Version July 2025
INTRODUCTION —
Nonsustained ventricular tachycardia (NSVT) is a common arrhythmia. It is usually asymptomatic and is typically diagnosed during external cardiac monitoring (eg, continuous ambulatory electrocardiography or inpatient telemetry), pacemaker interrogation, or exercise testing.
The presence of NSVT has long been recognized as a potential marker for developing sustained ventricular arrhythmias. NSVT in the presence of structural heart disease carries a more serious prognosis than NSVT in the absence of a cardiac abnormality. While NSVT in patients with structural heart disease predicts overall mortality, it does not predict sudden cardiac death.
There are two general goals in the management of NSVT:
●Identification of patients at risk for sustained arrhythmias and sudden cardiac death
●Treatment to suppress symptoms caused by NSVT (when present)
This topic will review the diagnosis and management of NSVT. The mechanism of NSVT in the structurally normal heart is addressed in more detail in another topic. (See "Nonsustained VT in the absence of apparent structural heart disease".)
Sustained ventricular tachycardia is addressed elsewhere:
●(See "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation".)
●(See "Ventricular tachycardia in the absence of apparent structural heart disease".)
DEFINITION —
The most commonly used definition of nonsustained ventricular tachycardia (NSVT) is an arrhythmia with all three of the following characteristics [1]:
●Three or more consecutive ventricular beats
●Rate of >100 beats per minute
●Duration of less than 30 seconds
The approach to distinguishing VT from other causes of wide QRS complex tachycardias (ie, supraventricular tachycardia [SVT] with aberrant conduction, SVT with preexcitation, pacemaker-associated tachycardia, or artifact) is discussed separately. (See 'Differential diagnosis' below and "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation", section on 'Differential diagnosis'.)
CLINICAL MANIFESTATIONS —
The history, physical examination, and 12-lead electrocardiogram (ECG) can all be helpful in establishing the diagnosis of nonsustained ventricular tachycardia (NSVT).
History — Patients with NSVT are usually asymptomatic, although some patients may notice symptoms associated with episodes of NSVT. Most patients with NSVT will have a history of underlying structural heart disease (eg, coronary artery disease, heart failure, hypertrophic cardiomyopathy, congenital heart disease), although NSVT can also be seen in patients without known structural heart disease. (See "Nonsustained VT in the absence of apparent structural heart disease".)
The type and intensity of symptoms, if present, will vary depending upon the rate and duration of the NSVT, along with the presence or absence of comorbid conditions such as cardiomyopathy or coronary artery disease. Symptomatic patients with NSVT typically present with one or more of the following:
●Palpitations
●Chest pain
●Shortness of breath
●Syncope or presyncope
Most commonly, symptomatic patients will report palpitations that may or may not be associated with chest pain or shortness of breath. If the duration of the episode lasts several seconds with an associated rate of NSVT that is rapid enough to result in hemodynamic compromise, patients may experience presyncope or even syncope.
Physical examination — Few physical examination findings in patients with NSVT are unique and specific. Patients will have a pulse exceeding 100 beats per minute during the episode. In addition, if the physical examination coincides with an episode of NSVT, this can reveal evidence of atrioventricular (AV) dissociation, which is present in up to 75 percent of patients with VT, although it is not always easy to detect [2-4]. During AV dissociation, the normal coordination of atrial and ventricular contraction is lost, which may produce characteristic physical examination findings including:
●Marked fluctuations in the blood pressure because of the variability in the degree of left atrial contribution to left ventricular filling, stroke volume, and cardiac output.
●Variability in the occurrence and intensity of heart sounds (especially S1) ("cacophony of heart sounds"), which is heard more frequently when the rate of tachycardia is slower.
●Cannon "A" waves – Cannon A waves are intermittent and irregular jugular venous pulsations of greater amplitude than normal waves. They reflect simultaneous atrial and ventricular activation, resulting in contraction of the right atrium against a closed tricuspid valve. Prominent A waves can also be seen during some SVTs. Such prominent waves result from simultaneous atrial and ventricular contraction occurring with every beat. (See "Assessment of the jugular venous pressure".)
DIAGNOSTIC EVALUATION —
Our approach to performing diagnostic testing and using the test results to guide patient management is found below.
