Case 1

64M with a history of HFrEF (LVEF 20-25%), CAD, AICD (unknown indication), COPD, CKD III presenting with gradual onset shortness of breath, progressive bilateral lower extremity edema.
Examination consistent with severe acute decompensated heart failure presumed secondary to left ventricular dysfunction.
Telemetry monitoring with multiple episodes of nonsustained ventricular tachycardia.

In the ED, the patient developed worsening respiratory failure despite initiation of therapy, requiring endotracheal intubation. Continuous cardiac monitoring revealed persistent salvos of NSVT, progressing to slow ventricular tachycardia without device intervention.
Device interrogation revealed multiple events, 3 shocks, several ATP’s over the recorded period.

Evaluation and Management:

• NSVT with known (severe) ischemic heart disease
• For repetitive monomorphic ventricular tachycardia: amiodarone, beta-blockade (if tolerated), procainamide (IIA, C)¹

ECG’s

Case 2

31F with autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), presenting with fever and cough.
Evaluation consistent with sepsis presumed secondary to pulmonary source.
Telemetry monitoring initially with ventricular bigeminy, then nonsustained ventricular tachycardia.

In the ED, the patient developed pulseless ventricular tachycardia – apparently polymorphic. Chest compressions and epinephrine produced return of spontaneous circulation with recovery to baseline neurologic function.
ECG revealed prolonged QTc and chemistry panel notable for critical hypokalemia/hypomagnesemia.

Evaluation and Management:

• NSVT progressing to VT
• Initially attributed to electrolyte disturbances. However, serial ECG’s continued to show prolonged QTc (possibly acquired, home medications included metoclopramide and erythromycin). Early echocardiography demonstrated global hypokinesis with EF 30-35% attributed to severe sepsis and recurrent defibrillation. Cardiac CT after resolution of acute illness showed persistently depressed ejection fraction without coronary atherosclerosis. The presence of NICM associated with malignant dysrhythmias warranted ICD placement.
• Cardioversion for hemodynamic compromise (I, B), B-blockade (I, B), amiodarone if no LQTS (I, C), urgent angiography if ischemia not excluded (I, C)¹
• Correction of electrolyte abnormalities (specifically hypokalemia) may decrease progression to VF.²

ECG’s

Definition^3,4

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

Epidemiology^3,5

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

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.^6,7,8

Evaluation

In 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

NSVT in the absence of structural heart disease

NSVT in Idiopathic Ventricular Tachycardia

Ventricular outflow arrhythmias:

RVOT: 70-80%, LBBB pattern

LVOT: 20-30%, RBBB pattern

Mechanism:

Adrenergically mediated

Occur during exercise, resolve as heart-rate increases, recur during recovery

Management:

Exclude arrhythmogenic right ventricular cardiomyopathy (imaging, myocardial biopsy)

If symptomatic, beta-blockade, ± IC anti-arrhythmic, CCB (verapamil) for ILVT

Prognosis:

Good, rare tachycardia-induced cardiomyopathy, rare SCD

NSVT in Polymorphic Ventricular Tachycardia

Mechanism

LQTS (acquired or inherited)

Familial catecholaminergic polymorphic VT

Management

Symptomatic (ex. syncope, cardiac arrest): ICD

Asymptomatic QTc > 550ms: consider ICD

Prognosis

Increased risk SCD

Arrhythmogenic Right Ventricular Cardiomyopathy

Mechanism

Fibrosis, fibro-fatty replacement of myocardium in RVIT/RVOT/RV apex

May occur with only subtle structural abnormalities of the right ventricle

LBBB morphology

Management

Anti-arrhythmics of limited utility

Catheter ablation, ICD backup

Prognosis

Increased risk SCD

NSVT with apparent structural heart disease1

Hypertension and LVH

Mechanism

Stretch-induced abnormal automaticity

Fibrotic tissue

Presence of NSVT correlates with degree of hypertrophy and subendocardial fibrosis

Management

Evaluation for ischemic heart disease

Aggressive medical management of hypertension (including beta-blockade)

Prognosis

Unclear

Valvular Disease

Mechanism

High incidence in AS, severe MR (25%)

Mechanical stress from dysfunctional valvular apparatus

Management

Beta-blockade if symptomatic

Prognosis

No evidence that NSVT is an independent predictor of SCD.

Ischemic Heart Disease^9-14

Mechanism

Monomorphic VT associated with re-entry at the borders of ventricular scars

Ischemia induces polymorphic NSVT/VF

Management

Revascularization, beta-blockade, statin, ACE/ARB

MADIT I, MUSTT: ICD for ICM LVEF <40%, NSVT, EPS inducible VT

MADIT II, SCD-HeFT: ICD for moderate-to-severe LV dysfunction irrespective of NSVT or EPS findings

Prognosis

NSTEMI with NSVT >48h after admission 2x risk SCD (MERLIN-TIMI 36)

STEMI with NSVT common, not as predictive of ACM or SCD as LVEF (CARISMA)

NSVT <24h after admission for NSTEMI/STEMI not of prognostic significance.

Hypertrophic Cardiomyopathy

Mechanism

Genetic myocardial disease

Myocyte disarray, fibrosis, ischemia result in arrhythmogenic substrate

Management

Restriction of physical activity

ICD (NSVT, LV thickness, FH SCD, syncope, abnormal BP response to exercise)

Beta-blockade, anti-arrhythmic for symptoms

Prognosis

Increased risk SCD (1% annual)

Other Conditions

• Non-ischemic dilated cardiomyopathy
• Giant-cell myocarditis
• Repaired TOF
• Amyloidosis
• Sarcoidosis
• Chagas cardiomyopathy

Algorithm for the Evaluation of NSVT¹

References

1. 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.
2. 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.
3. 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.
4. Katritsis DG, Camm AJ. Nonsustained ventricular tachycardia: where do we stand? Eur Heart J. 2004;25(13):1093–1099. doi:10.1016/j.ehj.2004.03.022.
5. Wellens HJ. Electrophysiology: Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart. 2001;86(5):579–585.
6. 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.
7. 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.
8. Udall JA, Ellestad MH. Predictive implications of ventricular premature contractions associated with treadmill stress testing. Circulation. 1977;56(6):985–989.
9. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med. 1989;321(6):406–412. doi:10.1056/NEJM198908103210629.
10. Goldstein S. Propranolol therapy in patients with acute myocardial infarction: the Beta-Blocker Heart Attack Trial. Circulation. 1983;67(6 Pt 2):I53–7.
11. Moss AJ. MADIT-I and MADIT-II. J Cardiovasc Electrophysiol. 2003;14(9 Suppl):S96–8.
12. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med. 1996;335(26):1933–1940. doi:10.1056/NEJM199612263352601.
13. 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.
14. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352(3):225–237. doi:10.1056/NEJMoa043399.
15. WikEM: Nonsustained Ventricular Tachycardia