Color Atlas and Synopsis of Electrophysiology, 1st Ed.


Yehoshua C. Levine, MD, and Alfred E. Buxton, MD


A 57-year-old man with a history of untreated hypertension presented to the emergency department with crushing substernal chest pain and diaphoresis lasting 6 hours. A 12-lead ECG upon arrival showed sinus tachycardia with 3 mm ST-segment elevations in leads V2-V5. The patient was emergently transported to the cardiac catheterization laboratory where coronary angiography demonstrated a subtotal occlusion of the proximal left anterior descending coronary artery. Percutaneous coronary intervention was performed, with export thrombectomy and drug-eluting stenting of the culprit vessel and immediate resolution of symptoms. Serum levels of Troponin-T peaked at 3.3 ng/mL. He was admitted to the coronary intensive care unit, where echocardiography the following day showed left ventricular (LV) hypertrophy with moderate hypokinesis of the anteroseptal and anterior walls and an estimated left ventricular ejection fraction (LVEF) of 35% to 40%. He remained asymptomatic and hemodynamically stable and was transferred to the floor later that day, where his cardiac medications were optimally titrated and cardiac rehabilitation planning was begun.

On the fourth hospital day, during the discharge planning process, the patient’s telemetry alarmed during a 14-beat run of a wide-complex tachycardia with heart rate approximately 250 bpm (Figure 17-1). He reported no symptoms during the episode. No further episodes of nonsustained ventricular tachycardia (NSVT) were observed for the duration of his hospitalization. The patient and nursing staff are concerned about the telemetry findings and wonder whether his hospital discharge should be delayed so that further evaluation can be performed. What is the significance of these findings on telemetry? Should they influence ongoing clinical management of this patient?


FIGURE 17-1 Telemetry monitor recording from the fourth day after the patient’s acute myocardial infarction (MI). Nonsustained ventricular tachycardia (NSVT) is demonstrated on the telemetry strip.


This patient has had an episode of NSVT 4 days after an acute anterior myocardial infarction (MI) in the setting of LV dysfunction documented on echocardiogram. Management considerations for this patient include determining the prognostic significance of his NSVT and determining whether further therapy is indicated either while he is still an inpatient or during outpatient follow-up.

Historically, NSVT has been defined in a number of ways based on the duration and rate of the observed arrhythmia.1 The standard definition is three or more consecutive ventricular premature depolarizations at a rate of at least 100 beats/min, lasting up to a maximum duration of 30 seconds before spontaneous termination.2 The rate cutoff of 100 beats/min is based on the observation that tachycardias slower than this rate do not generally confer adverse prognostic significance in patients who have a history of MI.3

The prevalence and prognostic significance of NSVT in a given patient depends upon the presence and extent of structural heart disease. Up to 3% of asymptomatic patients with no evidence of heart disease have been shown to experience runs of NSVT over the course of 24 hours of monitoring, but the prognostic significance of this finding remains unclear.4 In contrast, NSVT occurring in patients who have suffered an MI or have a history of idiopathic dilated cardiomyopathy,5 valvular heart disease such as mitral valve prolapse,6 longstanding hypertension and left ventricular hypertrophy,7 and hypertrophic cardiomyopathy8 is more common and may function as an independent predictor of mortality under certain situations. However, this does not mean that NSVT independently predicts arrhythmic death. NSVT in the post-MI period, such as that which occurred in the Case Presentation, portends a worse overall prognosis, but the incidence of sudden cardiac death (SCD) in patients with NSVT is not increased out of proportion to the increase in total mortality in this patient population.

In the following sections, we will outline the prognostic significance and management considerations of NSVT in patients with a history of MI.


