Ventricular Tachyarrhythmias

Ventricular Tachyarrhythmias is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • Ventricular tachyarrhythmias should be initially approached with assumption that they will have malignant course, until proven otherwise.
  • Characterization of the arrhythmia involves consideration of hemodynamic stability, duration and ECG morphology of tachycardia, and the presence or lack of underlying structural heart disease.
  • Characterization will aid in determining the patient’s risk for sudden cardiac arrest (SCA) and need for therapeutic intervention and/or device implantation.

Definition

  • Nonsustained ventricular tachycardia (NSVT): Three or more consecutive ventricular complexes (>100 bpm) that terminate spontaneously within 30 seconds.
  • Sustained monomorphic ventricular tachycardia (SMVT): Tachycardia of ventricular origin with single QRS morphology lasting longer than 30 seconds or requiring cardioversion due to hemodynamic compromise.
  • Polymorphic ventricular tachycardia (PMVT): VT is characterized by evolving QRS morphology. TdP is a variant of PMVT typically preceded by prolonged QT interval in SR. PMVT is associated with hemodynamic collapse or instability.
  • VF: Associated with disorganized mechanical contraction of ventricles, hemodynamic collapse, and sudden death. ECG reveals irregular and rapid oscillations (250–400 bpm) of highly variable amplitude without clearly identifiable QRS complexes or T waves.
  • Ventricular arrhythmias—major cause of sudden cardiac death (SCD).
    • SCD—unexpected death that generally occurs within 1 hour of onset of symptoms in person without prior condition that would appear fatal. In the US, approximately 350,000 cases of SCD occur annually.
      • Among patients with aborted SCD, ischemic heart disease is most commonly associated cardiac structural abnormality. Most cardiac arrest survivors do not have evidence of acute MI; however, >75% have evidence of previous infarcts.
      • Nonischemic cardiomyopathy (NICM) is also associated with an elevated risk for SCD.1

Etiology

  • VT associated with structural heart disease
    • Most ventricular arrhythmias are associated with structural heart disease, typically related to active ischemia or prior infarct.
      • Scar and the peri-infarct area provide substrate for reentry that produces SMVT.
      • PMVT and VF—commonly associated with ischemia and are presumed cause of most out-of-hospital SCD.
    • NICM typically involves progressive dilation and fibrosis of ventricular myocardium, providing arrhythmogenic substrate.
    • Infiltrative cardiomyopathies (secondary to sarcoidosis, hemochromatosis, amyloidosis, etc.) affect smaller patient population that is at significant risk for ventricular arrhythmias and whose management is less clearly defined.
    • Adults with prior repair of congenital heart disease are commonly afflicted with both VT and SVT.
    • Arrhythmogenic right ventricular dysplasia (ARVD) or cardiomyopathy—marked by fibrofatty replacement of the RV (and sometimes LV) myocardium giving rise to left bundle branch block (LBBB) morphology VT and is associated with sudden death, particularly in young athletes.
    • Bundle branch reentry VT—form of ventricular tachyarrhythmia that uses His–Purkinje system in a reentrant circuit and is typically associated with cardiomyopathy and abnormal conduction system.
  • VT in the absence of structural heart disease
    • Inherited ion channelopathies, such as those seen in Brugada syndrome and LQTS, can lead to PMVT and sudden death in patients without evidence of structural heart disease.
    • Catecholaminergic PMVT involves inherited, exercise-induced VT related to irregular calcium processing.
    • Idiopathic VT—diagnosis of exclusion that requires documented absence of structural heart disease, genetic disorders, and reversible etiologies (i.e., ischemia, metabolic abnormalities).
      • Most originate from RV outflow tract (RVOT) and are amenable to ablation.
      • LV outflow tract (LVOT) VTs, arising from near the coronary cusps or aortomitral continuity, or fascicular VTs (using anterior and posterior divisions of the left bundle branch) are less common forms of idiopathic VT.
      • Tachycardia-mediated cardiomyopathy can result if left untreated.

