Classification

Monomorphic VT

○Etiology and classification:

▪ Reentrant VT

• Scar-related: Slow conduction from myocardial fibrosis or scar

▫ Old myocardial infarction (MI)

▫ Dilated cardiomyopathy (DCM)

▫ Arrhythmogenic right ventricular cardiomyopathy (ARVC)

▫ Congenital heart disease with surgical scar (e.g., Tetralogy of Fallot)

• Reentry within the conduction system

▫ Fascicular VT (left posterior fascicular VT most common)

▫ Bundle branch reentry (ischemic cardiomyopathy or non-ischemic DCM with associated His-Purkinje disease)

▪ Enhanced automaticity

• Primary (idiopathic) VT

▫ Outflow tract VT (75%): Right ventricular outflow tract (RVOT)-VT, left ventricular outflow tract (LVOT)-VT, aortic cusp VT

▫ Non-outflow tract VT: Papillary muscle, mitral annular, tricuspid annular

▫ Acute post MI or surgery (myocardial injury)

▪ Triggered activity

• Acute post MI (usually arising near the His-Purkinje system)

Polymorphic VT

○Unstable VT with beat-to-beat QRS morphology variation (cycle length [CL] between 180 and 600 ms)

○Etiology and classification:

▪ Normal baseline QT

• Pathophysiology

▫ Can be due to reentry (e.g., acute MI, often degenerates to ventricular fibrillation [VF]), delayed afterdepolarization (e.g., catecholaminergic polymorphic VT (CPVT))

▫ Related to conditions of high sympathetic tone

▫ Acute ischemia (multiple reentrant circuits; abnormal automaticity)

▫ Channelopathies: Catecholaminergic polymorphic VT, Brugada syndrome, idiopathic polymorphic VT (PMVT)/VF

▪ Prolonged baseline QT

• Torsades de pointes

▫ Defined as a PMVT with a QRS amplitude and cardiac axis rotation over a sequence of 5–20 beats.

▫ Usually it is not sustained but recurs if the underlying cause is not corrected.

• Pathophysiology

▫ Due to early afterdepolarization

▫ Typical variant: Initiated by “short-long-short” coupling intervals (pause-dependent, typical for drug-induced)

▫ Short coupled variant: Initiated by “normal-short” coupling (induced by stress or startle, typical for congenital syndromes, adrenergic dependent)

• Etiology

▫ Acquired prolonged QT: Drugs (class Ia, III antiarrhythmic drug [AAD], phenothiazines, tricyclic antidepressant [TCA]), low Mg, or K

▫ Congenital prolonged QT

▪ Short QT syndrome

Ventricular Fibrillation (VF)

○Chaotic, rapid, disorganized wide-complex tachyarrhythmia (>300 bpm)

○Thought to be due to multiple reentrant wavefronts within the ventricle (wavelet hypothesis).

○All VT may degrade to VF.

○Etiology of primary VF is similar to polymorphic VT.

WCT: wide-complex tachycardia; SVT: supraventricular tachycardia; AVRT: atrioventricular reciprocating tachycardia; LBBB: left bundle branch block; RBBB: right bundle branch block.

○Ventricular rate 120–300 bpm (usually around 170)

○P waves

▪ AV dissociation (complete AV block) or retrograde P waves (intact VA conduction)

○Axis

▪ Change in axis of >40° from baseline or extreme (right superior) axis deviation

○QRS morphology and duration

▪ Left bundle branch morphology (Negative QRS complex in V1 – QS, rS) >160 ms

▪ Right bundle branch morphology (Positive QRS complex in V1 – qR, R, Rs, RSR′) >140 ms

▪ Variable with relatively narrow complexes in fascicular tachycardia (110–140 ms)

• Right bundle with left axis: Left anterior fascicular tachycardia

• Right bundle with right axis: Left posterior fascicular tachycardia

○ Fusion beat (almost pathognomonic of VT; generally only occurs with rates <160 bpm)

▪ A hybrid QRS is a result of the combination of normal atrial conduction down the His-Purkinje system and cell-to-cell conduction of a ventricular impulse.

▪ Fusion beats can also occur with PVC, ventricular escape, accelerated idioventricular rhythm, and Wolff-Parkinson-White syndrome (WPW).

