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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
21
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
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