Nonsustained ventricular tachycardia: Difference between revisions
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===Diagnosis===
===Diagnosis===
[[File:PMC2922873 ipej100357-01.png|thumb|Sinus rhythm with a five beat run of nonsustained ventricular tachycardia]]
*Based on [[ECG]]
*Based on [[ECG]]


Revision as of 03:27, 5 April 2019

Background

Definition[1][2]

  • >3-5 consecutive beats originating below the AV node
  • Rate > 100bpm
  • Duration <30s
  • Patient remains hemodynamically stable

Epidemiology

  • Occurs in 0-4% of ambulatory patients
  • Increased frequency in males and with increasing age

Clinical Features

  • Often asymptomatic
  • In some patients, NSVT is associated with an increased risk of sustained tachyarrhythmias and sudden cardiac death. In others it is of little prognostic significance.[3][4][5]

Differential Diagnosis

Most important distinction is whether dysrhythmia is associated with underlying structural heart disease.

NSVT in the absence of apparent structural heart disease

  • Idiopathic Ventricular Tachycardia: Ventricular outflow arrhythmias (RVOT > LVOT). Good prognosis, rarely associated with tachycardia-induced cardiomyopathy and sudden cardiac death (SCD).
  • Polymorphic ventricular tachycardia: Inherited or acquired long QT syndrome, familial catecholaminergic PMVT
    • Increased risk of sudden cardiac death, consideration for ICD if symptomatic (syncope, arrest) or asymptomatic QTc > 550ms.
  • Arrhythmogenic Right Ventricular Cardiomyopathy: Fibro-fatty deposition in RVIT/RVOT/RV apex. Increased risk of SCD, consideration for catheter ablation with ICD backup.

NSVT with apparent structural heart disease

  • Hypertension and LVH: warrants evaluation for ischemic heart disease, aggressive medical management of hypertension (including beta-blockade). Prognosis unclear.
  • Valvular disease: Highest incidence in AS and MR. No evidence that occurrence of NSVT associated with SCD.
  • Ischemic heart disease: Monomorphic NSVT around myocardial scars, active ischemia associated with both mono/polymorphic VT and VF. In ED, early NSVT (<24h) after NSTEMI/STEMI common and not associated with adverse outcomes.
  • Hypertrophic cardiomyopathy; myocyte disarray produces arrhythmogenic substrate. NSVT associated with increased risk of SCD.
  • Other conditions:

Evaluation

Workup

  • All patients
    • History: including arrhythmogenic medications/substances, pertinent family history
    • Physical examination
    • ECG/CXR
    • TTE
  • In selected patients
    • Exercise testing
    • Advanced imaging (CT/C-MR)
    • Electrophysiologic studies
    • Genetic testing

Diagnosis

Sinus rhythm with a five beat run of nonsustained ventricular tachycardia

Management

Algorithm for the Evaluation and Management of NSVT[6]

AHA Guidelines[7]

  • Nonsustained Repetitive Monomorphic VT: amiodarone, beta-blockade (if tolerated), procainamide (IIA, C)
  • Nonsustained Polymorphic VT: Cardioversion for hemodynamic compromise (I, B), B-blockade (I, B), amiodarone if no LQTS (I, C), urgent angiography if ischemia not excluded (I, C)
  • Correction of electrolyte abnormalities (specifically hypokalemia) may decrease progression to VF.[8]

Symptomatic Patients[9]

  • Beta blockers
    • Initial therapy
    • May benefit patients with coexisiting cardiac conditions (CAD, CHF)
  • Verapamil, diltiazem
    • Second line therapies
    • Do not use in patients with uncontrolled heart failure.
  • Antiarrhythmic medications are generally reserved for patients that have failed beta blocker or calcium channel blocking who are NOT candidates for ablation procedures. Expert consultation is advised.

Asymptomatic patients[10]

  • Do note require any specific therapy
  • Optimize underlying cardiac comorbidities

Disposition

  • Admit:
    • High-risk patients
      • Age >45 years
      • Symptomatic
      • Known structural heart disease
      • Concerning family history

See Also

External Links

References

  1. ↑ Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. J Am Coll Cardiol. 2012;60(20):1993–2004. doi:10.1016/j.jacc.2011.12.063.
  2. ↑ Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001;86(5):579–585.
  3. ↑ Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. 1999;341(25):1882–1890. doi:10.1056/NEJM199912163412503.
  4. ↑ Jouven X, Zureik M, Desnos M, Courbon D, Ducimetière P. Long-term outcome in asymptomatic men with exercise-induced premature ventricular depolarizations. N Engl J Med. 2000;343(12):826–833. doi:10.1056/NEJM200009213431201.
  5. ↑ Udall JA, Ellestad MH. Predictive implications of ventricular premature contractions associated with treadmill stress testing. Circulation. 1977;56(6):985–989.
  6. ↑ Adapted from Katritis et al (2012)
  7. ↑ Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death--executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(17):2099–2140. doi:10.1093/eurheartj/ehl199.
  8. ↑ Higham PD, Adams PC, Murray A, Campbell RW. Plasma potassium, serum magnesium and ventricular fibrillation: a prospective study. Q J Med. 1993;86(9):609–617.
  9. ↑ Gupta AK. Wide QRS Complex Tachycardias. Med Clin North Am. 2001 Mar; 85(2): 245-66.
  10. ↑ Gupta AK. Wide QRS Complex Tachycardias. Med Clin North Am. 2001 Mar; 85(2): 245-66.
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