Evaluation of all patients — All patients with nonsustained ventricular tachycardia (NSVT) should undergo a 12-lead electrocardiogram (ECG). On occasion, NSVT will occur during ECG acquisition. NSVT typically generates a wide QRS complex, usually with a QRS width >0.12 seconds. A full discussion of the ECG features of VT is presented separately. (See "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation", section on 'Electrocardiogram' and "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation", section on 'Additional diagnostic evaluation'.)
For patients with only a single episode of NSVT captured on cardiac monitoring or ECG, no further investigation is required.
For patients with more than one episode of NSVT on cardiac monitoring, we take the following approach:
●We evaluate for reversible, noncardiac causes of ventricular arrhythmias such as electrolyte imbalances, hypoxia, adverse drug effects (eg, drug-induced QT prolongation), anemia, and hypotension.
●We perform an echocardiogram to evaluate for structural heart disease including diagnoses such as dilated cardiomyopathy, hypertrophic cardiomyopathy, and severe valvular disease. Cardiac magnetic resonance (CMR) can be used selectively to complement echocardiography.
●We perform continuous ambulatory ECG monitoring for 14 to 30 days, with the duration of monitoring dependent on the frequency of symptoms. Ambulatory monitoring clarifies the frequency of NSVT and whether sustained VT is present. For patients with known NSVT who report vague symptoms that may not have correlated with the arrhythmia on previous monitoring, ambulatory monitoring will determine whether there is a correlation. If symptoms are found not to correlate with NSVT, other causes of the symptoms should be investigated.
Tests indicated for certain patients — For specific subsets of patients with NSVT, other testing may be indicated:
●For patients with either known coronary artery disease or exercise-related symptoms, stress testing is indicated. Because myocardial ischemia is a cause of ventricular arrhythmias, effective treatment of coronary artery disease (eg, antianginal medications, coronary revascularization) may prevent future episodes of NSVT.
●For patients whose ECG or echocardiogram is suggestive of arrhythmogenic right ventricular cardiomyopathy, CMR or signal-averaged ECG may be useful. Implantable cardioverter-defibrillator (ICD) is indicated for some patients with arrhythmogenic right ventricular cardiomyopathy and VT. (See "Arrhythmogenic right ventricular cardiomyopathy: Treatment and prognosis", section on 'Patients with an indication for an ICD'.)
●For patients with left ventricular ejection fraction >35 percent who experience syncope, near-syncope, or palpitations lasting for longer than 30 seconds, we often perform an electrophysiology study to evaluate for the presence of sustained VT. If sustained VT is induced, an ICD would be indicated [5,6].
A discussion of the diagnostic evaluation of patients with VT is presented separately. (See "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation", section on 'Additional diagnostic evaluation'.)
Classification of cardiac structure as normal or abnormal — Based on the results of diagnostic testing, we classify patients as having a structurally normal or structurally abnormal heart. The reason for this distinction is that patients with structurally abnormal hearts who have ventricular arrhythmias are at increased risk of sudden cardiac death, whereas those with normal hearts and VT are not at increased risk. For the purposes of this discussion, we consider a heart to be structurally abnormal if one of the following is present:
●Cardiomyopathy of any etiology (eg, ischemic, dilated, hypertrophic, restrictive)
●History of myocardial infarction with evidence of scar on noninvasive imaging
●Severe valvular disease
There are many echocardiographic findings that, while not normal, do not increase the patient’s risk of sudden cardiac death. Examples include mild or moderate valvular disease and concentric hypertrophy due to hypertension. If the classification of the patient is not straightforward, consultation with a cardiovascular specialist is advised.
DIFFERENTIAL DIAGNOSIS —
The differential diagnosis for a wide QRS complex tachycardia (WCT) includes nonsustained ventricular tachycardia (NSVT), supraventricular tachycardia with aberrant conduction (either preexistent or rate-related), supraventricular tachycardia with preexcitation, supraventricular tachycardia in a pacemaker-dependent patient, and electrocardiogram (ECG) artifact. Differentiating VT from other causes of WCT may be difficult, particularly if a high-quality 12-lead ECG is not available during the time of the arrhythmia. In general, a WCT, particularly when poorly tolerated, should be considered to be VT until proven otherwise.
The approach to differentiating VT from other causes of WCT is discussed separately. (See "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation", section on 'Differential diagnosis'.)
TREATMENT OF PATIENTS WITH STRUCTURALLY NORMAL HEARTS —
Our approach to the treatment of nonsustained ventricular tachycardia (NSVT) in patients with structurally normal hearts is described below (algorithm 1). A discussion about distinguishing normal from abnormal cardiac structure is found above. (See 'Classification of cardiac structure as normal or abnormal' above.)
