Idiopathic Ventricular

Arrhythmias
TO HUNG THUY
HUE CARDIOVASCULAR CENTER
Ventricular tachyarrhythmias
 Ventricular arhythmias
Arrhythmias that originate in the ventricular myocardium or His
Purkinje system include:
• Premature ventricular beats
• Ventricular tachycardia
• Ventricular fibrillation
Conduction through the ventricular myocardium is slower than
activation of the ventricles over the Purkinje system.
QRS wide, typically >0.12 s
 I.Mechanisms of VAs
• Reentrant
• Reentry circuit (fast and slow pathway) is confined to the ventricles and/or
bundle branches
• Automatic
• Automatic focus occurs within the ventricles
• Triggered activity
• Early afterdepolarizations (phase 3)
• Delayed afterdepolarizations (phase 4)
Reentrant
• Reentrant ventricular arrhythmias
• Premature ventricular complexes
• Idiopathic left ventricular tachycardia
• Bundle branch reentry
• Ventricular tachycardia and fibrillation when associated with chronic heart
disease:
• Previous myocardial infarction
• Cardiomyopathy
Automatic
• Automatic ventricular arrhythmias
• Premature ventricular complexes
• Ischemic ventricular tachycardia
• Ventricular tachycardia and fibrillation when associated with acute medical
conditions:
• Acute myocardial infarction or ischemia
• Electrolyte and acid-base disturbances, hypoxemia
• Increased sympathetic tone
Automaticity

Abnormal Acceleration of Phase 4

Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 16.

Triggered

Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 158.

 Different mechanisms of VAs

Focal Type Reentrant Type

Mapping and
Pace mapping, ablation
Activation map, VAs differ bytechnique,
Entrainment underlying
substrate
Unipolar electrogram morphology mapping, Electrogram
condition and tachycardia mechanism.
characteristics
Focal Ventricular Tachycardia
Reentrant Ventricular
Tachycardia
RVOT

Septum

LV apex

ICD Lead
Lin YJ et al. HRS abstract 2010
II.Manifestations of ventricular arrhythmias
 III.Classifications
I. ECG:
1. Monomorphic vs. Polymorphic
2. Sustained vs. non-sustained VT
• Sustained VT last at least 30 seconds
• Non-sustained VT last at least 6 beats but < 30 seconds more
commonly seen in structurally normal heart
II. Structural heart disease
Idiopathic vs. Abnormally structural heart
• 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.

• 10% of patients presenting with VT have no apparent structural

heart disease .
Klein LS et al Circulation 1992;85: 1666

• 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….

Premature Ventricular Contraction
• Premature ventricular ectopic beats arising in the diastolic period of
preceding sinus beat
• Unifocal
• Multifocal
• Ventricular Couplets
• Caused by electrical irritability: factors influencing
• Ischemia
• Electrolyte imbalances
• Drug intoxication
•
 PVCs : CLINICAL SIGNIFICANCE
• Bigeminy, trigeminy, couplet, triplet
• Three or more PVC's in a row (run of V-tach)
• They come close to or on top of a preceding T-wave (R on T)
• They are frequent (> 30% of complexes)
• PVC's come from different foci ("multifocal" or "multiformed")

May preclude the occurrence of :

• Ventricular Tachycardia
• Ventricular Fibrillation

“R on T phenomenon”

time

sinus beats V-tach Unconverted V-tach r V-fib

Ventricular couplets
IV.Idiopathic ventricular tachyarhthmias
Survival of VT Patients According to National
Mortality DataP=0.007
Base of Taiwan (up to 2011)
Fascicular VT

RV-VT

ARVC

Brugada,VF

CAD, DCM
PVC induced cardiomyopathy
• Frequent PVC can cause cardiomyopathy
• Chicken-egg dilenma
• Mechanisms:
• Dyssynchrony
• ↓ Ito IK1 current
• Change L-type Ca++ channel and
Ryanodine receptors
174 pts PVC, 57 pts EF↓. Correlation Improved EF post ablation
btwn PVC burden vs. EF
Topography
Continued..
How to Map
• Tools
• Surface ECG: origin, exit
• Pace mapping
• Activation time
• Entrainment technique: during VT,
• 3D activation and substrate mapping:
• Stable VT: NavX, Carto
• Unstable VT: Ensite Array, substrate map during sinus rhythm
• Location: RV, LV, and Epicardium
• ECG, substrate map, activation map
Specific Locations and ECG Features
Outflow Tract VT
RVOT Tachycardia
LVOT/Aortic Cusp Tachycardia
Epicardial Outflow Tract VT

