Mechanisms and Management of Ventricular Tachycardia in Ischemic Cardiomyopathy

Dr Ranjith MP
Senior Resident
Department of Cardiology
Government Medical college
Kozhikode

Mechanisms of VT
VT arises distal to the bifurcation of the His bundle in
the specialized conduction system, ventricular muscle,
or combinations of both

Disorders of impulse formation
 Enhanced automaticity
 Triggered activity

 Disorders of impulse conduction
 Re-entry (circus movements)

Mechanisms of VT
Disorders of impulse formation

Enhanced automaticity
 Can occur in virtually all cardiac tissues
 Occurs due to increasing the rate of diastolic
depolarization or changing the threshold potential
 Can arise from cells that have reduced maximum
diastolic potentials, often at membrane potentials
positive to −50 mV

Mechanisms of VT

Automatic ventricular arrhythmias

 Premature ventricular complexes
 Ventricular tachycardia associated with:
 Acute myocardial infarction or ischemia
 Electrolyte and acid-base disturbances, hypoxemia
 Increased sympathetic tone

Mechanisms of VT

Triggered activity
Pause-dependent triggered activity
 Early afterdepolarization (phase 3)
 Polymorphic ventricular tachycardia

Catechol-dependent triggered activity
 Late afterdepolarizations (phase 4)
 Idiopathic right ventricular tachycardia

Mechanisms of VT

Triggered activity

Figure A :- Early
afterdepolarizations in
phase 3 of the AP

Figure B :- Late
afterdepolarizations seen
in late phase 3 or phase 4
of the AP

Mechanisms of VT
Disorders of impulse conduction
Re-entry (circus movements)
Electrical Impulse Cardiac
Conduction Tissue

Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

 Two distinct pathways that come together at beginning
and end to form a loop
 A unidirectional block in one of those pathways
 Slow conduction in the unblocked pathway

Mechanisms of VT
Premature Beat Impulse Cardiac
Repolarizing Tissue (long Conduction
refractory period)) Tissue


 An arrhythmia is triggered by a premature beat
 The fast conducting pathway is blocked because of its long
refractory period so the beat can only go down the slow
conducting pathway

Mechanisms of VT
Re-entry (circus movements)
Cardiac
Conduction Tissue


The wave of excitation from the premature beat arrives at the
distal end of the fast conducting pathway, which has now
recovered and therefore travels retrogradely (backwards) up the
fast pathway

Mechanisms of VT
Re-entry (circus movements) Cardiac
Conduction Tissue


 On arriving at the top of the fast pathway it finds the
slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit

Mechanisms of VT

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

Coronary Artery Disease

Dilated Cardiomyopathy

Bundle Branch Re-entry Ventricular Tachycardia

Arrhythmogenic Right Ventricular Cardiomyopathies

Hypertrophic Cardiomyopathy

After Surgery for Congenital Heart Disease

Healed MI is the most frequent clinical setting for the
development of sustained VT

The first episode of VT can occur years after infarct
healing

Clinical presentation- tolerated sustained VT to SCD

Incidence reduced from 3% to 1%

Focal activation by abnormal automaticity in the ischemic
border zone

a/c ischemia activates KATP channels causing an increase in
extracellular K along with acidosis and hypoxia in the cardiac
muscle

Minor increases in extracellular K depolarize the
myocardiocyte’s RMP , which can increase tissue excitability
in early phases of ischemia

Focal discharge by Ca overload & triggered activity in the
form of delayed or early after-depolarizations - not been
proven experimentally

Reentry is the mechanism underlying the VT associated with
healed or healing MI (>95%)
 The ability to reproducibly initiate and terminate VT with
programmed ventricular extrastimuli- the sine qua non of
reentry
 Induction of VT in coronary disease is stimulation site specific
 An inverse relationship of the extrastimulus coupling interval to
the onset of the first tachycardia beat is observed in many VTs

Important determinants of arrhythmia risk after MI
 The extent of myocardial necrosis
 Presence of septal involvement
 Degree of left ventricular dysfunction

Anatomic substrate – extensive scar

VT consistently arises from surviving myocytes within
extensive areas of infarction

 Conduction is slow & discontinuous, owing to fibrosis and
abnormalities in gap junction distribution & function

Electrophysiologic substrate for VT develops in the first 2
weeks after MI - remain indefinitely

Triggers – Acute ischemia
– Surges in the autonomic tone
– Heart failure

Once sustained monomorphic VT occurs, risk continues
indefinitely, even if acute ischemia & heart failure are
adequately controlled

