ventricular tachycardia - bswhealth.med · idiopathic vt •presentation –frequent pvcs...

Ventricular Tachycardia

Javier E. Banchs, MD, FACC, FHRS

Director of Electrophysiology and Pacing

Scott & White Memorial Hospital

Temple, Texas

Objectives

• Understand the pathophysiology of

ventricular tachycardia (VT)

• Review the diagnosis and management of

VT

Ventricular Tachycardia

• Arrhythmia mechanisms

– Reentry

– Enhanced automaticity

– Triggered activity

Reentry

Begona B. Josephson ME. Rev Esp Cardiol. 2012;65:939-55

Lopera G. et al J Cardiovasc Electrophysiol. 2004;15: 52-58

Enhanced Automaticity

Iwasaki Y et al. Circulation. 2011; 124:2264-2274

Heart Rhythm 2010;7:117–126

Triggered Activity

Ventricular Tachycardia Classification

– Substrate

• Idiopathic : no structural heart disease

• Structural heart disease

– Ischemic

– Non ischemic – DCM, ACHD, ARVD, Sarcoidosis,

HCM…

• Channelopathies

Ventricular Tachycardia Classification

– Morphology

• Monomorphic

• Polymorphic

– Duration

• Sustained (>30 sec)

• Non sustained

– Hemodynamic stability

• Stable

• Unstable

VT Diagnosis

• Clinical presentation

– Symptoms: palpitations, chest pain, dyspnea,

syncope, cardiac arrest, ICD shocks

– Heart failure

– Asymptomatic

• Electrocardiographic

– Wide complex tachycardia

– AV dissociation

– ECG criteria

9

VT Diagnosis

Begona B. Josephson ME. Rev Esp Cardiol. 2012;65:939-55

1. AV relationship AV dissociation. Fusion and capture beats, VA ratio > 1

2. QRS Duration RBBB-like QRS >140 ms

LBBB-like QRS > 160 ms

QRS narrower than NSR

3. QRS Axis Right superior (negative concordance in I,II,III)

VT Diagnosis

Begona B. Josephson ME. Rev Esp Cardiol. 2012;65:939-55

4. Specific QRS patterns

Precordial leads Negative or Positive concordanceAbsence of RS in all precordial leadsRS complex with R to S nadir >100 ms

aVR Initial R waveWide (>40ms) or notched initial forces

V1 with RBBB-like QRS Monophasic R waveqR or Rs with > 30 ms R

V1 with LBBB-like QRS Broad r wave or deep S waveQS with slow initial forces (> 60 ms onset to nadir)

V6 with RBBB-like QRS Monophasic R waveDeep S wave (QS or rS) R/S<1

V6 with LBBB-like QRS Q waves (QR,QS, QrS)

SVT, AF, A flutter with aberrancy?

12

13

Other Diagnostic Tools (WCT)

• IV Adenosine

– Could worsen ischemia in ischemic VT

– Could cause A fib and lead to VF in wpw

• Esophageal atrial recording

• Electrophysiology study

• Pacemaker check if present

• Treadmill stress test

16

IDIOPATHIC VT

Idiopathic VT

• Presentation– Frequent PVCs

– Sustained or non sustained VT

– Monomorphic

• Origen– Focal (automaticity, reentry, triggered activity)

• Outflow tract – RVOT, LVOT, Coronary cusps, PA

• Mitral annulus

• Papillary muscle

• Fascicular VT

Treatment of idiopathic VT

• Identification and avoidance of triggers

• Antiarrhythmic drugs

• Ablation

• Consider cardiac MRI (ARVC)

• Ablation/AA drugs indicated for symptomatic

VT/PVCs with or without syncope

• 10.000 to 20.000 (15%) PVCs in 24 h could

lead to cardiomyopathy

Treatment of idiopathic VT

Frequent PVCs in the asymptomatic patient

• Monitor

– Symptoms

– Echocardiography

• Ablation/AA drugs

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Antiarrhythmic drugs

• Beta blockers

• Calcium channel blockers

• Flecainide

• Propafenone

• Dronedarone

• Mexiletine

• Sotalol, amiodarone, dofetilide

RVOT RVOT

PAPA

ISCHEMIC VT

26

Ischemic VT

• Usually scar related

– Monomorphic VT

– Multiple VT

• Polymorphic VT

– Ischemia

– Purkinje triggers

Ischemic/scar related VT Treatment

• Reversible cause

– Polymorphic VT - ischemia

– Electrolytes

– Heart failure

• Ablation

• Antiarrhythmic drugs

• Sudden death prevention - ICD

– ATP

– ICD shocks

Brugada J et al. J Am Coll Cardiol 2001;37:529–33

Revascularization

Revascularization

Brugada J et al. J Am Coll Cardiol 2001;37:529–33

VT Ablation

• Induction and mapping

• Targets: – Myocardial channels of slow conduction within

scar & border (tachycardia isthmus)

