---

MANAGEMENT OF VENTRICULAR TACHYCARDIA

A Comprehensive Presentation for Cardiology Fellows

---

SLIDE 1 — TITLE SLIDE

• Target: Cardiology Fellows
• Based on: 2017 AHA/ACC/HRS Guidelines, 2022 ESC Guidelines, VANISH/BERLIN-VT/VTACH Trials
• Sources: Braunwald's Heart Disease | Harrison's 22e | Goldman-Cecil Medicine | Fuster & Hurst

---

SLIDE 2 — OVERVIEW / LEARNING OBJECTIVES

1. Classify VT by mechanism, morphology, and clinical substrate
2. Apply a systematic approach to the wide-complex tachycardia (WCT)
3. Choose the correct acute termination strategy based on hemodynamic status
4. Select appropriate long-term therapy (AADs, ICD, ablation) for each VT substrate
5. Recognize and manage special situations: electrical storm, incessant VT, VT in channelopathies, and VT in structural heart disease
6. Apply current guideline recommendations (ESC 2022, AHA/ACC/HRS 2017)

---

SLIDE 3 — DEFINITION AND EPIDEMIOLOGY

• VT = 3 or more consecutive ventricular beats at rate >100 bpm, originating below the bundle of His
• Sustained VT: lasts >30 seconds or requires termination due to hemodynamic compromise
• Non-sustained VT (NSVT): <30 seconds, terminates spontaneously

• Responsible for ~80% of cases of sudden cardiac death (SCD) in structural heart disease
• Occurs in 6% of patients in early phase of acute MI
• Electrical storm occurs in 4% of primary prevention ICD patients and up to 20% in patients with known prior VT

---

SLIDE 4 — CLASSIFICATION OF VT

By Duration

By Morphology

By Substrate

---

SLIDE 5 — MECHANISMS OF VT

1. Reentry (most common in structural heart disease)

• Requires: slow conduction zone + unidirectional block
• Substrate: fibrotic scar from prior MI, cardiomyopathy, or infiltrative disease
• Surviving myocyte bundles within scar = slow conduction zone
• QRS on ECG inscribed when wavefront exits scar ("exit site")
• Single scar can support multiple reentry circuits → multiple VT morphologies
• Scar detectable as: LGE on CMR, low-voltage zones on EAM, abnormal electrograms

2. Triggered Activity

• Delayed afterdepolarizations (DADs): digoxin toxicity, catecholamines, CPVT
• Early afterdepolarizations (EADs): long QT, bradycardia - cause TdP
• RVOT/LVOT idiopathic VT: cAMP-mediated triggered activity, adenosine-sensitive

3. Abnormal Automaticity

• Enhanced normal automaticity or abnormal automaticity in depolarized cells
• Accelerated idioventricular rhythm (AIVR): common post-reperfusion, usually benign

---

SLIDE 6 — WIDE COMPLEX TACHYCARDIA: DIFFERENTIAL DIAGNOSIS

1. Monomorphic VT ← most important to rule in/out
2. SVT with bundle branch block aberrancy
3. SVT conducting over an accessory pathway (preexcited tachycardia)
4. SVT conducted with rate-related aberrancy
5. Ventricular pacing artifact

---

SLIDE 7 — ECG CRITERIA FOR VT vs SVT WITH ABERRANCY

Brugada Algorithm (1991) — stepwise, favor VT if:

1. No RS in any precordial lead → VT (100% sensitivity)
2. RS duration >100 ms in any precordial lead → VT
3. AV dissociation → VT (highly specific, present in ~50% of VTs)
4. Morphology criteria in V1 and V6 (LBBB or RBBB type)

Vereckei aVR Algorithm (2008)

• Initial R wave in aVR → VT
• Width of initial r or q in aVR >40 ms → VT
• Notch on downstroke of QRS in aVR → VT

Key ECG Signs Supporting VT:

• AV dissociation (P waves marching independently at slower rate) - most specific
• Fusion beats (hybrid of sinus + VT complex at slow VT rate)
• Capture beats (occasional narrow QRS = sinus capture)
• QRS duration >160 ms
• Absence of typical RBBB/LBBB morphology
• Concordance (all precordial leads positive or all negative)

---

SLIDE 8 — INITIAL EVALUATION OF A PATIENT WITH SUSPECTED VT

• Hemodynamic status: pulse? BP? consciousness?
• IV access, continuous monitoring, 12-lead ECG
• Defibrillator ready

• Prior MI, cardiomyopathy, family history of SCD
• Current medications (QT-prolonging drugs?)
• Electrolyte status

• 12-lead ECG (during tachycardia AND sinus rhythm)
• Cardiac biomarkers (troponin, BMP/BNP)
• Electrolytes: K+, Mg++, Ca++ (critical)
• Thyroid function, drug levels (digoxin)
• Echocardiogram (structure, function, LV dimensions)
• Cardiac MRI: scar characterization (LGE), myocarditis, ARVC
• Coronary angiography if ischemia suspected

---

SLIDE 9 — ACUTE MANAGEMENT: THE HEMODYNAMIC PIVOT POINT

Is the patient hemodynamically stable or unstable?

---

SLIDE 10 — ACUTE PHARMACOLOGICAL TERMINATION (STABLE VT)

Monomorphic VT — Stable:

• Loading dose: 150 mg IV over 10 min → then 1 mg/min × 6 h → 0.5 mg/min × 18 h
• Suitable for structural heart disease
• Most commonly used

• 1-1.5 mg/kg IV bolus, may repeat at 0.5-0.75 mg/kg every 5-10 min (max 3 mg/kg)
• Alternative to amiodarone in pulseless VT/VF
• Can be used in combination with amiodarone
• Note: Neither amiodarone nor lidocaine improves survival vs defibrillation alone in cardiac arrest (per ACLS evidence)

• 20-50 mg/min IV until conversion or max 17 mg/kg

• Useful in monomorphic VT, avoid in QT prolongation or structural disease

Wide-complex tachycardia of uncertain type:

• Treat as VT - procainamide is a reasonable choice
• Avoid adenosine unless absolutely certain of SVT

---

SLIDE 11 — POLYMORPHIC VT: MANAGEMENT OVERVIEW

---

SLIDE 12 — TORSADE DE POINTES: SPECIFIC MANAGEMENT

1. Immediate: DC cardioversion if sustained/unstable
2. Suppress recurrences: IV Magnesium sulfate 1-2 g over 1-2 min IV (repeat as needed)
3. Correct bradycardia: Isoproterenol infusion OR temporary transvenous pacing at 100-120 bpm (shortens QT, suppresses pause-dependent TdP)
4. Remove precipitants: Stop all QT-prolonging drugs (check CredibleMeds database)
5. Correct electrolytes: Potassium >4.5 mEq/L, Magnesium >2 mg/dL
6. Long-term: Patients with a history of TdP have a lifelong susceptibility - avoid all QT-prolonging agents

• LQTS1 & 2: Beta-blockers (nadolol preferred) - highly effective
• LQTS3 (SCN5A mutation): Beta-blockers less effective; mexiletine, flecainide, or ranolazine adjuncts
• High-risk patients: ICD; left cardiac sympathetic denervation (LCSD) if ICD contraindicated/recurrent shocks

---

SLIDE 13 — NONSUSTAINED VT (NSVT): WHEN TO TREAT

---

SLIDE 14 — SUSTAINED MONOMORPHIC VT: LONG-TERM MANAGEMENT OVERVIEW

1. Prevent SCD - ICD therapy
2. Reduce VT burden - Antiarrhythmic drugs (AADs)
3. Eliminate substrate - Catheter ablation

"Antiarrhythmic drugs may have utility for palliation of VT symptoms and prevention of ICD therapies; however, without an ICD, these drugs do not improve survival."

