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

VT Diagnosis


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


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

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

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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


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

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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


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

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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

Life Vest

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VEST Trial

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

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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

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

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