Josep Brugada et al JACC Vol. 37, No. 2, 2001:529–33

Reentry – macro/ micro reentry

Repolarization of individual myocardial cells not
homogenous. Some cells excitable, some refractory

Sinus rhythm mapping in a patient with VT in the setting of extensive healed anterior
infarction. The map is color-coded to represent bipolar electrogram voltage: red (representing
dense scar) denotes = 0.5 mV, purple = 1.5 mV, and the intervening colors represent voltage
values in between. Multiple inducible VTs of varied morphology were localized to
circuits within the scar

In the setting of an old MI, the ECG during VT is affected by

 The size of infarction

 The region of infarction

 The region within the scar where the circuit is located

 The proximity to the His-Purkinje system

 The influence of concomitant pharmacological agents

Presence of Q waves (qR, QR or Qr) in related leads

 Notched or wide QRS complexes

 Low QRS voltage

 Multiple ventricular tachycardia morphologies

 Paroxysmal sustained episodes

Surface ECG tends to locate the reentry circuit exit rather than
the VT origin

Location should be defined in 3 axes:

 septal vs lateral walls

 superior vs inferior walls

 apical vs basal regions

Bundle branch block patterns -sequence of ventricular activation

Lateral wall VT
 RBBB pattern
 Wider QRS complexes

Septal VT
 LBBB pattern

 Narrower QRS complexes

The QRS axis in inferior leads indicates the sequence of
activation between the superior and inferior walls

 Inferior MI
 Superior axis (80%)

Anterior MI
 Superior axis (55% )
 Inferior axis (45%)

Predominant polarity of QRS complexes in precordial leads
can help discriminate between VTs from the basal or the
apical regions

VT from the apex
 Negative concordant R progression

VT from the basal
 Positive concordant R progression

The key determinant of hemodynamic tolerance
 Tachycardia rate
 Left ventricular function
 Development of ischemia, and mitral insufficiency

Hemodynamic collapse – cardioversion

Intravenous procainamide, sotalol, and amiodarone have
been demonstrated to have superior efficacy

Goal of long-term therapy- prevention of SCD &
recurrence of symptoms

Asymptomatic NSVT with NLVEF- no treatment

Symptomatic NSVT in pts with NLVEF- betablockers

Cardiac arrest survivors / SUS VT in ↓LVEF- ICD

Primary pvt - ICD > Amiod- pvt of SCD

subendocardial resection of arrhythmogenic focus

Cryoablation

Laser vaporization

Photocoagulation

Patients resuscitated from VF when coronary
revascularization is not possible, and there is evidence of
prior MI and significant LV dysfunction I IIa
I IIa IIbIIb III
III

 LV dysfunction due to MI who present with
hemodynamically unstable VT I IIa
I IIa IIb
IIb III
III

Primary prevention - LV dysfunction due to prior MI who
are at least 40 days post-MI and have an LVEF 30%-40% &
NYHA II or III
I
I IIa
IIa IIb
IIb III
III

Primary prevention ICD is reasonable in patients with LV
dysfunction due to prior MI who are at least 40 days post-MI,
and have an LVEF 30%-35% & NYHA I I IIa
I IIa IIb
IIb III
III

 ICD implantation is reasonable in patients with post-MI
with normal LV function and recurrent VT
I
I IIa
IIa IIb
IIb III
III

DCM has a propensity to the development of
ventricular arrhythmias and sudden death

Incidence of DCM - 4 to 8 cases per 100,000 population

Incidence of VT – 50-60% DCM, resp for 8-50% deaths

Genetics - Relationship between individual genotypes
and arrhythmogenicity is poorly understood

Multiple factors responsible for VT in DCM

Myocardial fibrosis/scar - may act as sites for reentry
 At autopsy, extensive subendocardial scarring in the LV in 33% &
multiple patchy areas of replacement fibrosis in 57%

Sustained stretch-induced shortening of refractory period
and AP duration, predisposing to reentry

Short, pulsatile, stretch-induced after depolarizations

Diastolic Ca overload caused by decreased sacrcoplasmic
reticulum Ca2+–adenosine triphosphatase pump

Afterdepolarizations induced by increased Na+-Ca2+ exchanger
activity

Hypokalemia, hypomagnesemia (often related to diuretic use)

Increased circulating catecholamines

Increased sympathetic tone

Purkinje system conduction delay

 Increased endocardial surface area in dilated atrium or
ventricle

 Drugs (antiarrhythmics, digoxin, sympathomimetic)

Macro reentry - dominant mechanism

Bundle branch reentry ventricular tachycardia (BBRVT)
is the most characteristic

BBRVT - Responsible for VT in up to 41% of DCM

Macro-reentrant circuit involving the His-Purkinje
system, usually with antegrade conduction over the
RBB and retrograde conduction over the LBB