---

SLIDE 15 — IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR (ICD)

Secondary Prevention Indications (Class I):

• Cardiac arrest from VF or hemodynamically unstable sustained VT (not due to reversible cause)
• Sustained VT with structural heart disease
• Syncope of undetermined origin with inducible sustained VT at EPS

Primary Prevention Indications (Class I):

• ICM with prior MI (≥40 days), LVEF ≤35%, NYHA class II/III on GDMT
• Non-ischemic CM with LVEF ≤35%, NYHA class II/III on GDMT (if expected survival >1 year)
• Certain inherited arrhythmia syndromes (LQTS, Brugada, HCM with high-risk features, CPVT)

ICD Types:

• Transvenous ICD (TV-ICD): Standard; offers ATP + antitachycardia pacing
• Subcutaneous ICD (S-ICD): No transvenous leads; preferred when pacing not needed and lead infection risk high (KNOPS et al., NEJM 2020 - noninferior to TV-ICD for prevention of death)
• Wearable cardioverter-defibrillator (WCD): Bridge in early post-MI or newly diagnosed CM while awaiting ICD decision

Programming Pearls for Fellows:

• ATP (antitachycardia pacing) terminates >70% of VT episodes - program aggressively to reduce shocks
• Long detection times reduce unnecessary shocks for self-terminating VT
• VF detection zone >220 bpm for primary prevention - reduces inappropriate shocks significantly

---

SLIDE 16 — ANTIARRHYTHMIC DRUGS FOR VT: OVERVIEW

---

SLIDE 17 — CATHETER ABLATION FOR VT: PRINCIPLES

Mechanisms Targetable by Ablation:

• Scar-related reentry (ischemic/non-ischemic) - endocardial or epicardial substrate
• Bundle branch reentry - ablation of right bundle branch is curative
• Idiopathic focal VT (RVOT, LVOT) - focal ablation, success ~80%
• Fascicular VT - ablation of posterior fascicle or false tendon region

Mapping Approaches:

1. Activation mapping during VT - identifies exit site; feasible only if VT hemodynamically stable and inducible
2. Entrainment mapping - confirms critical isthmus; post-pacing interval (PPI) matches TCL
3. Substrate mapping (in sinus rhythm) - identifies low-voltage scar, abnormal electrograms, late potentials → applicable even when VT not inducible; now preferred approach
4. Electroanatomic mapping (CARTO, EnSite) - 3D scar reconstruction

Endpoints:

• Noninducibility of clinical VT
• Elimination of all inducible VTs
• Scar homogenization (ablation of all abnormal electrograms within scar)

---

SLIDE 18 — CATHETER ABLATION: KEY CLINICAL TRIALS

• Strongly recommends catheter ablation for ICM patients failing or intolerant of AADs
• Allows ablation as alternative to long-term amiodarone (toxicity avoidance) even before AAD failure

---

SLIDE 19 — VT IN ISCHEMIC CARDIOMYOPATHY

• Most common form of structural VT in the Western world
• Scar-related reentry, usually in LV or LV-side of interventricular septum
• 70% recurrence within 2 years despite therapy
• Typically presents years after remote MI in a remodeled, dilated ventricle

• Even with acute biomarker rise, suspect old scar substrate (not just new ischemia) when presentation is remote from first MI
• Scar-related VT is NOT prevented by revascularization alone (CABG does not cure reentrant VT based on scar)
• CABG may be indicated for angina, ongoing ischemia, or hemodynamic reasons - but VT-specific therapy also needed

1. ICD - mandatory for secondary prevention
2. Beta-blockers (reduce sympathetic tone, reduce ICD shocks)
3. Amiodarone or sotalol - reduce VT burden, reduce ICD shocks
4. Catheter ablation - after AAD failure or as alternative to long-term amiodarone
5. Surgical ablation/subendocardial resection - reserved for refractory cases or concurrent cardiac surgery (success 85-90%, operative mortality 5-15%)

---

SLIDE 20 — VT IN NON-ISCHEMIC CARDIOMYOPATHY

• Scar often intramural or subepicardial (unlike post-MI subendocardial scar)
• Located near valve annuli (mitral, tricuspid, perivalvular)
• Progressive replacement fibrosis, often occult genetic etiology
• LGE on CMR identifies scar but may be intramural - harder to reach endocardially

