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 the assumption that they will have a malignant course until proven otherwise.
  • Characterization of the arrhythmia involves consideration of hemodynamic stability, duration and ECG morphology of the tachycardia, and presence or lack of underlying structural heart disease.
  • Ultimately, this characterization will aid in determining the patient’s risk for sudden cardiac arrest (SCA) and the 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 that lasts longer than 30 seconds or requires cardioversion because of hemodynamic compromise.
  • Polymorphic ventricular tachycardia (PMVT): VT characterized by an evolving QRS morphology. Torsades de Pointes (TdP) is a variant of PMVT that is typically preceded by a prolonged QT interval in sinus rhythm. Polymorphic VT is associated with hemodynamic collapse or instability.
  • Ventricular fibrillation (VF) is associated with disorganized mechanical contraction, hemodynamic collapse, and sudden death. The ECG reveals irregular and rapid oscillations (250–400 bpm) of highly variable amplitude without uniquely identifiable QRS complexes or T waves.
  • Ventricular arrhythmias are the major cause of sudden cardiac death (SCD). SCD is defined as unexpected death that generally occurs within 1 hour of the onset of symptoms in a person without any prior condition that would appear fatal. In the United States, approximately 350,000 cases of SCD occur annually. Among patients with aborted SCD, ischemic heart disease is the most common associated cardiac structural abnormality. Most cardiac arrest survivors do not have evidence of an 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 the substrate for reentry that produces SMVT.
      • PMVT and VF are commonly associated with ischemia and are the presumed cause of most out-of-hospital SCD.
    • NICM typically involves progressive dilation and fibrosis of the ventricular myocardium, providing an arrhythmogenic substrate.
    • Infiltrative cardiomyopathies (secondary to sarcoidosis, hemochromatosis, amyloidosis, etc.) affect a 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 (ARVC) is marked by fibrofatty replacement of the RV (and sometimes LV) myocardium that gives rise to left bundle branch block (LBBB) morphology VT and is associated with sudden death, particularly in young athletes.
    • Bundle branch reentry VT is a form of ventricular tachyarrhythmia that uses the His-Purkinje system in a reentrant circuit and is typically associated with cardiomyopathy and an 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 on imaging.
    • Catecholaminergic PMVT involves inherited, exercise-induced VT that is related to irregular calcium processing.
    • Idiopathic VT is a diagnosis of exclusion that requires the documented absence of structural heart disease, genetic disorders, and reversible etiologies (i.e., ischemia, metabolic abnormalities). Most idiopathic VTs originate from the RV outflow tract (RVOT) and are amenable to ablation. Less commonly, LV outflow tract (LVOT) VT or fascicular VT (using anterior and posterior divisions of the left bundle branch) may be discovered on EPS.

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General Principles

  • Ventricular tachyarrhythmias should be initially approached with the assumption that they will have a malignant course until proven otherwise.
  • Characterization of the arrhythmia involves consideration of hemodynamic stability, duration and ECG morphology of the tachycardia, and presence or lack of underlying structural heart disease.
  • Ultimately, this characterization will aid in determining the patient’s risk for sudden cardiac arrest (SCA) and the 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 that lasts longer than 30 seconds or requires cardioversion because of hemodynamic compromise.
  • Polymorphic ventricular tachycardia (PMVT): VT characterized by an evolving QRS morphology. Torsades de Pointes (TdP) is a variant of PMVT that is typically preceded by a prolonged QT interval in sinus rhythm. Polymorphic VT is associated with hemodynamic collapse or instability.
  • Ventricular fibrillation (VF) is associated with disorganized mechanical contraction, hemodynamic collapse, and sudden death. The ECG reveals irregular and rapid oscillations (250–400 bpm) of highly variable amplitude without uniquely identifiable QRS complexes or T waves.
  • Ventricular arrhythmias are the major cause of sudden cardiac death (SCD). SCD is defined as unexpected death that generally occurs within 1 hour of the onset of symptoms in a person without any prior condition that would appear fatal. In the United States, approximately 350,000 cases of SCD occur annually. Among patients with aborted SCD, ischemic heart disease is the most common associated cardiac structural abnormality. Most cardiac arrest survivors do not have evidence of an 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 the substrate for reentry that produces SMVT.
      • PMVT and VF are commonly associated with ischemia and are the presumed cause of most out-of-hospital SCD.
    • NICM typically involves progressive dilation and fibrosis of the ventricular myocardium, providing an arrhythmogenic substrate.
    • Infiltrative cardiomyopathies (secondary to sarcoidosis, hemochromatosis, amyloidosis, etc.) affect a 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 (ARVC) is marked by fibrofatty replacement of the RV (and sometimes LV) myocardium that gives rise to left bundle branch block (LBBB) morphology VT and is associated with sudden death, particularly in young athletes.
    • Bundle branch reentry VT is a form of ventricular tachyarrhythmia that uses the His-Purkinje system in a reentrant circuit and is typically associated with cardiomyopathy and an 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 on imaging.
    • Catecholaminergic PMVT involves inherited, exercise-induced VT that is related to irregular calcium processing.
    • Idiopathic VT is a diagnosis of exclusion that requires the documented absence of structural heart disease, genetic disorders, and reversible etiologies (i.e., ischemia, metabolic abnormalities). Most idiopathic VTs originate from the RV outflow tract (RVOT) and are amenable to ablation. Less commonly, LV outflow tract (LVOT) VT or fascicular VT (using anterior and posterior divisions of the left bundle branch) may be discovered on EPS.

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