Severity of LV dysfunction - most powerful predictor

SCD is significantly greater in patients with syncope

 Laboratory values - low serum sodium and increased
plasma norepinephrine, renin, and ANP,BNP

LBBB & of first- and second-degree AV block has been
associated with poor outcome

 Vesnarinone Trial (VEST) showed a significant association
between the degree of QRS prolongation and mortality

Gottipaty V, et al. J Am Coll Cardiol 33:145A, 1999

ACEI – reduction in SCD due to VT (37% vs 46%)

 new VT developed less frequent at 1,2 yrs in enalapril
group (VHeFT-II trial)

Amiodarone
 Used only on specific arrhythmic indications
 Reduces ICD shock frequency , without worsening heart
failure (SCDHeFT)

Implantable Cardioverter-Defibrillators
 AMIOVIRT- No difference in mortality ( amio vs ICD)
 SCD-HeFT - Significant reduction in total mortality in ICD group

Catheter ablation

Biventricular pacing- severe drug refractory heart failure ,
in elderly

 Improve systolic function by shortening the duration of mechanical
systole and increasing dP/dt
 Improve diastolic function by prolonging diastolic filling time
 Reduce presystolic MR by earlier activation of the lateral papillary
muscle without the adverse effect on the sympathetic nervous
system seen with inotropic agents

Commonly occurs in disease with severe LV dysfunction
like DCM & conduction abnormalities in the HPS

BBR VT may also be seen in:
 Myotonic dystrophy
 Hypertrophic cardiomyopathy
 Ebstein anomaly
 Following valvular surgery
 Proarrhythmia due to Na channel blockers

 Presyncope, syncope or sudden death - VT with fast
rates > 200 bpm

Macro re-entrant circuit employing
 His Bundle
 Both bundle branches
 Ramifications of left bundle
 Transeptal myocardium

May present with LBBB or RBBB morphology depending
on the antegrade conduction

LBBB morphology is common

BBR –LBBB: - antegrade direction -RB
& reterograde LB

BBR –RBBB:- antegrade direction-LB
& reterograde RB

VT QRS Activation
Morphology Sequence

LBBB LB-H-RB-V

RBBB RB- H-LB-V

Surface ECG in sinus rhythm - non-specific or typical
bundle branch block patterns with prolonged QRS
duration

Total interruption of conduction in one of the BB would
theoretically prevent occurrence of reentry

Can occur in patients with relatively narrow QRS complex
- functional conduction delay

Electrophysiologic features
 During tachy QRS morphology is commonly LBBB type

 His electrograms precede each V

 HV interval during tachycardia > HV in baseline

 Changes in V–V interval follow the changes in H–H

 Delay in HPS conduction facilitates induction

Electrophysiologic features
Block in Bundle branches or HPS will terminate the tachy

 Ablation of RB renders tachycardia noninducible

VT of myocardial origin mimics BBR-LB pattern VT – can
be differentiated by the presence of rapid intrinsicoid
deflection due to initial ventricular activation through the
HPS in the later

The reentrant circuit involves superior and inferior
division of the left bundle

RBBB and anterior or posterior fascicular block is
present during sinus rhythm

usually has RBBB morphology

Antegrade - LAF & retro – LPF –RAD

Antegrade- LPF & retro – LAF- LAD

HV interval shorter than sinus rhythm

LB potential before HIS deflections

High recurrence rate after drugs

RFA - first line therapy

 Treatment of choice for BBR VT is ablation of the RB

A PPI should be implanted if the post-ablation HV
interval is 100 ms or longer

ICD implant should be considered if myocardial VT
occur spontaneously or are inducible or if EF < 35%

Most frequent – ARVD

Extensive myocardial fibrosis - substrate for reentry

RV outflow tract
RV apex
RV inflow segments

Marcus fi et al.Circulation 1982; 65:384–398

ECG in sinus rhythm
1. Prolonged QRS duration ≥ 110 ms in V1-V3 (Sens-55%, Spec-100%)

2. T wave inversion in right precordial leads (Seen in 60%)

3. Epsilon wave (Seen in 30%)

4. Low-voltage QRS amplitude

(Indicate severe cases)

Ventricular arrhythmias are usually exercise-related

Sensitive to catecholamines

Most Common- LBBB morphology VT

Up to 12 VT morphologies have been reported in a
single patient

RBBB VT - LV involvement or a left septal breakthrough
site

VT in ARVD may be confused with RVOT VT

O’Donnell D ET et al. Eur Heart J.
2003;24:801-810, 2003.