• Cardiac sarcoidosis: Granulomatous infiltration → heterogeneous scar; VT often multimorphic; responds to corticosteroids in acute phase; ablation often needed
• Chagas' disease (Trypanosoma cruzi): Apical aneurysm, posterolateral scar; endemic to Latin America; high VT burden
• Lamin A/C cardiomyopathy (LMNA mutations): Progressive AV block + VT; extremely high SCD risk; ICD early; male sex, NSVT, non-sinus rhythm, truncating mutations = high-risk markers
• ARVC: Fibrofatty replacement of RV (and sometimes LV); VT with LBBB morphology; epsilon waves; ICD, ablation, sotalol/flecainide (structural heart disease exception)

• More complex due to intramural/epicardial substrate
• Epicardial access frequently required (subxiphoid pericardial puncture)
• Success rates lower than ischemic CM but improving with substrate mapping

---

SLIDE 21 — IDIOPATHIC VT (NO STRUCTURAL HEART DISEASE)

Outflow Tract VT (most common idiopathic form)

• Young to middle-aged patients, no structural disease
• Often provoked by exercise, emotional stress, caffeine
• In women: perimenstrual, perimenopausal, gestational triggers
• Usually RVOT origin; also LVOT, aortic sinus of Valsalva, LV summit

• LBBB morphology in V1 + inferior axis (tall R waves in II, III, aVF)
• V1 or V2 prominent R waves → suspect LVOT origin

• Beta-blockers, CCBs (verapamil/diltiazem), flecainide (safe - no structural disease)
• Catheter ablation: first-line if symptomatic and medications not preferred; success ~80%; most favorable for RVOT
• ICD: NOT indicated in isolated idiopathic VT (SCD risk is very low)

Fascicular VT (Belhassen's / Verapamil-sensitive VT)

• Second most common idiopathic VT
• RBBB-like configuration, negative inferior leads; exercise-induced; more common in men
• Mechanism: small reentry circuit in/near LV Purkinje system (septal ramifications), often associated with LV false tendon
• Acute termination: IV verapamil
• Chronic: Oral verapamil (not always effective); catheter ablation if preferred or CCBs fail
• Prognosis: benign course; SCD rare

---

SLIDE 22 — ELECTRICAL STORM / VT STORM

• 4% of primary prevention ICD patients
• Up to 20% of patients with known prior VT or resuscitated SCD
• Associated with worsening HF, acute ischemia, or proarrhythmic drug effect

1. Hemodynamic support - invasive monitoring, consider VA-ECMO or IABP if cardiogenic shock
2. Identify and reverse triggers:
   • Ischemia → emergent PCI/CABG
   • Electrolyte imbalance → aggressive K+ and Mg++ repletion
   • Drug-induced proarrhythmia → stop offending drug
   • New HF exacerbation → diurese, unload
3. Deep sedation/anesthesia - reduces sympathetic tone; crucial step often forgotten
4. Pharmacological suppression:
   • IV amiodarone (loading + infusion) - first-line
   • IV beta-blockers (propranolol, metoprolol) - especially if sympathetically driven
   • For refractory cases: IV bretylium (where available)
   • Special case - Brugada VT storm: IV isoproterenol + quinidine (not amiodarone or flecainide)
5. Stellate ganglion block (left) - effective adjunct in refractory VT storm; reduces sympathetic outflow
6. Emergent catheter ablation - life-saving in refractory VT storm; improves survival (per Braunwald's references)
7. Refractory: Stereotactic body radiotherapy (SBRT/STAR) - emerging salvage therapy

---

SLIDE 23 — INCESSANT VT

• Usually monomorphic
• Can be hemodynamically stable but leads to gradual cardiac decompensation (tachycardia-induced CM)
• Sometimes results from proarrhythmic effect of amiodarone or flecainide

