Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation

INTRODUCTION — Sustained monomorphic ventricular tachycardia (SMVT) is defined by the following characteristics:

●A regular (<50 msec beat-to-beat cycle length variation) wide QRS complex (≥120 milliseconds) tachycardia at a rate greater than 100 beats per minute

●The consecutive beats have a uniform and stable QRS morphology

●The arrhythmia lasts ≥30 seconds or causes hemodynamic collapse in <30 seconds

In patients with coronary heart disease (CHD) or other structural heart disease, a wide QRS complex tachycardia (WCT) should be considered to be ventricular tachycardia until proven otherwise. (See "Wide QRS complex tachycardias: Approach to the diagnosis".)

This topic will focus on the clinical presentation, diagnosis, and evaluation of SMVT. The approach to treatment of SMVT, the approach to patients with monomorphic VT and no apparent heart disease, and the management of non-sustained VT are discussed separately. (See "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis" and "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features" and "Nonsustained ventricular tachycardia: Clinical manifestations, evaluation, and management" and "Ventricular tachycardia in the absence of apparent structural heart disease".)

EPIDEMIOLOGY AND RISK FACTORS — Cardiovascular disease (CVD) is common in the general population, affecting the majority of adults past the age of 60 years. In 2012 and 2013, CVD was estimated to result in 17.3 million deaths worldwide on an annual basis [1,2]. Many patients who die from CVD experience unexpected sudden cardiac death (SCD), with more than 50 percent of SCD episodes occurring as a first event in persons thought to be at low risk [3]. Along with ventricular fibrillation, SMVT is responsible for nearly all of the arrhythmic SCD, although ventricular arrhythmias are fairly uncommon in the general population populations. Among a prospective cohort of more than half a million United Kingdom residents, the prevalence of ventricular arrhythmias (which included ventricular premature beats, as well as ventricular tachycardia [VT] and ventricular fibrillation [VF]) was approximately 12 per 10,000 persons under age 55 and increased to between 20 (females) and 59 (males) per 10,000 persons ≥65 years of age [4]. These data are most likely weight toward VPBs rather than VT or VF in this cross-sectional community population. (See "Overview of sudden cardiac arrest and sudden cardiac death" and "Overview of established risk factors for cardiovascular disease".)

SMVT may be idiopathic but occurs most frequently in patients with underlying heart disease of various types including:

●Coronary heart disease (CHD), especially with prior myocardial infarction

●Dilated cardiomyopathy

●Infiltrative cardiomyopathy

●Chagas heart disease

●Complex congenital heart disease

●Cardiac sarcoidosis

●Arrhythmogenic right ventricular cardiomyopathy

●Left ventricular noncompaction

CHD is responsible for the majority of cases of SMVT. Approximately 70 percent of the cases of SCD in the United States are due to CHD, resulting in hundreds of thousands of deaths. However, SCD can result from VT that occurs in the absence of known heart disease. Monomorphic VT occurring in the absence of apparent structural heart disease is discussed in detail separately. (See "Ventricular tachycardia in the absence of apparent structural heart disease".)

Drugs — Flecainide and encainide have been associated with ventricular proarrhythmia in patients with prior infarct. By extension, propafenone is usually not recommended in this setting. Antiarrhythmic drugs in general can lead to more frequent (and at times incessant, albeit slower) SMVT. Inotropes, sympathomimetic agents, and other stimulants have been associated with SMVT. A number of other agents have been implicated in SMVT but at very low frequencies. A 2020 scientific statement from the American Heart Association details drugs associated with SMVT [5].

CLINICAL MANIFESTATIONS AND ECG FINDINGS — The history, physical examination, and 12-lead electrocardiogram (ECG) during SMVT and in sinus rhythm can all provide information to help confirm the diagnosis of SMVT. Because time may not allow for extensive questioning or examination, identifying a history of coronary heart disease (CHD) or other structural heart disease is the most important piece of historical information, along with obtaining an accurate list of medications and potential intoxicants (eg, flecainide, digoxin, etc) to identify any potential triggers for SMVT. (See "Wide QRS complex tachycardias: Approach to the diagnosis".)

History and associated symptoms — The clinical presentation of SMVT is highly variable, ranging from sudden cardiac arrest to mild symptoms. Although most patients with SMVT experience symptoms, in the occasional patient, symptoms may be minimal. Most patients with SMVT will have a history of underlying structural heart disease (eg, CHD, heart failure, hypertrophic cardiomyopathy, congenital heart disease, etc), although SMVT can also be seen in patients without known structural heart disease. Although SMVT is most commonly related to the development of reentrant circuits that follow healing of a prior myocardial infarction (MI), patients with prior MI may also develop SMVT due to non-reentrant mechanisms. (See "Ventricular tachycardia in the absence of apparent structural heart disease".)

In the most severe instances, when SMVT significantly impairs cardiac output and results in immediate hemodynamic collapse, patients may briefly experience the onset of symptoms prior to the abrupt loss of consciousness and sudden cardiac arrest. Patients with faster ventricular rates, underlying heart disease, and decompensated heart failure with reduced left ventricular systolic function are more likely to develop hemodynamic instability. In such cases, prompt defibrillation and resuscitation to restore a perfusing heart rhythm is required. (See "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis", section on 'Unstable patients'.)