High Risk Features
Younger patients

Recurrent syncope

History of cardiac arrest or sustained VT

Clinical signs of RV failure or LV involvement

Patients with or having a family member with the high
risk ARVD gene (ARVD2)

Increase in QRS dispersion ≥ 40 msec
 QRS dispersion = max measured QRS minus min measured QRS

Documented VT/VF on c/c OMT, have reasonable expectation of
survival- ICD to prevent SCD I
I IIa
IIa
IIa IIb
IIb III
III

B

Severe disease LV inv, FH of SCD, undiagnosed syncope, on c/c OMT
I
I IIa
IIa
IIa IIb
IIb III
III

C

Amiodarone or sotalol effective , when ICD not feasible
I
I IIa
IIa
IIa IIb
IIb III
III

C

Ablation can be adjunctive
I
I IIa
IIa
IIa IIb
IIb III
III

C

EP testing might be useful for risk assessment
I
I IIa
IIa
IIa IIb
IIb III
III

C

SCD in adults with asymptomatic HCM- 1%

NSVT – 8%

On 24-hr Holter -90% have ventricular arrhythmias

Prevalence of ventricular and
supraventricular arrhythmias on
24-hour Holter recording in 178
patients from a community-based
population of patients with
hypertrophic cardiomyopathy
J Am Coll Cardiol 45:697-704, 2005

In LVH action potential prolongation is due to a decrease in
Ito. This results in nonhomogeneous repolarization and
propensity for EAD

 Hypertrophied myocytes may produce DAD due to an
increase in Ca load

Abnormal pacemaker current (If) has been reported in
LVH. Intensity of this current increases with beta
adrenergic stimulation

In LVH the density of Ito is reduced. The density of ICaL
and IK is unchanged and density of If is increased

Pharmacologic Treatment
 Beta-blockers, verapamil, amiodarone
 Long term prophylactic pharmacologic therapy
now not recommended in high-risk population

ICD implantation is reasonable for patients who have 1
or more major risk factor for SCD. (Level of Evidence: C)

1. Family history of premature HCM-related death

2. Unexplained syncope, particularly in young patients,
or if demonstrated to be arrhythmia-based

3. Frequent, multiple, or prolonged episodes of NSVT

4. Hypotensive or attenuated BP response to exercise

5. Extreme LVH with maximum wall thickness ≥ 30 mm

Presence or magnitude of LVOT obstruction has not proved to be a
consistently strong independent risk factor for SCD in HCM and therefore
does not constitute a sole justification for prophylactic ICD implantation

Ventricular Tachycardia in Patients after
Surgery for Congenital Heart Disease

Most information concerning patients with VT and
congenital heart disease pertains to TOF

VT in these patients are due to the effect of
 Years of chronic cyanosis
 Presence of a ventriculotomy
 Elevation of RV pressures
 Severe pulmonic regurgitation with RV dysfunction

These factors lead to myocardial fibrosis, resulting
reentrant circuits


Mechanism of VT is reentry involving the RVOT, either
at the site of anterior rt. ventriculotomy or at VSD patch

The incidence of VT significantly higher in patients with
RVSP >60 mm Hg and RVEDP > 8 mm Hg

Zeltser et al showed RV volume overload is the most
important predictor of inducible ventricular arrhythmias

J Thorac Cardiovasc Surg 130:1542-1548, 2005


The risk of VT can be assessed by QRS duration

Syncope & VT- squares
Sudden death- triangles
Syncope with Afl- star

Gatzoulis MA et al. Circulation 95:401-404, 1997

Ventricular Tachycardia in Patients after Surgery for Congenital Heart Disease

Treatment

Antiarrhythmics medication

Radiofrequency catheter ablation

Surgical Cryoablation

ICD implantation

A combined approach of correcting significant structural
abnormalities with intra-operative EP-guided ablation
may reduce the potential risk of deterioration in
ventricular function

References- Journal
1. Relationship between the 12-lead electrocardiogram during ventricular tachycardia
and endocardial site of origin in patients with coronary artery disease. John M. et al.
Circulation 77, No. 4, 759-766, 1988.