– Triggers of VT

• Limitations:– Multiple morphologies

– Frequently unstable VT

– Limited lesion depth

– Frequent recurrences

231 patients53% free of VT in 6 monthsAll VT abolished in 49%Frequency of VT episodes reduced by 75% in 67% of patients

Stevenson W et al. Circulation. 2008;118:2773-2782

Intracardiac Recordings in Sinus

A A

V VV LP LP LP

CS

ABL

I

aVF

V1

VT Induction

Mid diastolic potentials in VT

CS

ABL

I

aVF

V1

Ablation in VT

Mid diastolic potentials in VT

VT TerminationAblation ON

CS

ABL

I

aVF

V1

Intracardiac US

LV

Prophylactic VT Ablation for

Prevention of ICD Shocks

Reddy et al. NEJM 2007;357:2657-65

SMASH-VT TRIAL

Ablation vs. Antiarrhythmic Drugs

Sapp JL, et al. N Engl J Med 2016;375:111-21

VANISH TRIAL

Antiarrhythmic drugs

• IV lidocaine

• IV procainamide

• Beta blockers

• Sotalol

• Amiodarone

• Mexiletine

• Dofetilide

AmiodaroneCASCADE SUTDY

Green HL. Am J Cardiol 1993;72:70F-74F

AMIO

d,l-SOTALOL IMPLANTABLE CARDIOVERTER–

DEFIBRILLATOR STUDY GROUP

Pacifico A. et al. N Engl J Med 1999;340:1855-62

Optimal Pharmacological Therapy in Cardioverter

Defibrillator Patients (OPTIC)

Connolly SJ. Et al. JAMA. 2006;295:165-171

OPTIC SUTDY

Baquero GA. Et al. J Cardiovasc Electrophysiol, Vol. 23, 296-301, 2012

Treatment of idiopathic VT

ICD indications

• Secondary prevention – Cardiac arrest– Symptomatic sustained VT– Inducible sustained VT at EP study

• Primary prevention– Previous MI > 40 days, EF <35% with optimal Rx, 3

months after CABG/PCI– Dilated CM > 3 months, EF <35% with optimal Rx,

NYHA II-III– Long QT, HOCM, Brugada

– Expected survival > 1 year– No NYHA class IV

Sudden Cardiac DeathSecondary Prevention – ICD Trials

Lee, DS et al . J Am Coll Cardiol 2003;41:1573

Sudden Cardiac Death in Heart FailureSCD-HeFT – Primary prevention

47

N Engl J Med 2005; 352:225-237

ATP works

VT ATP

ATP SINUS

ICD shock

LONG QT

50

N Engl J Med 2008;358:169-76

Long QT

N Engl J Med 2008;358:169-76

Prognosis

• High risk

– Recurrent syncope on BB

– QTc > 500 ms

– Male in LQT3

– Individual genes

Therapy

• Beta blockers (LQT1, LQT2)

• Flecainide (LQT7 – Andersen-Tawil Syndrome)

• Flecainide, mexiletine, ranolazine (?LQT3)!

• QT prolonging drug avoidance– CredibleMeds.org (ARIZONACERT)

• ICD secondary prevention + high risk patients– Clinical events

– Family history ?

– Genetic markers – SCN5A

Therapy

• Beta blockers (LQT1, LQT2)

• Flecainide (LQT7 – Andersen-Tawil Syndrome)

• Flecainide, mexiletine, ranolazine (?LQT3)!

• QT prolonging drug avoidance– CredibleMeds.org (ARIZONACERT)

• ICD secondary prevention + high risk patients– Clinical events

– Family history ?

– Genetic markers – SCN5A

Life Vest

58

VEST Trial

59

JE Olgin et al. N Engl J Med 2018;379:1205-1215.

60

VEST Trial

JE Olgin et al. N Engl J Med 2018;379:1205-1215.

Conclusions

• Ventricular tachycardia can occur with our

without structural heart disease

• The diagnosis of VT could be challenging

• Treatment of VT may require

antiarrhythmic drugs, catheter ablation,

device therapy or a combination of both