Treatment

1. PREMATURE
VENTRICULAR
CONTRACTION :
Treat it or Leave it
Dr. Ardian Rizal, SpJP
Arrhythmia and Electrophysiology Division
Cardiology and Vascular Medicine
Faculty of Medicine, Brawijaya University

2. Introduction

3. 40–75%
In General
Population
PVCs in Numbers
1.39
Male compared
to female
3.5%
incidence of
sustained
VT or SCD
Mostly
Only need
reassurance

4. Ventricular Arrhythmia
Clinical Spectrum
Asymptomatic and Benign
Frequent and Symptomatic
Sudden Cardiac Death
Heart Rhythm, Vol 11, No 10, October 2014
Reassurance
ICD and
Ablation

5. Ventricular Arrhythmia
Diagnosis Work UP
Structural heart disease ?
inherited and acquired cardiomyopathies?
myocardial ischemia ?
12 Lead ECG & Specific Morphology
Echocardiography
Holter Monitoring
Other imaging

6. Expert Consensus EHRA/HRS/APHRS
Diagnosis Work UP
• All patients should have a resting ECG and echocardiogram to detect underlying
heart disease including inherited and acquired cardiomyopathies. Especially in
patients in whom the arrhythmia morphology suggests such a specific etiology
(II a ; LOE B)
Heart Rhythm, Vol 11, No 10, October 2014
• A test for myocardial ischaemia should be considered in all patients with VAs in
whom the clinical presentation and/or the type of arrhythmia suggests the
presence of coronary artery disease. (II a ; LOE C)
• Prolonged ECG monitoring by Holter ECG, prolonged ECG event monitoring, or
implantable loop recorders should be considered when documentation of
further, potentially longer arrhythmias would change management. (II a ; LOE C)

7. First of All, Be sure that it is VT
Jenis Aritmia Insiden
Ventricular Tachycardia (VT) 80%
SVT dengan konduksi aberan
- RBBB atau LBBB sebelumnya
- BBB fungsional (mis : RBBB terkait takikardia)
15-20 %
SVT lainya :
- AVRT antidromik (mis : sindroma WPW)
- Atrial takikardia, flutter atau AVNRT dengan jalur asesoris (bystander)
- SVT dengan delay induksi intramiokard (hipertrofi, kardiomiopati, dan kelainan kongenital)
- SVT dan Intoksikasi obat (Anti aritmia kelas 1A, 1C amiodarone)
- SVT dan hiperkalemia
1-5 %
Irama pacu jantung ventrikel

8. Clinical Finding
VT lebih Mungkin SVT lebih Mungkin
Umur > 35 tahun Usia < 35 tahun
Adanya kelainan jantung struktural Kelainan jantung struktural tidak ada
PJK dan penyakit jantung iskemia Keluhan pertama muncul lebih lama(<3tahun)
CHF EKG sebelum SVT menunjukkan BBB
Kardiomiopati EKG sebelum SVT menunjukan adanya WPW
Riwayat keluarga (Brugada, LQTS atau ARVD) Riwayat SVT membaik dengan adenosisn atau vagal
maneuver

9. ECG Finding
VT lebih mungkin SVT lebih mungkin
EKG awal Infark, Brugada, ARVD Normal, WPW
Durasi QRS Lebih lebar (RBBB > 140 ms, LBBB > 160
ms)
Lebih sempit
Aksis QRS Deviasi aksis ekstrem (positif di AVR dan
negati di lead 1)
Aksis normal
Hubungan AV Rasio AV < 1
Disosiasi AV
Fussion beat, capture beat
Rasio AV ≥ 1
Konkordansi Konkordansi positif atau negatif Diskordans
Lead aVR Gelombang R atau q > 40 ms
Lain - lain Tanda Brugada
Tanda Josephson’s
RBBB dengan RSR’ dimana puncak kiri lebih
lebar
RBBB dengan RSR’ dimana puncak kanan
lebih lebar

11. AV dissociation is Always VT

14. Concordance
• Present of concordance strongly suggest VT (90% sensitivity)
• Absent is not helpful diagnostically (20% spesificity)
• Higher sensivity for positive compare to negative concordance
(95% vs 90%)

15. Negative concordance

16. Positive concordance

18. VT Classification

19. 10%
90%
VT Etiology
structurally normal heart
structural heart diasese
• Ischemic Cardiomyopathy
• Non – Ischemic Cardiomyopathy
• Hypertrophic Cardiomyopathy
• Arrhythmogenic Right
Ventricular Dysplasia
• Sarcoidosis
• Outflow Tract VT (80-90 %)
• ILVT
• Idiopathic Propanolol VT
• Cathecolaminergic Polymorphic
VT
• Inherited Channelopathies
(Brugada and Long QT
Syndrome)
SUPPLEMENT OF JAPI • APRIL 2007 •

20. VT/PVC in Structurally Normal Heart
SUPPLEMENT OF JAPI • APRIL 2007 •

21. Also called Idiopathic VT
Outflow tract VT (RVOT/LVOT) 90 %
Manifest at a relatively early age
Female  RVOT ; Male  LVOT
Symptoms :
• Most patients (48% to 80%) experience palpitations
• Presyncope and lightheadedness may also be observed
(28% to 50%)
• True syncope  rarely seen
VT / PVC in Structurally Normal
Heart
Huang et all, 2011
Am Heart J 1992; 124: 746