Asymptomatic patients — NSVT may be detected in asymptomatic patients on routine pacemaker or defibrillator interrogation, ambulatory rhythm monitoring, inpatient telemetry monitoring, or exercise testing. Beta blockers, antiarrhythmic medications, and implantable cardioverter-defibrillators (ICDs) are not indicated for patients with structurally normal hearts who have asymptomatic NSVT because no studies have suggested these interventions improve outcomes. One prospective observational cohort study of 582 patients, most of whom had a normal left ventricular ejection fraction, found that asymptomatic NSVT detected on routine pacemaker interrogation did not impact survival [7].
Symptomatic patients — While NSVT is usually asymptomatic, some patients experience palpitations, chest pain, shortness of breath, presyncope, or syncope. Because many of the symptoms that may be attributed to NSVT are vague and nonspecific, it is important to try to correlate symptoms to episodes of NSVT on rhythm monitoring before initiating therapy specifically to treat NSVT.
Initial treatment — For the initial treatment of patients with structurally normal hearts who have symptomatic NSVT, we suggest beta blockers. Metoprolol (usual effective dose 50 to 200 mg daily) and carvedilol (usual effective dose 6.25 to 25 mg twice daily) are commonly prescribed. While beta blockers have been shown to reduce ventricular arrhythmias and sudden cardiac death only in patients with structural heart disease, we have found beta blockers to be helpful for controlling symptoms in some patients with structurally normal hearts. [1]
For patients with symptomatic NSVT and structurally normal hearts who remain symptomatic on beta blockers, or who are unable to take beta blockers, we suggest adding a nondihydropyridine calcium channel blocker. We typically use verapamil (usual effective dose of 360 to 480 mg daily) or diltiazem (usual effective dose of 240 to 360 mg daily). While this class of drugs does not have demonstrated efficacy in suppressing VT, it may be helpful in certain cases. (See "Calcium channel blockers in the treatment of cardiac arrhythmias", section on 'Ventricular arrhythmia'.)
Persistent symptoms — In patients with structurally normal hearts who have persistent symptoms despite treatment with a beta blocker and/or calcium channel blocker, we proceed with radiofrequency catheter ablation (RFA) or the addition of antiarrhythmic drug therapy.
●Radiofrequency catheter ablation versus antiarrhythmic drugs – RFA and antiarrhythmic drugs are both options for patients with structurally normal hearts who have symptomatic monomorphic NSVT despite treatment with beta blockers and/or calcium channel blockers [1]. RFA is particularly effective in patients whose ECG suggests an idiopathic, triggered arrhythmia that originates in the outflow tracts, septum, or papillary muscles [1,8]. For patients who are not good RFA candidates due to the location of the VT origin or other patient-related factors, antiarrhythmic medications are preferred. More details about the treatment of VT in the absence of apparent structural heart disease are found elsewhere. (See "Ventricular tachycardia in the absence of apparent structural heart disease".)
●Choice of antiarrhythmic drug – For patients who are not considered to be good candidates for RFA, or for whom the procedure was not successful, we choose an antiarrhythmic medication based on the risk of coronary artery disease.
•Low coronary artery disease risk – For patients with symptomatic NSVT and structurally normal hearts who are at low risk for coronary artery disease, we typically use an antiarrhythmic drug in class IC (eg, flecainide, propafenone) (table 1). The initial dosing is flecainide 100 mg twice daily or propafenone 150 mg every eight hours. Class IC agents are safe and effective for the suppression of ventricular arrhythmias in patients with a normal ejection fraction and without coronary artery disease.
•Intermediate or high coronary artery disease risk – For patients with frequent, symptomatic NSVT and structurally normal hearts who are at intermediate or high risk for coronary artery disease, or who have documented coronary artery disease, we use a class III agent (eg, sotalol, amiodarone) because class IC agents have been shown to increase the risk of sudden cardiac death in this population. The use of dofetilide, another class III agent, for the treatment of NSVT is off-label, and recent data indicate dofetilide fails to suppress the occurrence of NSVT in the majority of patients [9]. Of the class III agents, sotalol is less effective than amiodarone but carries a lower risk of long-term toxicity. Initiation of sotalol is discussed elsewhere (see "Clinical uses of sotalol", section on 'Initiation of therapy' and "Clinical use of dofetilide", section on 'Protocol for administration'). Amiodarone is initiated at a dose of 200 mg three times daily for two weeks, then 200 mg two times daily for two weeks, and then 200 mg daily. The dose can be further reduced to 100 mg daily if there is concern over toxicity, and follow-up monitoring of liver, thyroid, and lung function should be performed. (See "Amiodarone: Clinical uses" and "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring".)