▪ Atrial impulse induces ventricular activation via the normal conduction system, resulting in a normal narrow QRS that is earlier than expected in the cardiac cycle.

○See page 91 about the differentiation of VT from SVT

○When describing VT, it is important to comment on:

▪ Duration: Non-sustained or sustained (lasts >30 seconds or associated with hemodynamic instability)

▪ Variability: Monomorphic or polymorphic

▪ Ventricular rate

▪ QRS morphology: Left or right bundle branch block morphology

▪ Axis: Right/inferior or left/superior

Localizing the Exit Site

○QRS morphology

▪ Left bundle morphology (negative QRS complex in V1: QS, rS): RV or LV septum

▪ Right bundle morphology (positive QRS complex in V1: qR, R, Rs, RSR′): LV

○Axis

▪ Superior (negative in II, III, aVF): Inferior wall or inferior septum

▪ Inferior (positive in II, III, aVF): Anterior wall or anterior septum

▪ Rightward: Lateral LV wall or apex

○Precordial transition

▪ Left bundle morphology VT

• ≤V3: Basal LV; RV septum

• ≥V4: Apical LV; RV free wall

• Negative concordance (all negative QRS V1–V6): Apical LV

▪ Right bundle morphology VT (reverse transition)

• ≤V2: Basal LV

• V3–V4: Mid cavity LV

• ≥V5: Apical LV

• Positive concordance (all positive QRS V1–V6): Mitral valve apparatus

○Variants and other features:

▪ Outflow tract VT (~LBBB morphology with an inferior axis)

• V1, V2 R-wave duration

▫ >50% of QRS: LVOT (left coronary cusp)

▫ <50% of QRS: RVOT or LVOT (right coronary cusp)

• V2 R:S ratio

▫ >1: left ventricular outflow tract (LVOT)

▫ <1: right ventricular outflow tract (RVOT)

• QRS transition in tachycardia compared to normal sinus rhythm (NSR)

▫ Earlier transition in NSR: RVOT

▫ Earlier transition in PVC/VT: LVOT

ARVC: arrhythmogenic RV cardiomyopathy; CPVT: catecholaminergic polymorphic ventricular tachycardia; DCM: dilated cardiomyopathy; HCM: hypertrophic cardiomyopathy; HR: heart rate; ILR: insertable looprecorder; IVCD: intraventricular conduction delay; LVEF: LV ejection fraction; LVH: LV hypertrophy; MRI: magnetic resonance imaging; SAECG: signal averaged ECG; WMA: wall motion abnormality; WPW: Wolff-Parkinson-White syndrome.

Management

Acute Management

○Non-sustained VT and PVCs

▪ No evidence that suppression of non-sustained VT (NSVT) prolongs life except with very rapid or repetitive (incessant) NSVT that compromises hemodynamic stability.

▪ First-line therapy

•β-blockers

▪ Second-line therapy

• Amiodarone + β-blockers

• Sotalol

• Catheter ablation

○Sustained monomorphic VT

▪ First-line therapy

• Direct-current cardioversion (DCCV)

▪ Second-line therapy

• IV procainamide is a reasonable alternative; use with caution if it is congestive heart failure (CHF) or hypotension.

• IV lidocaine: This is more effective if the cause is ischemic.

• IV amiodarone

▫ Hemodynamically unstable, refractory to cardioversion, or recurrent despite AAD

• Transvenous pace-termination

▫ Refractory to cardioversion, recurrent despite medical therapy

○Polymorphic VT with a normal baseline QTc

▪ First-line therapy

• DCCV

• IV β-blockers

• IV amiodarone

• Note: Calcium-channel blockers (CCB) may be effective for DAD (caused by inward calcium current).

• For Brugada or idiopathic VF consider IV isoproterenol infusion (target HR >100–120 bpm) or PO quinidine.

○Polymorphic VT with a prolonged baseline QTc

▪ Treat the underlying cause.

• Remove offending or unnecessary drugs (including AAD).

• Treat ischemia.

• Electrolyte abnormalities (keep K⁺ >4.0–4.5 mmol/L)

▪ Adjunctive therapy

• IV magnesium sulfate

▫ This is only useful with prolonged baseline QTc.