22. ECG Presentation
LBBB Type
Inferiror Axis

23. VT localization : General Principle
VT Localization: General ECG Principle
1. LV free wall VT shows RBBB
configuration, while VT
exiting from IVS or RV
displays LBBB configuration.
2. Septal exits are associated
with narrower QRS
consistent with synchronous
rather than sequential
ventricular activation.
3. Basal sites show positive
precordial concordance,
while negative concordance
is seen in apical sites of
origin.
8
 RBBB/LBBB morphology:
 RBBB: origin in the left ventricle
 LBBB: origin in the right ventricle
 Inferior/superior axis (lead II, III and
aVF):
 Inferior axis (positive in lead II, III and aVF):
origin superior wall
 Superior axis (negative in lead II, III and aVF):
origin inferior wall
 Basal/apical (lead V5-V6):
 Positive concordance in V5-6: basal origin
 Negative concordance in V5-6: apical origin

24. Differentiate LVOT and RVOT

25. Distinguish LVOT from RVOT : V2 transition ratio
• Measure R and S waves in V2 of SR QRS and PVC QRS
• Transition ration is (R/R+S) VT / (R/R+S) SR
Transition Ratio:
< 0.6 = RVOT
> 0,6 = LVOT
Betensky et al. JACC 2011

26. Transition of PVC and SR
PVC after SR = RVOT 100% PVC at/before SR = LVOT 71%
Betensky et al. JACC 2011

27. Diagnostic Algorithm for Outflow tract VT
Di
a
g
n
o
st
i
c
Al
g
o
r
i
t
With Lead V3 P
V2 Transition Ratio
Betensky et al. JACC 2011

30. • Reentry (Verapamil-sensitive)
• 3 Types :
• Left posterior type
(RBBB+LAD, common form)
• Left Anterior type
(RBBB+RAD, uncommon form)
• Left Upper Septal type
(Narrow QRS+IA, rare form)
Idiopathic Left Ventricular Tachycardia
(Fasicular VT)

31. Substrate and Anatomy
“Slow-Fast” Type “Fast-Slow” Type (Upper septal)
False Tendon or Fibromuscular band

32. Posterior Fasicular VT
RBBB morphology with Left axis deviation

33. Anterior Fasicular VT
RBBB morphology with Right axis deviation

34. • Narrow QRS complex (100 msec)
• R/S transition between V3-V4
• Inferior axis
Left Upper septal VT

35. Patophysiology

36. Patophysiology and Classification
Substrate
Trigger
Arrhythmia
Mechanism

37. Pathophysiology
Automaticity
Ectopic
Automatic
Focus
heightened
adrenergic
state
myocardial
ischemia
Acid-base
disorders
Sympathomi
metic agent
Anaerobic
glycolysis

38. Pathophysiology
Re - entry
• two parallel conducting pathways connected
proximally and distally
• reentrant circuits arise in areas in which normal
cardiac tissue becomes interspersed with patches of
fibrous (scar) tissue
• Such as after a myocardial infarction or with
cardiomyopathic diseases

40. Pathophysiology
Triggered activity
abnormal fluxes of positive ions
• Abnormal fluxes of positive ions into cardiac
cells
• Trigger the rapid sodium channels (which are
voltage dependent) and cause another
action potential to be generated
• triggered activity appears to be the dominant
mechanism in reperfusion injury

41. Substrate : Long QT Syndrome
Trigger : PVC
Arrhythmia Mechanism :
Triggered Activity

42. Management

43. PVC
Induced Cardiomyopathy
• Several studies have demonstrated an association
between PVCs and a potentially reversible
cardiomyopathy
• Risk predictors :
• high-frequency PVCs
• longer duration of PVCs
• epicardial or broad QRS complex PVCs
• interpolated PVCs
• male sex
Rev Esp Cardiol. 2016;69(4):365–369

44. Management of PVCs

45. • The first step is education of the benign nature of
this arrhythmia and reassurance
• The most common indication for treating PVCs
remains the presence of symptoms
• Medical tx :
• Beta – blocker and non-dihydropyridine calcium
antagonists
Treatment
In Structural Normal Heart

46. PVC/NSVT Management
in Normal Heart

47. PVC/NSVT Management
in Structural Heart Disease

48. Drug Therapy
for PVC/NSVT Supression

49. Catheter Ablation
• catheter ablation should only be considered for patients who are markedly symptomatic
with very frequent PVC
• Multiple studies indicate high efficacy of ablation with PVC elimination in 74 – 100% of
patients
• Procedural success may be dependent on site of origin and number of PVC morphology
• Although complete PVC elimination is the goal of ablation, it should be noted that partial
success may still be associated with significant improvement in LV systolic function
• Catheter ablation for idiopathic ventricular tachycardia For focal VT (esp RVOT VT) 
highly successful and carries low procedural risk

51. Management of SMVT

52. Intra Cardiac Defibrillator (ICD) Indications

53. Treatment
In Structural Heart : Ischemic VT
• ICD first
• most agree that ablation therapy is palliative
and adjunctive to ICD therapy
• The typical patient considered for VT
ablation has frequent VT episodes resulting
in multiple ICD shocks due to rapid VT
Huang et all, 2011
Am Heart J 1992; 124: 746