Nonsustained ventricular tachycardia: Difference between revisions

No edit summary
 
(17 intermediate revisions by 6 users not shown)
Line 1: Line 1:
==Background==
==Background==
===Definition<ref>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.</ref><ref>Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001;86(5):579–585.</ref>===
===Definition<ref>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.</ref><ref>Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001;86(5):579–585.</ref>===
* >3-5 consecutive beats originating below the AV node
*>3-5 consecutive beats originating below the AV node
* Rate > 100bpm
*Rate > 100bpm
* Duration <30s
*Duration <30s
*Patient remains hemodynamically stable


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


==Clinical Features==
==Clinical Features==
* Often asymptomatic
*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.<ref>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.</ref><ref>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.</ref><ref>Udall JA, Ellestad MH. Predictive implications of ventricular premature contractions associated with treadmill stress testing. Circulation. 1977;56(6):985–989.</ref>
*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.<ref>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.</ref><ref>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.</ref><ref>Udall JA, Ellestad MH. Predictive implications of ventricular premature contractions associated with treadmill stress testing. Circulation. 1977;56(6):985–989.</ref>


==Differential Diagnosis==
==Differential Diagnosis==
Most important distinction is whether dysrhythmia is associated with underlying structural heart disease.
{{Tachycardia (wide) DDX}}
===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 LQTS, familial catecholaminergic PMVT. Increased risk of SCD, 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===
==Evaluation==
* Hypertension and LVH: Occurrence of NSVT warrants evaluation for ischemic heart disease, aggressive medical management of hypertension (including beta-blockade). Prognosis unclear.
===Workup===
* Valvular disease: Highest incidence in AS and MR. No evidence that occurrence of NSVT associated with SCD.
*All patients
* 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.
**History: including arrhythmogenic medications/substances, pertinent family history
* Hypertrophic cardiomyopathy: Genetic myocardial disease, myocyte disarray produces arrhythmogenic substrate. NSVT associated with increased risk of SCD.
**Physical examination
* Other conditions:
**[[ECG]]/[[CXR]]
** Non-ischemic dilated cardiomyopathy
**[[Echocardiography|TTE]]
** Giant-cell myocarditis
*In selected patients
** Repaired TOF
**Exercise testing
** Amyloidosis
**Advanced imaging (CT/C-MR)
** Sarcoidosis
**Electrophysiologic studies
** Chagas cardiomyopathy
**Genetic testing


==Diagnosis==
===Diagnosis===
===In all patients:===
[[File:PMC2922873 ipej100357-01.png|thumb|Sinus rhythm with a five beat run of nonsustained ventricular tachycardia]]
* History: including arrhythmogenic medications/substances, pertinent family history
*Based on [[ECG]]
* Physical examination
*Most important distinction is whether dysrhythmia is associated with underlying structural heart disease.
* ECG/CXR
* TTE


===In selected patients:===
====NSVT in the absence of apparent structural heart disease====
* Exercise testing
*Idiopathic [[Ventricular Tachycardia]]: Ventricular outflow arrhythmias (RVOT > LVOT). Good prognosis, rarely associated with tachycardia-induced cardiomyopathy and sudden cardiac death (SCD).
* Advanced imaging (CT/C-MR)
*[[Polymorphic ventricular tachycardia]]: Inherited or acquired [[long QT syndrome]], familial catecholaminergic PMVT
* Electrophysiologic studies
**Increased risk of sudden cardiac death, consideration for ICD if symptomatic (syncope, arrest) or asymptomatic QTc > 550ms.
* Genetic testing
*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:
**Non-ischemic dilated cardiomyopathy
**Giant-cell [[myocarditis]]
**Repaired [[TOF]]
**[[Amyloidosis]]
**[[Sarcoidosis]]
**[[Chagas]] cardiomyopathy


==Management==
==Management==
===Algorithm for the Evaluation and Management of NSVT===
[[File:Nonsustained Ventricular Tachycardia.png|thumb|Algorithm for the Evaluation and Management of NSVT<ref>Adapted from Katritis et al (2012)</ref>]]
[[File:Nonsustained Ventricular Tachycardia.png|800px|Adapted from Katritis et al (2012)]]
===AHA Guidelines<ref>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.</ref>===
*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.<ref>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.</ref>


===AHA Guidelines<ref>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.</ref>===
===Symptomatic Patients<ref>Gupta AK. Wide QRS Complex Tachycardias. Med Clin North Am. 2001 Mar; 85(2): 245-66.</ref>===
* Nonsustained Repetitive Monomorphic VT: amiodarone, beta-blockade (if tolerated), procainamide (IIA, C)
*[[Beta blockers]]
* 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)
**Initial therapy
* Correction of electrolyte abnormalities (specifically hypokalemia) may decrease progression to VF.<ref>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.</ref>
**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<ref>Gupta AK. Wide QRS Complex Tachycardias. Med Clin North Am. 2001 Mar; 85(2): 245-66.</ref>===
*Do note require any specific therapy
*Optimize underlying cardiac comorbidities


==Disposition==
==Disposition==
High-risk patients (age > 45yo, symptomatic, or with known structural heart disease) warrant immediate and appropriate evaluation. This includes echocardiography to identify underlying structural heart disease, exercise testing to evaluate whether NSVT represents underlying ischemic heart disease, and specialized testing in selected patients (ex. EPS, genetic testing in young symptomatic patients, or those with concerning family histories).
*Admit:
**High-risk patients
***Age >45 years
***Symptomatic
***Known structural heart disease
***Concerning family history
 
==See Also==
*[[Tachyarrhymias]]
*[[Wide Tachycardia]]
*[[Ventricular Tachycardia]]
*[[Polymorphic ventricular tachycardia]]


==External Links==
==External Links==
* [http://ddxof.com/nonsustained-ventricular-tachycardia/ DDxOf: Differential Diagnosis of Nonsustained Ventricular Tachycardia]
*[http://ddxof.com/nonsustained-ventricular-tachycardia/ DDxOf: Differential Diagnosis of Nonsustained Ventricular Tachycardia]


==References==
==References==

Latest revision as of 15:56, 25 September 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

Wide-complex tachycardia

Assume any wide-complex tachycardia is ventricular tachycardia until proven otherwise (it is safer to incorrectly assume a ventricular dysrhythmia than supraventricular tachycardia with abberancy)

^Fixed or rate-related

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
  • Based on ECG
  • 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:

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.
Retrieved from "https://www.wikem.org/w/index.php?title=Nonsustained_ventricular_tachycardia&oldid=230069"