Unlike sustained tachyarrhythmias, NSVT is usually not associated with symptoms in patients with structural heart disease (because most episodes are brief); rather, it is usually discovered incidentally during electrocardiographic monitoring. Early studies that identified NSVT as a risk factor for the development of sudden death in patients with a recent MI were based on the observation that ventricular fibrillation in the acute phase of MI was often preceded by escalating frequency of ventricular ectopy and NSVT. Later studies demonstrated an association between the presence of NSVT discovered in the early postinfarction period and risk of SCD in patients with reduced left ventricular ejection fraction (LVEF).9 With rare exception, most data suggest that NSVT within the first 48 hours after an MI does not carry prognostic significance.10 By contrast, NSVT occurring after the first 48 hours after an MI has been linked with an increased risk of both SCD and total mortality in pre-reperfusion era studies,11 and NSVT was accordingly used as a qualifying characteristic in early implantable cardioverter-defibrillator (ICD) trials in patients with prior MI and LV systolic dysfunction.12,13 It is important to note, however, that the increased risk of SCD in patients with NSVT is due to the increased risk of total mortality in these patients and not due to any specific predilection to sustained ventricular arrhythmias. Indeed, in a subgroup analysis of the first 1480 patients enrolled in the MUSTT study, Buxton et al found that electrocardiographic characteristics of spontaneous NSVT in patients with coronary artery disease cannot differentiate between patients with and those without sustained VT inducible by programmed stimulation.14,15 In these patients, NSVT portends a worse overall prognosis, but the risk of SCD is not increased out of proportion to the risk of total mortality. A post-hoc analysis of the relation of LVEF and inducible VT to mode of death in MUSTT-enrolled patients (who all had significant LV dysfunction and spontaneous asymptomatic NSVT) demonstrated a significantly higher risk of mortality in those patients whose LVEF was <30%, regardless of the presence or absence of inducible sustained VT that might predict risk for VT. In these patients, it is the presence and severity of heart failure that serves as a major determinant of total mortality. Furthermore, the percent of total mortality accounted for by arrhythmic events was similar regardless of whether the LVEF was <30% or ≥30% and would likely also be similar whether or not there was a history of documented NSVT.16

In the reperfusion era, the presence of NSVT has become a less significant risk stratification tool following an MI, as newer data have not identified an independent association between NSVT and worse prognosis in many situations.17,18 In the absence of other risk factors such as low LVEF, NSVT predicts neither inducibility of sustained monomorphic VT nor total mortality in patients post-MI. The reason for this is probably multifactorial and has to do with the fact that early reperfusion strategies and the ubiquitous use of β-blocker therapy have reduced both the incidence of NSVT and postinfarction scar burden even in patients who do have NSVT.


The patient described in the Case Presentation has been noted to have asymptomatic NSVT in the setting of an LVEF estimated to be between 35% and 40% after his acute MI. The first question is whether this observation portends worse prognosis. As discussed in the previous section, the more significant issue is his LV dysfunction (reflected both by EF and clinical evidence of heart failure), and he will require optimal medical management and follow-up echocardiography as an outpatient to determine his long-term total mortality. Demonstrating persistent LV dysfunction during follow-up 2 to 3 months after his MI is likely to have greater prognostic utility than observing episodes of NSVT. If LV dysfunction persists in the months-to-years after his MI, his total mortality risk will be higher, but his risk of SCD requires other prognostic variables for accurate risk stratification. Unfortunately, while the LVEF correlates with overall survival, it tells us nothing about how patients die (suddenly versus nonsuddenly).

The next issue is whether the presence of NSVT on routine monitoring should alter medical management for this patient. The historical approach of suppressing NSVT with class I or III antiarrhythmic medications in patients after MI in an effort to reduce the incidence of malignant arrhythmias and SCD has become extinct, as controlled trials showed no evidence that pharmacologic antiarrhythmic therapy reduces overall mortality in this population.19Importantly, the CAMIAT trial found that although amiodarone reduced the annual rate of arrhythmic death or resuscitated ventricular tachyarrhythmias in patients who have frequent ventricular premature depolarizations or at least one episode of NSVT between 6 and 45 days post-MI, it did not affect all-cause or cardiac mortality in these patients.20 β-Blockers are recommended to reduce total mortality in the post-MI period, but do not benefit patients who have NSVT more than patients who do not have NSVT. Therefore, in asymptomatic patients with a history of MI who have NSVT on cardiac monitoring, no medication adjustment is indicated based on the presence of NSVT alone.

The most important practical consideration for this patient is whether to perform an electrophysiology study (EPS) to determine inducibility of sustained monomorphic VT. Indeed, determining the utility of EPS in preparation for possible primary prophylactic ICD implantation is the only way that documenting NSVT might change management. Patients with NSVT in the context of LVEF ≤40% who have inducible sustained monomorphic VT at EPS have a significantly higher risk of SCD and total mortality at 2 years than patients without inducible VT, as demonstrated in the MUSTT trial. Furthermore, noninducible patients in the MUSTT trial had a significantly lower risk of SCD compared with inducible patients at 2 and 5 years (12% versus 18% and 24% versus 32%, respectively).13,21 There is also evidence that inducibility of ventricular arrhythmias is predictive of subsequent appropriate ICD therapies for VT/VF in patients who undergo ICD implantation.22 EPS is often performed in borderline-risk patients to determine whether their level of risk justifies ICD implantation, and many of these patients have NSVT. Indeed, a recent National Cardiovascular Data Registry (NCDR) ICD Registry analysis of patients undergoing EPS for improved risk stratification of SCD observed that patients undergoing EPS more often had NYHA class I symptoms and NSVT than patients who did not undergo EPS prior to ICD implantation.23 If our patient’s LVEF remains 35% to 40% at least 3 months after his MI—or if his LVEF becomes 30% to 35% at that point but he has New York Heart Association (NYHA) class I symptoms—NSVT justifies further risk stratification with an EPS to determine whether he is likely to derive improved survival with an ICD.