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General Principles

  • Ventricular tachyarrhythmias should be initially approached with assumption that they will have malignant course, until proven otherwise.
  • Characterization of the arrhythmia involves consideration of hemodynamic stability, duration and ECG morphology of tachycardia, and the presence or lack of underlying structural heart disease.
  • Characterization will aid in determining the patient’s risk for sudden cardiac arrest (SCA) and need for therapeutic intervention and/or device implantation.

Definition

  • Nonsustained ventricular tachycardia (NSVT): Three or more consecutive ventricular complexes (>100 bpm) that terminate spontaneously within 30 seconds.
  • Sustained monomorphic ventricular tachycardia (SMVT): Tachycardia of ventricular origin with single QRS morphology lasting longer than 30 seconds or requiring cardioversion due to hemodynamic compromise.
  • Polymorphic ventricular tachycardia (PMVT): VT is characterized by evolving QRS morphology. TdP is a variant of PMVT typically preceded by prolonged QT interval in SR. PMVT is associated with hemodynamic collapse or instability.
  • VF: Associated with disorganized mechanical contraction of ventricles, hemodynamic collapse, and sudden death. ECG reveals irregular and rapid oscillations (250–400 bpm) of highly variable amplitude without clearly identifiable QRS complexes or T waves.
  • Ventricular arrhythmias—major cause of sudden cardiac death (SCD).
    • SCD—unexpected death that generally occurs within 1 hour of onset of symptoms in person without prior condition that would appear fatal. In the US, approximately 350,000 cases of SCD occur annually.
      • Among patients with aborted SCD, ischemic heart disease is most commonly associated cardiac structural abnormality. Most cardiac arrest survivors do not have evidence of acute MI; however, >75% have evidence of previous infarcts.
      • Nonischemic cardiomyopathy (NICM) is also associated with an elevated risk for SCD.1

Etiology

  • VT associated with structural heart disease
    • Most ventricular arrhythmias are associated with structural heart disease, typically related to active ischemia or prior infarct.
      • Scar and the peri-infarct area provide substrate for reentry that produces SMVT.
      • PMVT and VF—commonly associated with ischemia and are presumed cause of most out-of-hospital SCD.
    • NICM typically involves progressive dilation and fibrosis of ventricular myocardium, providing arrhythmogenic substrate.
    • Infiltrative cardiomyopathies (secondary to sarcoidosis, hemochromatosis, amyloidosis, etc.) affect smaller patient population that is at significant risk for ventricular arrhythmias and whose management is less clearly defined.
    • Adults with prior repair of congenital heart disease are commonly afflicted with both VT and SVT.
    • Arrhythmogenic right ventricular dysplasia (ARVD) or cardiomyopathy—marked by fibrofatty replacement of the RV (and sometimes LV) myocardium giving rise to left bundle branch block (LBBB) morphology VT and is associated with sudden death, particularly in young athletes.
    • Bundle branch reentry VT—form of ventricular tachyarrhythmia that uses His–Purkinje system in a reentrant circuit and is typically associated with cardiomyopathy and abnormal conduction system.
  • VT in the absence of structural heart disease
    • Inherited ion channelopathies, such as those seen in Brugada syndrome and LQTS, can lead to PMVT and sudden death in patients without evidence of structural heart disease.
    • Catecholaminergic PMVT involves inherited, exercise-induced VT related to irregular calcium processing.
    • Idiopathic VT—diagnosis of exclusion that requires documented absence of structural heart disease, genetic disorders, and reversible etiologies (i.e., ischemia, metabolic abnormalities).
      • Most originate from RV outflow tract (RVOT) and are amenable to ablation.
      • LV outflow tract (LVOT) VTs, arising from near the coronary cusps or aortomitral continuity, or fascicular VTs (using anterior and posterior divisions of the left bundle branch) are less common forms of idiopathic VT.
      • Tachycardia-mediated cardiomyopathy can result if left untreated.

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