetic syndromes
1. Long QT
2. Brugada Syndrome
3. CPVT
LIFE-THREATENING
(TYPICALLY POLYMORPHIC VT)

42. 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 torsade de pointes VT

43. Seven types, based on different genes involved
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

44. • 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
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.

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

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

48. • 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
• Surgical left cardiac sympathetic denervation for recurrent
arrhythmias resistant to BB therapy (class IIb, LOA-B)
• Catheter ablation of triggering PVCs-abolish recurrent VT/VF

49. 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.

50. 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

51. 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 (Class IC)
• 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

52. ROLE OF ICD
• ICD are effective in preventing SCD and are indicated for cardiac
arrest survivors (Class IC)
• Major management dilemma arises in decision to place
prophylactically an ICD based on patient’s perceived risk of SCD

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

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

55. • 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)
• RyR2 and CASQ2 mutations cause intracellular calcium
overload and DAD -basis of arrhythmogenesis

56. • 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 bidirectional VT
• Mean age for presentation with syncope is 7.8 - 4 years
• Electrophysiology study is not helpful in risk stratification

57. • 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

58. • 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

59. THANK YOU