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Sustained VentricularTachycardia

Chapter 261 | Harrison's 22e · Part 6 – Cardiovascular Disorders · Chapter 261

Key Clinical Points

  1. Sustained monomorphic VT is defined as a wide QRS arrhythmia lasting ≥ 30 s or requiring intervention such as antitachycardia pacing from a defibrillator or cardioversion for termination.
  2. Accelerated idioventricular rhythm (AIVR) is a slow, regular wide-complex rhythm often seen in acute MI, cardiomyopathy, or during sleep apnea; it can also be idiopathic.
  3. Fusion beats are a reliable marker of ventriculoatrial (VA) dissociation and confirm a ventricular origin for the tachycardia.
  4. Clinical presentation varies based on heart rate, underlying cardiac function, and autonomic response; rapid VT may cause hypotension/syncope, while slower VT may present as palpitations.
  5. Sustained monomorphic VT must be distinguished from supraventricular tachycardia (SVT) with bundle branch block (aberrancy).
  6. Specific ECG markers for VT include R or Rs waves in lead aVR and precordial concordance (absence of R/S waves in V1–V6).
  7. Outflow tract VT is differentiated by transition: RVOT shows late transition; LVOT shows early transition with prominent R wave in V1–V3.
  8. Polymorphic VT and ventricular fibrillation (VF) should prompt immediate evaluation for ischemia.
  9. Nonischemic cardiomyopathies (e.g., sarcoidosis, Chagas disease, Lamin A/C mutations) can cause monomorphic VT due to fibrotic scars.
  10. Genetic syndromes like LQTS, Brugada, and CPVT present with specific patterns of polymorphic or bidirectional VT.

DEFINITION & CLASSIFICATION

• Sustained monomorphic VT:

Definition (Harrison's 22e): an arrhythmia with a wide QRS lasting for at least 30 s or requiring an intervention such as antitachycardia pacing from a defibrillator or a cardioversion for termination. • Accelerated idioventricular rhythm (AIVR): • Description: Slow regular wide-complex rhythm. • Clinical Context: Common during acute MI, in patients with cardiomyopathies, or during sleep apnea; can also be idiopathic (often emerging when the sinus rate slows during sleep).

ETIOLOGY & PATHOPHYSIOLOGY

• Mechanism of VT: • Structural heart disease: Usually related to reentry or automaticity in diseased conduction pathways (e.g., areas of patchy replacement fibrosis due to infarction, fibrosis, inflammation, or prior cardiac surgery). • Idiopathic VT: Occurs in structurally normal hearts; due to a focal region of automaticity in the myocardium or reentry involving a portion of the Purkinje system. • Clinical Contexts (Table 261-1): • Outflow tract origin: RVOT (LBBB pattern, inferior axis) and LVOT (inferior axis, early transition). • Ischemic cardiomyopathy: Monomorphic VT common with prior large MI; Polymorphic VT/VF prompt ischemia evaluation. • Nonischemic cardiomyopathy: Fibrotic scars from sarcoidosis, Chagas disease, or Lamin A/C mutations. • Arrhythmogenic RV cardiomyopathy: Monomorphic VT usually of RV origin (LBBB morphology in V). • Repaired tetralogy of Fallot: Monomorphic VT of RV origin (LBBB morphology in V). • Hypertrophic cardiomyopathy: Polymorphic VT or VF; monomorphic VT associated with myocardial scars. • Genetic arrhythmia syndromes: • LQTS → Torsades de pointes. • Brugada → Ventricular fibrillation (often nocturnal). • CPVT → Polymorphic or bidirectional VT. • Short QT and early repolarization → Ventricular fibrillation.

CLINICAL FEATURES

• Presentation: • Varies based on: rate of arrhythmia, underlying cardiac function, and autonomic adaptation. • Rapid VT: • Can produce hypotension → may present as syncope (especially in patients with significant ventricular dysfunction). • Slower VT: • In patients with normal cardiac function, may be tolerated and present as simple palpitations. • Progression: • Monomorphic VT that is rapid or associated with structural heart disease may eventually deteriorate to ventricular fibrillation (VF).