TREATMENT OF PATIENTS WITH STRUCTURALLY ABNORMAL HEARTS —
Our approach to the treatment of nonsustained ventricular tachycardia (NSVT) in patients with structurally abnormal hearts is described below (algorithm 1). A discussion about distinguishing normal from abnormal cardiac structure is found above. (See 'Classification of cardiac structure as normal or abnormal' above.)
Asymptomatic patients — NSVT may be detected in asymptomatic patients on routine pacemaker or defibrillator interrogation, ambulatory rhythm monitoring, inpatient telemetry monitoring, or exercise testing. Patients with asymptomatic NSVT and structurally abnormal hearts are typically already receiving a beta blocker because it is indicated due to their cardiac condition. However, if they are not, we start a beta blocker. Metoprolol succinate (usual effective dose 50 to 200 mg daily) and carvedilol (usual effective dose 6.25 to 25 mg twice daily) are commonly prescribed. We do not recommend using antiarrhythmic medications or radiofrequency catheter ablation (RFA) for most asymptomatic patients with structurally abnormal hearts because these therapies do not reduce the risk of sudden cardiac death even when they successfully suppress arrhythmias. However, there are two types of asymptomatic patients for whom RFA or an antiarrhythmic medication may be useful:
●Patients with reduced ejection fraction that is thought to be secondary to frequent ventricular ectopy, in which case suppressing the arrhythmia may improve the ejection fraction. (See "Arrhythmia-induced cardiomyopathy".)
●Patients with biventricular pacemakers whose pacing is compromised by frequent ventricular arrhythmias.
Our antiarrhythmic drug recommendations are the same as for symptomatic patients. (See 'Persistent symptoms' below.)
Symptomatic patients — Patients with structurally abnormal hearts who have symptoms are initially treated with beta blockers. Those with persistent symptoms may be treated with either antiarrhythmic drug therapy or catheter ablation.
Initial treatment — For the initial treatment of patients with structurally abnormal hearts who have symptomatic NSVT, we suggest beta blockers for patients who are not already taking them. Metoprolol succinate (usual effective dose 50 to 200 mg daily) and carvedilol (usual effective dose 6.25 to 25 mg twice daily) are commonly prescribed. Beta blockers have been shown to reduce ventricular arrhythmias and sudden cardiac death in structural heart disease (eg, heart failure with reduced ejection fraction, post-myocardial infarction, certain channelopathies).
We do not recommend the use of nondihydropyridine calcium channel blockers for most patients with structural heart disease, with occasional exceptions (eg, hypertrophic cardiomyopathy). Nondihydropyridine calcium channel blockers may increase the risk of decompensated heart failure in patients with reduced ejection fraction [1].
Persistent symptoms — For patients with structurally abnormal hearts who have persistent, symptomatic NSVT despite beta blockers, RFA and antiarrhythmic medications are both valid options. Physicians who practice at an institution with expertise in VT ablation may prefer to start with RFA, while others may choose an antiarrhythmic agent. RFA is more challenging to perform for patients with scar-related VT than for VT in structurally normal hearts. [1]
For patients with structurally abnormal hearts who have persistent, symptomatic NSVT for whom an antiarrhythmic strategy has been chosen, we favor sotalol and amiodarone, which are class III antiarrhythmic medications. (table 1). Dofetilide, which is another class III agent, may not be as effective as sotalol and dofetilide [9]. Class IC drugs (eg, flecainide, propafenone) should not be used in patients with structural heart disease or coronary artery disease because they have been shown to increase arrhythmic sudden death and total cardiovascular mortality even when they successfully suppress ventricular ectopy [10,11]. We often start with sotalol, despite the fact that it is less effective than amiodarone, because it carries a lower risk of long-term toxicity [12]. Initiation of sotalol is discussed elsewhere. (See "Clinical uses of sotalol", section on 'Initiation of therapy' and "Clinical use of dofetilide", section on 'Protocol for administration'.).