Mechanism
triggered activity due to catecholamine-mediated delayed after-
depolarizations.This triggered activity results from a catecholamine-mediated
increase in cyclic adenosine monophosphate, with subsequent increase in
intracellular calcium from the sarcoplasmic reticulum, resulting in delayed after-
depolarizations and triggered activity. This underlying mechanism leads to
tachycardia initiation with catecholamines and termination with adenosine, -
blockers, or calcium channel blockers.
RVOT Tachycardia
most common IPVT-70%
LBBB/Inf axis
F>X2M
triggered by exercise or stress, and may also occur during hormonal
cycles in women
third to fifth decade of life
 C/F: palpitations/chest pain, fatigue, and presyncope or
syncope/isolated PVCs/nonsustained VT/sustained VT.
9/19/2017 HN Tim mạch Miền Trung Trung Tâm TM Huế
Tr hợp bn: Võ Văn Gia L.
Thường xuyên luyên cơn nhịp nhanh thất cơn ngắn
không bền bĩ
RF trước vách RVOT
24 h sau thủ thuật
Tr hợp bn : Nguyễn Minh L
RF vị trí đích
Trước và sau đốt sau 3 phút
Siêu âm
Siêu âm tim sau đốt
LVOT/Aortic Cusp Tachycardia
 10%-15% of IPVT,M>F
 Anatomy
Noncoronary cusp does not directly contact ventricular myocardium,
ventricular arrhythmias are rare.
The base of the left and right coronary cusps lies in direct contact to the
ventricular myocardium, and LV muscle fibers may extend into the aortic
root,serving as a source of these PVCs. These extensions may be a remnant
from embryonic development, and these myocardial fibers persist providing
an arrhythmogenic substrate. When mapping more inferiorly in the aortic
root, successful ablation may be related to necrosis of ventricular myocytes
arising from the most superior portion of the ostium of the LV.
ECG classification of RVOT-VT versus
LVOT/aortic cusp VT
Chuyển tiếp trước V3

9/19/2017 HN Tim mạch Miền Trung Trung Tâm TM Huế

 Tr. T. Yen L Đỗ Tấn V.

ParaHis PA

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Trần Thị Thu T. SoV PVC Lê Thị N. 80t SoV L

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Lê Thị N. 80 yrs

Prior abl Post abl

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Fascicular VT
 Idiopathic left fascicular VT= fascicular VT=LBB-ANT/POST
 ECG classify to left posterior fascicular VT, left anterior fascicular VT,
and left upper septal VT.
 LPFVT- most common then LAFVT & septal is rare
 young male(60%)- 15 and 40 years, younger female.
 paroxysmal
 Exertion.
 Symptoms – palpitations/syncope /tachycardia-mediated
cardiomyopathy .
IFVT
Zipes’ triad
 RBBB/LAD/ VT induced by atria pacing.
 Verapamil sensitive
 tachycardia originates from the Purkinje network of the
 mechanism of verapamil-sensitive left VT is reentry/induced,
entrained, and terminated by ventricular or atrial stimulation. The
proposed reentrant circuit consists of an area of slow conduction
that forms the orthodromic limb in the LV septum from base to
apex, with the retrograde limb using the Purkinje network
 false tendons is arrythmogenic.
ECG Characteristics
 RBBB/left superior axis pattern/narrow/confused for SVT
LPFT - RBBB and left axis deviation(LAFB)
• LAFT-RBBB/RAD(LFBB)
 septal VT demonstrates an incomplete
RBBB and normal axis.
Management
Excellent prognosis
Medical Therapy
Intravenous verapamil is effective for acute termination. Chronic oral verapamil therapy is
often an effective regimen for patients with symptoms who do not wish to pursue
catheter ablation.-adrenergic blockers have also been used with some success.
Catheter Ablation: successful-90%,
Trường hợp 1
• Bn Nguyễn Văn Y. 48 tuổi
• Vv: VT storm 5 lần schock điện dù xylocain , Amiodaron IV.
• H/o:
• Bệnh cơ tim dãn QRS rộng có VT → CRT –D
• Nhiều lần shock chuyển nhịp ( kiểm tra máy)
• Nhiều lần nhập viện >5 lần/năm
• Chuyển viện TT TM Huế
HA 70/40 mmHg
RBBB S@V6 neg inf leads
Siêu âm tim
Thăm dò ĐSL
Điều trị RF
Vị trí đích
→ nhịp xoang có block nhĩ thất thoáng qua
Điện tâm đồ sau đốt
Theo dõi 5 ngày sau đốt
Diastolic potential & Purkinje potential
Lê Thị N. 80 yrs