• Pacing

▫ Overdrive pacing (acute)

▫ Chronic pacing: Pause-dependent TdP

• Isoproterenol

▫ IV infusion to a target HR >100–120 bpm

• IV lidocaine or mexilitine

▫ LQT3 with TdP

Chronic Management

Table 10.4 Strategies for Chronic Management of Ventricular Arrhythmias

ICD: implantable cardioverter-defibrillator; SCD: sudden cardiac death.

▪ An ICD may be the only way to reduce the risk of death in the majority of high-risk patients.

▪ Primary prevention

○Pharmacologic therapy

▪ Suppression of ventricular ectopy with AADs does not decrease the risk of SCD.

• CAST: Suppression of ambient ventricular ectopy either increased mortality (encainide, flecainide) or had no effect (moricizine).

▪ Empiric amiodarone may reduce the arrhythmia burden but it does not generally reduce the risk of SCD.

• CHF-STAT: 674 patients; LVEF <40%; complex ectopy

▫ No difference in survival overall vs. placebo (non-ischemic dilated cardiomyopathy [NIDCM] had a trend towards increased survival)

• CASCADE: 228 patients; survivors of VF arrest

▫ Amiodarone resulted in less ICD shocks or syncope vs. other AAD

• CAMIAT: 1202 patients; survivors of MI; complex ectopy

▫ No survival benefit vs. placebo

• EMIAT: 1500 patients; survivors of MI; LVEF <40%

▫ No survival benefit vs. placebo

• SCD-HeFT: 2521 patients; LVEF ≤35%; NYHA 2–3

▫ No survival benefit with amiodarone

○Invasive therapy

▪ Ablation of reentrant foci is an effective method of treating some types of VT.

CATHETER ABLATION OF VENTRICULAR TACHYCARDIA (VT)

Indications

○Frequent monomorphic PVCs and NSVT

▪ This is particularly true if it is associated with LV dysfunction (LV dilatation or decline in LVEF).

○Monomorphic VT: Sustained (class I), non-sustained (class IIa)

▪ Patients may be drug resistant or drug intolerant.

▪ They do not want a long-term drug therapy.

○Bundle-branch reentrant VT (class I)

○Adjunctive therapy in those with an ICD (class I)

▪ Patients receiving multiple shocks as a result of sustained VT that cannot be managed by device programming, changes in AAD therapy, or they do not want long-term drug therapy.

○Idiopathic ventricular tachycardia (e.g., RVOT or fascicular VT) 80%–90%, if inducible

○Bundle branch reentry: 80%–90%

○Ischemic VT: 60%–70%

○Dilated cardiomyopathy: 50% (usually requires epicardial ablation)

○ARVC: 70% (usually requires epicardial ablation)

Anticipated Complications

○Similar to all invasive ablation procedures

○3%–5% major complications

▪ Vascular access: hematoma, AV fistula, arterial pseudoaneurysm

▪ Catheter manipulation: vascular damage, microemboli/stroke, coronary dissection

▪ RF application: cardiac perforation/tamponade, coronary damage, AV block

○Mortality 1%–3%

Patient Preparation

○Use echocardiography (± contrast) to exclude the presence of LV thrombus (if LV ablation is anticipated).

○Stop all AAD for 5 half-lives before the procedure (especially for RVOT VT, fascicular VT).

○Conscious sedation is preferred to general anesthesia due to the risk of rendering the VT non-inducible.

Set-Up

○3D mapping system

▪ Focal VT: Set window to 50–80 ms prior to surface QRS onset

▪ Reentrant VT: Set window to >90% of tachycardia cycle length

○Diagnostic catheters

▪ Quadripolar catheters in right ventricular apex (RVa) and at the His

▪ Deflectable decapolar in CS (reference and pacing)

○Endocardial RV VT

▪ Non-irrigated RF: D-curve (medium/blue), C-curve (green), or bidirectional [D-curve (medium/blue)/F-curve (large/orange)]

▪ Irrigated RF: D-curve (medium/blue) or bidirectional [D-curve (medium/blue)/F-curve (large/orange)]

▪ Consider long sheath for improved stability in the RVOT (LAMP, SL0, or steerable sheath).

○Endocardial LV VT

▪ Irrigated RF ablation: F-curve (large/orange), D-curve (medium/blue), J-curve (extra large/black), or bidirectional (D/F, D/J, F/J)

▪