If amiodarone is selected, we initiate this medication at a dose of 200 mg three times daily for two weeks, then 200 mg two times daily for two weeks, and then 200 mg daily. The dose can be further reduced to 100 mg daily if there is concern over toxicity, and follow-up monitoring of liver, thyroid, and lung function should be performed (see "Amiodarone: Clinical uses" and "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring"). Multiple trials in post-myocardial infarction and heart failure patients have demonstrated that amiodarone reduces ventricular arrhythmias and does not impact mortality [13-16].
If class III agents cannot be used or are inadequate to suppress symptomatic NSVT, a class IB (eg, mexiletine) or class ID (eg, ranolazine) agent may be added. We typically start with mexiletine 150 to 200 mg every eight hours. However, there is no high-quality evidence to guide therapy with these agents.
Implantable cardioverter-defibrillators — Patients with structurally abnormal hearts and NSVT may be at increased risk of sudden cardiac death. Implantation of a cardioverter-defibrillator may be indicated. Discussions about determining implantable cardioverter-defibrillator
(ICD) candidacy are found elsewhere. (See 'Tests indicated for certain patients' above and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Ventricular arrhythmias".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Ventricular tachycardia (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition – The most common definition of nonsustained ventricular tachycardia (NSVT) is ≥3 consecutive ventricular beats, a heart rate of >100 beats per minute, and a duration of less than 30 seconds. (See 'Definition' above.)
●Clinical manifestations – Patients with NSVT are usually asymptomatic, but some patients may notice palpitations, chest pain, shortness of breath, syncope, or presyncope. (See 'Clinical manifestations' above.)
●Diagnostic evaluation – Patients with NSVT should have a 12-lead electrocardiogram (ECG). Reversible noncardiac causes of VT should be considered. Patients should undergo an echocardiogram or cardiac magnetic resonance (CMR) to assess for structural heart disease. Stress testing and electrophysiology study are appropriate for certain patients. Test results will determine if structural heart disease is present. (See 'Diagnostic evaluation' above.)
●Treatment of patients with structurally normal hearts
•Asymptomatic patients – Asymptomatic patients do not require any specific therapy directed toward the NSVT. (See 'Treatment of patients with structurally normal hearts' above.)
•Symptomatic patients – We suggest beta blockers rather than calcium channel blockers or antiarrhythmic medications (Grade 2C). For patients with NSVT who remain symptomatic despite beta blockers, we suggest adding a nondihydropyridine calcium channel blocker (ie, verapamil or diltiazem) rather than an antiarrhythmic medication (Grade 2C). For patients with structurally normal hearts who have persistent symptomatic NSVT, radiofrequency catheter ablation (RFA) and antiarrhythmic drugs are both valid options. RFA is most effective for an idiopathic, triggered arrhythmia that originates in the outflow tracts, septum, or papillary muscles. For patients whose arrhythmias originate in other locations, we typically start with an antiarrhythmic medication. (See 'Treatment of patients with structurally normal hearts' above.)
●Treatment of patients with structurally abnormal hearts
•Beta blocker for all patients – For patients with structurally abnormal hearts and NSVT, we suggest adding a beta blocker (Grade 2C), if they are not already taking one, to reduce the likelihood of sustained VT. We do not use nondihydropyridine calcium channel blockers for patients with reduced rejection fraction due to an increased risk of decompensated heart failure. (See 'Treatment of patients with structurally abnormal hearts' above.)
•Asymptomatic patients – We do not use antiarrhythmic medications or radiofrequency ablation (RFA) for asymptomatic patients with reduced ejection fraction, with rare exceptions. (See 'Treatment of patients with structurally abnormal hearts' above.)
•Symptomatic patients – For patients with persistent symptoms despite beta blockers, RFA and antiarrhythmic medications are both valid options. Physicians who practice at an institution with expertise in VT ablation may prefer to start with RFA, while others may choose an antiarrhythmic agent. (See 'Treatment of patients with structurally abnormal hearts' above.)
•Implantable cardioverter-defibrillators – Some patients with structurally abnormal hearts and NSVT are at increased risk of sudden cardiac death. Implantable cardioverter-defibrillator (ICD) may be indicated. Discussions about determining ICD candidacy are found elsewhere. (See 'Tests indicated for certain patients' above and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)
ACKNOWLEDGMENT —
The UpToDate editorial staff acknowledges the late Mark E. Josephson, MD, who contributed to an earlier version of this topic review.