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9/19/2017 Hue CV Centre 13th National Congress of Cardiology 71

Papillary Muscle VT
 2008, Doppalapudi et al. first to report idiopathic VT from posterior PM
 Posterior papillary muscle origin is more common.
Papillary muscle VT is usually exercise induced and is catecholamine
sensitive, requiring isoproterenol or epinephrine for induction
 mechanism is typically focal in nature and not reentrant. This VT cannot
be entrained, and has a lack of late potentials at the site of ablation.
 Papillary muscle VT often exhibits multiple QRS morphologies, with
subtle changes seen spontaneously or during ablation. These subtle
morphologic changes are thought to be from preferential conduction to
different exit sites or multiple regions of origins within the complex
structure of the papillary muscles.
 RFA-quite usuful.
Mitral Annular VT
 majority from anterior mitral annulus
ECG in MAVT:RBBB pattern/ monophasic R or Rs in leads V2-V6.
Catheter ablation is highly successful with ablation delivered at the
site of earliest ventricular activation or sites with a 12/12 pace-map
match by mostly endocardial approach or coronary venous
system(GCV)
Lê Thị N. 80 yrs

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9/19/2017 Hue CV Centre 13th National Congress of Cardiology 74

Tricuspid Annular VT
 8% of IPVT
 5% of right-sided VT
 Septal sites > free-wall sites
 septal locations-anteroseptal or para-Hisian.
 ECG: A positive component (any r or R) was recorded in lead aVL in 95% of patients
 QRS duration and Q-wave amplitude V1-V3 were greater in VT/PVCs arising from the
free wall of the tricuspid annulus compared with the septum. Notching of the QRS
complex was seen more often in free-wall sites, as well as later precordial transition. A
Q-wave in lead V1 was observed more often in septal tricuspid annular VTs.
 RF catheter ablation successful for the free wall (90%) compared with the septal
(57%) group. Low success rate in the septal tricuspid annular group was thought to be
due to the likelihood of impairing AV nodal conduction with RF ablation.
 Arrhythmogenic RV Dysplasia
 Cardiomyopathy begins in RV with poor contractile function
and dilatation, progresses to LV finally.
 Histology: RV muscle becomes replaced by adipose and
fibrous tissue.
 Arrhythmia: Re-entrant Type (scarring & late Potentials) with
LBBB type ECG;
 ECG: Diffuse T wave inversion over precordial leads, and
Epsilon Wave.
 Ablation: The effect of catheter ablation is temporizing, 1/3
epicardium, mostly reentry. Implanted cardioverter
defibrillator (ICD) is the only reliable therapy for sudden
cardiac death.
ECG of End stage ARVC
RVEF=10%, LVEF=15%
RV-VT, ARVC/D
Conclusions:
• Treatment of idiopathic VAs is effective.
• Preventing: arrhythmia induced cardiomyopathy
• Improving symtomps
• Effective enough with conventional RF ablation in majority of cases.
• 3D helpful in some difficult cases.
Chân thành cảm ơn quý Thầy Cô và quý đồng nghiệp.