Whether this patient should be discharged with a wearable cardiac defibrillator (WCD) during this 3-month period is not clearly indicated from an evidence-based perspective. An ongoing randomized clinical trial is evaluating the ability of the WCD to reduce mortality in the first 3 months after MI. It is important to remember that although this period is the single time when patients with MI have highest risk of SCD, many of the SCD occurring during this period appear not to result from arrhythmias. A substudy of the VALIANT trial reviewed autopsy records of patients who suffered SCD early after acute MI and found that at 3 months after the MI, only approximately 30% to 35% of the sudden deaths were considered presumed arrhythmic.24 These data suggest that a defibrillator, which would terminate ventricular arrhythmias, may not reduce mortality in many patients who experience sudden death early after an acute MI. While current evidence does not demonstrate a reduction in mortality with a WCD, it is nonetheless reasonable to discharge such a patient with this temporary device if the physician is concerned about the patient’s risk of arrhythmic SCD.

There are two special situations that should be highlighted:

1. NSVT morphology may be prognostically and diagnostically important. With repeated episodes of NSVT, a 12-lead ECG should be performed to characterize the morphology of VT and to evaluate for an idiopathic VT, most commonly arising from the right ventricular outflow tract (Figure 17-2). In patients with a history of MI whose NSVT morphology suggests right ventricular outflow tract origin, the NSVT is probably not related to the MI and does not carry adverse prognostic significance.


FIGURE 17-2 A 12-lead electrocardiogram tracing from a 60-year-old man with a history of a remote inferior MI who was hospitalized for pneumonia and was incidentally noted to have evidence of ventricular ectopy during his hospitalization. The premature ventricular depolarizations captured on this tracing—and the NSVT documented on cardiac monitoring—arose from the right ventricular outflow tract and had no relation to his prior inferior MI.

2. Management differs for patients with symptoms (such as palpitations, lightheadedness) that are attributable to NSVT, or patients who develop cardiomyopathy as a direct result of frequent episodes of NSVT. Patients with symptomatic NSVT are more likely to have structurally normal hearts and may not already be treated with β-blockers. By contrast, patients with cardiomyopathy attributable to high NSVT burden will likely already have been started on β-blocker therapy for management of their cardiomyopathy, and the β-blockers may aid in controlling the NSVT burden. Patients in these categories may benefit from antiarrhythmic therapy and/or catheter ablation for symptom relief and/or for optimal treatment of their cardiomyopathy25 (Figure 17-3). Note that the reason to treat NSVT is for symptom relief, not to reduce mortality risk.


FIGURE 17-3 Induction of NSVT with double extrastimuli in a 76-year-old man with a history of coronary artery disease who presented with NSVT in the setting of presyncope and palpitations and was referred to for ablation.


The patient presented has had NSVT incidentally noted a few days after his acute MI. As discussed, the more significant prognostic indicator of adverse cardiovascular events is his LV dysfunction, reflected by an LVEF of 35% to 40%. Having had documented NSVT should not affect his post-MI medication regimen and should not result in further monitoring or risk stratification at the current time. However, if he remains a borderline candidate for ICD implantation for primary prevention of SCD in 3 months, that is, if his LVEF remains 35% to 40% or if his LVEF becomes 30% to 35% and he has NYHA class I symptoms—the presence of NSVT would justify further risk stratification with an EPS to determine his candidacy for ICD implantation.


  1. Buxton AE. Nonsustained ventricular tachycardia: clinical significance and mechanisms. In: Josephson ME, Wellens HJJ, eds. Tachycardias: Mechanisms and Management. Mount Kisco, NY: Futura Publishing Co Inc; 1993;353-361.

  2. Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006 key data elements and definitions for electrophysiological studies and procedures: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology). Circulation. 2006;114:2534-2570.