• Hemodynamic support if deteriorating
• Withdraw precipitating antiarrhythmic if proarrhythmic cause suspected
• Correct underlying triggers
• Urgent catheter ablation is often the definitive treatment
• Note: Slow incessant VT may fall below ICD detection threshold → interrogate device and reprogram

---

SLIDE 24 — VT IN SPECIAL SUBSTRATES: BRUGADA SYNDROME

• Type 1: Coved ST-elevation ≥2 mm in V1-V3 (spontaneous or drug-induced)
• Risk of polymorphic VT and VF, not VT storm in typical form
• Associated with SCN5A mutations (~20-25% of cases)

• Spontaneous type 1 pattern + history of cardiac arrest/syncope = highest risk → ICD
• Spontaneous type 1, asymptomatic: EPS-guided; risk low but debated
• Drug-induced type 1 pattern only: lower risk

• IV isoproterenol (increases ICaL, restores action potential dome) - drug of choice for storm
• Quinidine (IKto blocker, prevents ST elevation, prevents arrhythmia) - oral prevention

• RVOT epicardial ablation eliminates Brugada phenotype in selected patients
• Efficacy per systematic review (Kotake 2023, PMID 35451610)

---

SLIDE 25 — VT IN SPECIAL SUBSTRATES: CPVT

• Autosomal dominant: RYR2 mutations (ryanodine receptor) → DAD-mediated triggered VT
• Classic presentation: exercise/emotion-triggered bidirectional or polymorphic VT → syncope, SCD in young
• Normal ECG at rest, no structural disease

• Beta-blockers (nadolol preferred) - cornerstone; reduces but does not eliminate risk
• Flecainide - adjunct; reduces DADs by stabilizing RYR2; reduces VT burden
• ICD if cardiac arrest or breakthrough VT despite beta-blockers; NOTE: shocks can cause sympathetic surge → VT storm → consider combined with beta-blocker
• Left cardiac sympathetic denervation (LCSD): Option for breakthrough arrhythmias or ICD-intolerant patients
• Avoid isoproterenol (worsens DADs)

---

SLIDE 26 — VT IN SPECIAL SUBSTRATES: ARVC

• Fibrofatty replacement of RV myocardium, sometimes biventricular
• Autosomal dominant mutations in desmosomal proteins (PKP2, DSC2, DSG2, DSP, JUP)
• Classic ECG: Epsilon waves, T-wave inversions V1-V3, LBBB-morphology VT

• Prior cardiac arrest, syncope, sustained VT, severe RV dysfunction → high risk → ICD
• NSVT, inducible VT at EPS, family history SCD → intermediate risk

• Sotalol or amiodarone - first-line for VT burden reduction
• Flecainide - used in ARVC (exception to structural HDD rule) per some centers
• Beta-blockers - adjunctive

• Important role; RV scar mapping; epicardial approach often required
• High recurrence rate reflects progressive nature of disease

---

SLIDE 27 — BUNDLE BRANCH REENTRY VT

• Uncommon (<10% of patients referred for VT ablation)
• Requires Purkinje system disease
• VT circuit: Down right bundle branch, through septum, up left bundle branch
• QRS resembles LBBB (or rarely RBBB in reverse circuit)
• Rate often rapid (>200 bpm)
• Associated with severe LV dysfunction, dilated CM, interventricular conduction delay in sinus rhythm

• Can mimic SVT with aberrancy (important to recognize)
• Curative by ablation: right bundle branch ablation eliminates VT
• BUT: poor anterograde His-Purkinje conduction afterward → pacemaker/ICD usually required
• Most patients have additional scar-related VTs → ICD implant indicated regardless

---

SLIDE 28 — MANAGEMENT OF ICD SHOCKS

• Confirm by interrogation: appropriate for VT/VF (not lead malfunction or AF with rapid rate)
• If isolated, stable, no deterioration: follow-up within 1-2 days + remote monitoring
• Evaluate for triggers: electrolyte disturbance, ischemia, drug changes