DIAGNOSTIC APPROACH

  1. Differentiate monomorphic VT from SVT with aberrancy (Flowchart 261-1): • Step 1: Is there an R or Rs wave in lead aVR? → Yes → VT → No → Proceed to Step 2 • Step 2: Are there no R or S or Rs waves in any of V1 to V6 (Precordial Concordance)? → Yes → VT → No → Possible SVT with aberrancy; VT still possible
  2. Identify specific VT morphology and etiology: • Outflow tract differentiation: • RVOT: LBBB pattern in V, inferior axis (tall QRS in inferior leads), late transition in precordial leads. • LVOT: Similar inferiorly directed axis, early precordial transition with prominent R wave in V1–V3. • Ischemic cardiomyopathy: • Monomorphic VT is common with prior large MI. • Polymorphic VT and VF → prompt ischemia evaluation. • Nonischemic cardiomyopathy: • Fibrotic scars (sarcoidosis, Chagas disease, Lamin A/C mutations) cause monomorphic VT. • Arrhythmogenic RV cardiomyopathy: Monomorphic VT usually of RV origin (LBBB morphology in V). • Repaired tetralogy of Fallot: Monomorphic VT of RV origin (LBBB morphology in V). • Hypertrophic cardiomyopathy: Polymorphic VT or VF; monomorphic VT associated with myocardial scars. • Genetic arrhythmia syndromes: • LQTS → Torsades de pointes. • Brugada → Ventricular fibrillation (often nocturnal). • CPVT → Polymorphic or bidirectional VT. • Short QT/Early repolarization → Ventricular fibrillation.
  3. Identify specific markers for VT: • Fusion beats: Reliable marker of ventriculoatrial (VA) dissociation; occurs when the atrial rate is slower than the ventricular rate. • Precordial Concordance: Absence of R or S waves in V1–V6. • aVR Morphology: Monophasic R wave or Rs in aVR is relatively specific for VT.

MANAGEMENT & TREATMENT

  1. Identify and treat underlying cause: Target the primary cause of the arrhythmia.
  2. Manage bradycardia in AIVR: • If loss of atrioventricular synchrony causes hemodynamic compromise → Atropine may be administered to increase the sinus rates.
  3. Note on asymptomatic rhythms: Specific antiarrhythmic therapy for asymptomatic idioventricular rhythm is not necessary.

KEY PEARLS & HIGH-YIELD POINTS

• SVT vs VT Differentiation: Critical distinction; use aVR morphology and precordial concordance to rule out SVT with aberrancy. • Fusion Beats: A key indicator of ventriculoatrial (VA) dissociation, confirming a ventricular origin. • Ischemia Alert: Polymorphic VT and VF should always prompt an evaluation for acute ischemia. • Outflow Tract Distinction: RVOT presents with LBBB pattern and late transition; LVOT presents with similar axis but early transition in V1–V3. • AIVR Management: Focus on underlying cause and correction of bradycardia; no specific antiarrhythmic therapy needed for asymptomatic cases.

Reference Tables

TABLE 261-1 Sustained Ventricular Arrhythmias 1. Idiopathic ventricular tachycardia (VT) without structural heart…