2. Coronary Artery Revascularization in Patients With Sustained Ventricular Arrhythmias
in the Chronic Phase of a Myocardial Infarction: Effects on the Electrophysiologic
Substrate and Outcome. Josep Brugada et al JACC Vol. 37, No. 2, 2001:529–33

3. Ventricular Tachycardia in Coronary Artery Disease . B. Benito, M.E. Josephson / Rev
Esp Cardiol. 2012;xx(x):xxx–xxx

4. Role of Ablation Therapy in Ventricular Arrhythmias. Mithilesh K. Das et al. Cardiol Clin
26 (2008) 459–479

5. Ventricular Arrhythmias in Heart Failure Patients Ronald Lo, Henry H. Hsia. Cardiol Clin
26 (2008) 381–403

References- Journal
5. A Comprehensive Approach to Management of Ventricular Arrhythmias, Fred
Kusumoto. Cardiol Clin 26 (2008) 481–496

6. Relationship between the 12-lead electrocardiogram during ventricular tachycardia
and endocardial site of origin in patients with coronary artery disease, J M Miller et al.
Circulation. 1988;77:759-766

7. Arrhythmogenic right ventricular cardiomyopathy: A cause of sudden death in young
people, A. Thomas mcrae et al, Cleveland clinic journal of medicine volume 68 ,No.5,
2001:459-467

8. Ventricular arrhythmias in idiopathic dilated cardiomyopathy K Von Olshausen et al. Br
Heart J 1984; 51: 195-201

9. Non-Sustained Ventricular Tachycardia in Hypertrophic Cardiomyopathy: An
Independent Marker of Sudden Death Risk in Young Patients. Lorenzo Monserrat et al,
Vol. 42, No. 5, 2003:873–9

10. Sustained Ventricular Tachycardia in Adult Patients Late After Repair of Tetralogy of
Fallot. David A. Harrison et al. JACC Vol. 30, No. 5,November 1, 1997:1368–73

References – Text Books

1. Zipes 5th ed. Cardiac Electrophysiology From Cell to Bedside

2. Basic Cardiac Electrophysiology for the Clinician .2nd ed. José Jalife, MD

3. Clinical arrhythmology and electrophysiology: a companion to
Braunwald’s heart disease 8th ed.

4. Handbook of Cardiac Electrophysiology. Andrea Natale MD.

5. Management of Cardiac Arrhythmias, edited by Leonard I. Ganz, MD,
2002

MCQ-1
True statement regarding AVRD

A. Ventricular arrhythmias are usually exercise-related

B. Sensitive to catecholamines

C. Most Common- LBBB morphology VT

D. All are true

MCQ-2
12 lead ECG of BBR-VT is given below. The antegrade conduction
through------------
A. Right bundle branch

B. Left bundle branch

C. Left posterior fascicle

D. Left anterior fascicle

MCQ-3
 Exists site of the VT circuit given below is ?

A. LV lateral wall

B. Septum

C. Right ventricle

D. Both B & C

MCQ-4
A 45yr old smoker with past history of hospitalization for chest pain presented to
causality with palpitation and hypotension. Patient was stabilized with DC cardio
version and taken to echo lab. His presentation ECG shown below. Echo likely to
show?

A. LV apical aneurysm

B. RWMA anterior wall

C. RWMA Inferior wall

D. RV outflow aneurysm

MCQ-5
A 39 yr old smoker with hypotension in ED was stabilized with DC cardio version and
his echo is shown below(Left side) . His presentation ECG is most likely to be ?
B
A

C D

MCQ-6

All are true about BBR- VT except?

A. High recurrence rate after drugs

B. Treatment of choice for BBR VT is ablation of the RB

C. Usually has LBBB morphology

D. V precede each his electrograms

MCQ-7
VT in post TOF repair patients are due to the effect of all except?

A. Years of chronic cyanosis
B. Presence of a ventriculotomy
C. Elevation of RV pressures
D. Severe pulmonic regurgitation with RV dysfunction
E. None

MCQ-8
 Sudden death risk factors in HCM are all except?

A. Family history of premature HCM-related death

B. Unexplained syncope, particularly in young patients, or if demonstrated to be
arrhythmia-based

C. Hypotensive or attenuated BP response to exercise

D. Presence or magnitude of LVOT obstruction

Mechanisms and Management of Ventricular Tachycardia in Ischemic Cardiomyopathy

Empfohlen

Empfohlen

Weitere ähnliche Inhalte

Was ist angesagt?

Was ist angesagt? (20)

Andere mochten auch

Andere mochten auch (20)

Ähnlich wie Mechanisms and Management of Ventricular Tachycardia in Ischemic Cardiomyopathy

Ähnlich wie Mechanisms and Management of Ventricular Tachycardia in Ischemic Cardiomyopathy (20)

Mehr von drranjithmp

Mehr von drranjithmp (8)

Kürzlich hochgeladen

Kürzlich hochgeladen (20)

Mechanisms and Management of Ventricular Tachycardia in Ischemic Cardiomyopathy