• Patient must call EMS; do NOT drive
• Activate VT storm protocol (see Slide 22)
• Reprogram ATP parameters; extend detection windows
• Consider AAD add-on or catheter ablation

• Causes: AF/flutter with rapid ventricular rate, T-wave oversensing, lead fracture/noise
• Consequences: reduced QoL, PTSD, increased mortality risk
• Prevention: optimal programming (long detection windows, high rate cutoffs), ATP programming

• Patients with ICD shocks have significantly higher rates of anxiety, depression, and PTSD
• Refer to cardiac psychology/liaison psychiatry as appropriate

---

SLIDE 29 — ADVANCED/EMERGING THERAPIES

Stereotactic Body Radiotherapy (SBRT / STAR)

• Non-invasive cardiac radiation targeting arrhythmia substrate
• Used for truly refractory VT failing all conventional therapies
• Target defined by cardiac MRI, ECG vest (ECGI), or prior ablation maps
• Mechanism: myocardial fibrosis and substrate modification
• Multiple systematic reviews now available (Gupta 2024, PMID 39716963; Greiner 2025, PMID 40883833)
• ~70-80% reduction in VT burden in initial series; multicenter trials ongoing

Noninvasive Cardiac Mapping (ECG Vest - ECGI)

• 252-electrode vest + CT/MRI → noninvasive mapping of VT origin
• Can guide ablation and SBRT target planning

Novel Ablation Energy Sources:

• Pulsed field ablation (electroporation): Nonthermal cell death, more tissue-selective
• Bipolar ablation: Two catheters generating energy between them to reach deep intramural substrate
• Needle catheter ablation: Direct delivery into deep intramural scar

VT Ablation in LVAD Patients

• Meta-analysis (Barrera 2025, PMID 41078026): catheter ablation feasible in LVAD patients; VT recurrence ~45% at 1 year; procedural mortality ~3%
• Access through LVAD inflow cannula occasionally required

---

SLIDE 30 — KEY CLINICAL TRIALS SUMMARY TABLE

---

SLIDE 31 — GUIDELINE SUMMARY: 2017 AHA/ACC/HRS AND 2022 ESC

2017 AHA/ACC/HRS (Al-Khatib et al., Heart Rhythm 2018)

2022 ESC (Zeppenfeld et al., Eur Heart J 2022)

• Strengthened role of catheter ablation earlier in management (not just after AAD failure)
• Emphasized substrate-based ablation strategies
• Expanded guidance on channelopathies and inherited arrhythmia syndromes
• New sections on SBRT as salvage therapy

---

SLIDE 32 — VT IN PREGNANCY

• Most AADs cross the placenta; balance maternal/fetal risk
• Safe in pregnancy: Beta-blockers (first-line), digoxin, sotalol (2nd/3rd trimester), flecainide, verapamil
• Avoid: Amiodarone (neonatal thyroid disease, growth retardation), Class IA agents if possible
• DC cardioversion: Safe in all trimesters; use standard settings; fetal monitoring recommended
• ICD therapy: continue existing ICD; S-ICD may be preferred for new implants to avoid fluoroscopy
• Idiopathic RVOT VT: generally well-tolerated; beta-blockers first-line

---

SLIDE 33 — APPROACH TO VT IN THE ACUTE MI SETTING

• PMVT/VF: up to 10% in early STEMI; associated with larger infarct, worse LV function
• Immediate defibrillation/cardioversion
• IV amiodarone or lidocaine for recurrent VT
• Beta-blockers for electrical storm driven by adrenergic activation
• Reperfusion (primary PCI) is the primary intervention
• Important: Early VF (<48h) after STEMI does not independently predict long-term arrhythmia risk or mandate ICD if no underlying reduced EF

• Portends worse prognosis
• Indicates larger scar, higher SCD risk
• Monomorphic sustained VT = scar-based reentry
• ICD indicated if VF/sustained VT occurs >48h post-MI (not acute ischemia-related)
• Reassess EF at 40 days post-MI before ICD decision

