Dr ranjith mp,ventricular tachycardia in abnormal heart dr ranjith mp

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 VTDisorders 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


Automatic ventricular arrhythmias

Premature ventricular complexes

Ventricular tachycardia associated with:

Acute myocardial infarction or ischemia

Electrolyte and acid-base disturbances, hypoxemia

Increased sympathetic tone


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


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 VTDisorders of impulse conduction

Fast Conduction PathSlow Recovery

Slow Conduction PathFast Recovery

Electrical Impulse Cardiac Conduction Tissue

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





Premature Beat Impulse Cardiac Conduction 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

Repolarizing Tissue (long refractory period))


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



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



Cardiac Conduction Tissue



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 voltagevalues in between. Multiple inducible VTs of varied morphology were localized tocircuits 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

LV dysfunction due to MI who present with hemodynamically unstable VT

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

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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

ICD implantation is reasonable in patients with post-MI with normal LV function and recurrent VT


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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

Morphology

Activation

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


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 tractRV apexRV inflow segments

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

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)

ECG in sinus rhythm

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

Severe disease LV inv, FH of SCD, undiagnosed syncope, on c/c OMT

Amiodarone or sotalol effective , when ICD not feasible

Ablation can be adjunctive

EP testing might be useful for risk assessment


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SCD in adults with asymptomatic HCM- 1%

NSVT – 8%

On 24-hr Holter -90% have ventricular arrhythmias

J Am Coll Cardiol 45:697-704, 2005

Prevalence of ventricular and supraventricular arrhythmias on24-hour Holter recording in 178 patients from a community-based population of patients with hypertrophic cardiomyopathy

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 ICaLand 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- trianglesSyncope with Afl- star

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


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- Journal1. 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 Clin26 (2008) 459–479

5. Ventricular Arrhythmias in Heart Failure Patients Ronald Lo, Henry H. Hsia. Cardiol Clin26 (2008) 381–403

References- Journal5. 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

THANK YOU

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 ?

AB

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

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