  3. Anderson KP, DeCamilla J, Moss AJ. Clinical significance of ventricular tachycardia (3 beats or longer) detected during ambulatory monitoring after myocardial infarction. Circulation. 1978;57:890.

  4. Hinkle LE, Carver ST, Stevens M. The frequency of asymptomatic disturbances of cardiac rhythm and conduction in middle-aged men. Am J Cardiol. 1969;24:629-650.

  5. Doval HC, Nul DR, Grancelli HO, et al. Nonsutained ventricular tachycardia in severe heart failure. Independent marker of increased mortality due to sudden death. GESICA-GEMA Investigators. Circulation. 1996;94:3198-3203.

  6. Kligfield P, Hochreiter C, Kramer H, et al. Complex arrhythmias in mitral regurgitation with and without mitral valve prolapse: contrast to arrhythmias in mitral valve prolapse without mitral regurgitation. Am J Cardiol. 1985;55:1545.

  7. McLenaghan JM, Henderson E, Morris KL, et al. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med. 1987;317:787-792.

  8. McKenna WJ, England D, Doi YL, et al. Arrhythmia in hypertrophic cardiomyopathy: influence on prognosis. Br Heart J. 1981;46:168.

  9. Buxton AE, Marchlinski FE, Waxman HL, et al. Prognostic factors in nonsustained ventricular tachycardia. Am J Cardiol. 1984;53:1275-1279.

 10. Heidbuchel H, Tack J, Vanneste L, et al. Significance of arrhythmias during the first 24 hours of acute myocardial infarction treated with alteplase and effect of early administration of a beta-blocker or a bradycardic agent on their incidence. Circulation. 1994;89:1051-1059.

 11. Bigger JT Jr, Fleiss JL, Rolnitzky LM. Prevalence, characteristics and significance of ventricular tachycardia detected by 24-hour continuous electrocardiographic recordings in the late hospital phase of acute myocardial infarction. Am J Cardiol. 1986;58(13):1151.

 12. Buxton AE, Lee KL, Fisher JD, et al. 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.

 13. 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.

 14. Buxton AE, Lee KL, DiCarlo L, et al. Nonsustained ventricular tachycardia in patients with coronary artery disease: relationship to inducible sustained ventricular tachycardia. Ann Intern Med. 1996;125:35-39.

 15. Buxton AE, Hafley GE, Lehmann MH, et al. Prediction of sustained ventricular tachycardia inducible by programmed stimulation in patients with coronary artery disease: utility of clinical variables. Circulation. 1999;99:1843-1850.

 16. Buxton AE, Lee KL, Hafley GE, et al. Relation of ejection fraction and inducible ventricular tachycardia to mode of death in patients with coronary artery disease: an analysis of patients enrolled in the Multicenter Unsustained Tachycardia Trial. Circulation. 2002;106:2466-2472.

 17. Hohnloser SH, Klingenheben T, Zabel M, et al. Prevalence, characteristics and prognostic value during long-term follow-up of nonsustained ventricular tachycardia after myocardial infarction in the thrombolytic era. J Am Coll Cardiol. 1999;33(7):1895.

 18. Bloch Thomsen PE, Jons C, Raatikainen MJ, et al. Long-term recording of cardiac arrhythmias with an implantable cardiac monitor in patients with reduced ejection fraction after acute myocardial infarction: the Cardiac Arrhythmias and Risk Stratification After Acute Myocardial Infarction (CARISMA) study. Circulation. 2010;122:1258-1264.

 19. Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324(12):781.

 20. Cairns JA, Connolly SJ, Roberts R, Gent M. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators. Lancet. 1997;349(9053):675.

 21. Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. J Am Coll Cardiol. 2012;60(20):1993.

 22. Daubert JP, Winters SL, Subacius H, et al. Ventricular arrhythmia inducibility predicts subsequent ICD activation in nonischemic cardiomyopathy patients: a DEFINITE substudy. Pacing Clin Electrophysiol. 2009;32:755-761.

 23. Cheng A, Wang Y, Berger RD, et al. Electrophysiology studies in patients undergoing ICD implantation: findings from the NCDR®. Pacing Clin Electrophysiol. 2012;35(8):912-918.

 24. Pouleur AC, Barkoudah E, Uno H, et al. Pathogenesis of sudden unexpected death in a clinical trial of patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. Circulation. 2010;122:597-602.

 25. Chen T, Koene R, Benditt DG, Lu F. Ventricular ectopy in patients with left ventricular dysfunction: should it be treated? J Card Fail. 2013;19(1):40-49.