• 60-100 bpm, occurs within 12h, often heralds reperfusion
• Benign; does NOT predict sustained VT/VF
• No antiarrhythmic therapy required (unless hemodynamically compromising)

---

SLIDE 34 — PRACTICAL ALGORITHMS

Algorithm 1: Acute Wide Complex Tachycardia

Wide Complex Tachycardia
        ↓
   Is there a pulse?
   /            \
 No               Yes
  ↓                ↓
CPR + Unsync    Hemodynamically stable?
shock (200J)    /                    \
             No                      Yes
              ↓                        ↓
      Sync cardioversion         12-lead ECG
      (brief sedation)           VT vs SVT distinction
                                  ↓
                          IV Amiodarone 150mg
                          (or Procainamide if no SHD)
                          → If fails: Sync cardioversion

Algorithm 2: Long-term VT Management (Structural Heart Disease)

Sustained VT + Structural Heart Disease
        ↓
1. ICD (secondary prevention - mandatory)
        ↓
2. Optimize GDMT (beta-blocker, ACEi/ARNi, MRA)
        ↓
3. VT recurrence on ICD?
        ↓
  Yes → Add amiodarone or sotalol
        ↓
  VT persists? → Catheter ablation
        ↓
  Refractory? → Combination therapy / SBRT / Advanced center

---

SLIDE 35 — KEY TAKE-HOME POINTS

1. Hemodynamic stability drives the immediate action - cardiovert if unstable; pharmacology if stable
2. Treat any WCT in structural heart disease as VT until proven otherwise
3. ICD is the cornerstone of secondary prevention - antiarrhythmic drugs do not improve survival without an ICD
4. Amiodarone remains the most effective AAD for VT in structural disease despite long-term toxicities
5. VANISH trial (2025 updated NEJM): Catheter ablation is superior to escalating AADs in ischemic CM with VT
6. Torsade de pointes: IV magnesium + overdrive pacing + remove precipitants; NOT amiodarone
7. Electrical storm: Deep sedation + IV amiodarone + beta-blockers + emergent ablation
8. Idiopathic VT (RVOT, fascicular) = benign prognosis; ablation is curative and preferred; ICD not indicated
9. Substrate-based catheter ablation in sinus rhythm has transformed management - no need for inducible VT
10. Emerging: SBRT, electroporation, ECG vest mapping - expanding options for truly refractory VT

---

SLIDE 36 — REFERENCES (KEY)

1. Al-Khatib SM et al. 2017 AHA/ACC/HRS Guideline for Management of Patients with Ventricular Arrhythmias and Prevention of SCD. Heart Rhythm 2018;15:e73
2. Zeppenfeld K et al. 2022 ESC Guidelines for Ventricular Arrhythmias and SCD. Eur Heart J 2022;43:3997-4126
3. Cronin EM et al. 2019 HRS/EHRA/APHRS/LAHRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias. Europace 2019;21:1143
4. Sapp JL et al. Catheter Ablation or Antiarrhythmic Drugs for Ventricular Tachycardia (VANISH-2). NEJM 2025 (PMID 39555820)
5. Knops RE et al. Subcutaneous or Transvenous Defibrillator Therapy (ATLAS trial). NEJM 2020;383:526-536
6. Gupta A et al. Stereotactic Cardiac Radiotherapy for Refractory VT. Europace 2024 (PMID 39716963)
7. Joglar JA et al. 2023 HRS Expert Consensus on Arrhythmias During Pregnancy. Heart Rhythm 2023 (PMID 37211147)
8. Kotake Y et al. Catheter Ablation for Brugada Syndrome - Updated Systematic Review. Clin Res Cardiol 2023 (PMID 35451610)
9. Braunwald's Heart Disease, 11th Ed (Elsevier, 2022), Chapter 67
10. Harrison's Principles of Internal Medicine, 22nd Ed (McGraw-Hill, 2025), Chapters 261, 263
11. Fuster & Hurst's The Heart, 15th Ed, Chapter 37
12. Goldman-Cecil Medicine, International Edition, Chapters 49, 53-54

---