Harrison's 22e, p.1964

    1. Idiopathic ventricular tachycardia (VT) without structural heart disease
      A. Outflow tract origin
      • Right ventricular (RV) outflow tract: left bundle branch block pattern in
      V with inferior axis (tall QRS in inferior leads) and late transition in the
      1
      precordial leads
      • Left ventricular (LV) outflow tract: similar inferiorly directed axis but
      with early precordial transition with prominent R wave in V–V
      2 3
      B. LV fascicular VT: Typical right bundle branch block pattern in V with sharp
      1
      intrinsicoid deflection and left axis deviation (arising from left posterior
      fascicle in its most common form)
      C. Papillary muscle VT
      • Posteromedial: atypical right bundle branch block pattern in V with
      1
      monophasic R wave and left axis deviation
      • Anterolateral: atypical right bundle branch block pattern in V with
      1
      positive deflection in lead III and negative deflection in lead I
      2. Ischemic cardiomyopathy
      • Monomorphic VT is common with prior large myocardial infarction
      • Polymorphic VT and ventricular fibrillation (VF) should prompt ischemia
      evaluation
      3. Nonischemic cardiomyopathy
      • Fibrotic scars can cause monomorphic VT, especially with sarcoidosis
      or other inflammatory cardiomyopathies, Chagas’ disease, and
      familial arrhythmogenic cardiomyopathies such as Lamin A/C genetic
      cardiomyopathy
      • Polymorphic VT and VF can also occur independently or related to
      degeneration of monomorphic VT
      4. Arrhythmogenic RV cardiomyopathy
      • Monomorphic VT usually of RV origin (left bundle branch morphology in V)
      1
      • Polymorphic VT and VF can occur independently or related to degeneration
      of monomorphic VT
      5. Repaired tetralogy of Fallot
      • Monomorphic VT of RV origin (usually left bundle branch morphology in V)
      1
      6. Hypertrophic cardiomyopathy
      • Polymorphic VT or ventricular fibrillation
      • Less commonly, monomorphic VT associated with myocardial scars,
      particularly apical aneurysms
      7. Genetic arrhythmia syndromes
      A. Long QT syndrome
      • Torsades des pointes VT
      B. Brugada syndrome
      • Ventricular fibrillation episodes, often nocturnal
      C. Catecholaminergic polymorphic VT
      • Polymorphic VT or bidirectional VT
      D. Short QT and early repolarization syndromes
      • Ventricular fibrillation
      8. Idiopathic polymorphic VT or ventricular fibrillation
      • Usually triggered by recurrent premature ventricular contractions; the most
      common site of origin is the left posterior fascicle (right bundle branch
      block/left anterior fascicular block pattern)

TABLE 261-2 Summary of Randomized Controlled Studies Assessing Catheter Ablation of Ventricular Tachycardia in Patients…

Harrison's 22e, p.1966

STUDY,
YEAR		 STUDY
PERIOD		 SAMPLE SIZE INCLUSION CRITERIA CONTROL ARM AGE
(years)		 MALE
(%)		 ICM
(%)		 BASELINE
LVEF (%)		 FOLLOW-UP
(months)
CA OC
2000–2006 64 64 Prior MI, ICD for VF or unstable VT Medical therapy 67 ± 10 87 100 32 ± 9
VTACH, 2010 2002–2006 52 55 Prior MI, LVEF ≤50%, ICD indicated
for stable VT		 ICD + medical therapy 66 ± 8 93 100 34 ± 9 22.5 ± 9
2012–2014 13 14 IHD, ≥1 ICD shock or ≥3 ATP
therapies for monomorphic VT in
last 6 months		 AAD therapy 63 ± NR 93 100 30 ± NR
VANISH,
2016		 2009–2015 132 127 Prior MI, ICD in situ, ≥1 episode of
VT while on a class I/III AAD		 Escalation of AAD
therapy		 69 ± 8 93 100 31 ± 11 27.9 ± 17.1
2002–2010 54 57 IHD, LVEF ≤40%, unstable VT ICD + medical therapy 67 ± 8 84 100 31 ± 7
BERLIN-VT,
2020		 2015–2018 76 83 Prior MI, LVEF 30–50%, ICD in situ
for life-threatening VT		 Medical therapy until
third ICD shock (then
VT ablation)		 66 ± 10 87 100 41 ± 6 13.2 ± 9.5
2012–2021 23 24 Cardiomyopathy, had first ICD
shock		 Medical therapy 68 ± 9 85 81 32 ± 9
SURVIVE-VT,
2022		 2010–2017 71 73 Prior MI, sustained VT causing ICD
shock or syncope		 AAD therapy 70 ± 9 96 100 33 ± 11 23
2015–2020 60 61 LVEF <50%, ICD indicated for
secondary prevention or inducible
monomorphic VT on EPS		 ICD + medical therapy 55 (46–64) 81 35 40 (30–49)