For patients without immediate sudden cardiac arrest, the type and intensity of symptoms will vary depending upon the rate and duration of SMVT along with the presence or absence of significant comorbid conditions. Patients with SMVT typically present with one or more of the following symptoms:

●Shortness of breath/dyspnea

●Chest discomfort

●Palpitations

●Syncope or presyncope

●General malaise

Most commonly, symptomatic patients will report chest discomfort and/or shortness of breath. Palpitations are less common during VT in persons with significant ventricular dysfunction because the heart does not contract with enough vigor to cause palpitations. If the associated rate of SMVT is rapid enough to result in hemodynamic compromise, patients may experience presyncope or even syncope and further deterioration into cardiac arrest. On occasion, patients may experience syncope at the onset of SMVT and then recover consciousness while remaining in VT. The patient's medication list should be reviewed carefully, with special attention for rate-controlling drugs and antiarrhythmic drugs, to assess potential proarrhythmic effects and to guide therapy. QT-prolonging drugs, however, typically cause torsades de pointes (ie, polymorphic VT). (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes".)

Physical examination — Few physical examination findings in patients with SMVT are unique and specific. By definition, patients will have a pulse exceeding 100 beats per minute during the episode. In addition, if the physical examination is performed while SMVT persists, this can reveal evidence of atrioventricular (AV) dissociation, although it is not always easy to detect [6]. During AV dissociation, the normal coordination of atrial and ventricular contraction is lost, which may produce characteristic physical examination findings including (see "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'AV dissociation'):

●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, which is heard more frequently when the rate of the 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 "Examination of the jugular venous pulse".)

Electrocardiogram — In patients with sudden cardiac arrest or hemodynamically unstable SMVT, often the only ECG available is a single-lead assessment from the telemetry monitor or defibrillator showing a wide QRS complex tachycardia (WCT); in such instances, a full 12-lead ECG is not typically obtained until the patient has been stabilized. However, for patients with suspected SMVT who are hemodynamically stable, a 12-lead ECG should be performed as this provides the maximal ECG information for making an accurate diagnosis and determining a possible etiology and may help to direct future therapy. If available, a previous ECG when the patient was in normal sinus rhythm is very helpful for comparison. For example, if a patient with underlying bundle branch block develops wide QRS complex tachycardia with a bundle branch block pattern opposite to the baseline bundle branch block (ie, a left bundle branch block pattern in a patient with right bundle branch block during NSR), the tachycardia is very likely to be VT, not SVT with aberrant conduction.

SMVT typically generates a WCT, usually with a QRS width >0.12 seconds (waveform 1). WCT occurring in patients with prior MI is almost always SMVT. In rare instances, SMVT may present as a relatively narrow complex tachycardia (algorithm 1). Such an arrhythmia may be incorrectly diagnosed and treated as a supraventricular tachycardia [7]. Although uncommon, a QRS complex that is narrower during tachycardia than during sinus rhythm (usually in patients with chronic bundle branch block or intraventricular conduction delay during sinus rhythm) is diagnostic of SMVT. (See "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Idiopathic left ventricular tachycardia'.)

A detailed discussion of the ECG characteristics of SMVT is found elsewhere (see "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Evaluation of the electrocardiogram'). Summarized briefly:

●The ECG hallmark for the diagnosis of SMVT is a wide complex tachycardia with the obvious presence of AV dissociation (waveform 2). If not obvious, AV dissociation is suggested by the presence of fusion complexes (which reflect a supraventricular impulse coming from above the AV node fusing with an impulse generated in the ventricle) or sinus capture complexes (which reflect an impulse coming from above the AV node that depolarizes the ventricles when they are no longer refractory but before the next VT-generated complex). The occurrence of persistent or intermittent retrograde block is virtually diagnostic of SMVT. However, up to 40 percent of patients have intact ventriculoatrial (VA) conduction during SMVT, and AV dissociation is not seen (waveform 3) [8]. VA conduction may occur in a 1:1 pattern or with second-degree VA block (eg, 2:1 or 3:1).

●Variability in the ST and T waves may be present, reflecting superimposed P waves as well as changes in ventricular repolarization.

●The tachycardia rate is usually constant but may warm up at start and may exhibit some subtle variability.

●While concordance, or the presence of monophasic QRS complexes with the same polarity in leads V1 through V6, has been reported to have a specificity of greater than 90 percent for VT, positive concordance can also be present in preexcited tachyarrhythmias, specifically antidromic reciprocating tachycardia, which occur less frequently than VT [9]. Negative concordance is rarely seen but is consistent with VT.

●The specific QRS morphology, particularly when a shift in QRS axis occurs during WCT, may be helpful.

Given the number of exceptions and the need to establish the correct diagnosis, ECG criteria may only be suggestive of SMVT. Confirmation sometimes requires other means, such as intracardiac ECGs from an implantable cardioverter-defibrillator (ICD) or pacemaker or invasive electrophysiologic testing. If a patient with sustained tachycardia has an ICD or pacemaker, interrogation and review of intracardiac electrograms are often diagnostic.

DIAGNOSIS — The diagnosis of SMVT should be suspected in a patient who presents with either sudden cardiac arrest, syncope, or sustained palpitations, particularly in a patient with a known history of structural heart disease.

The diagnosis of SMVT is typically confirmed following review of an ECG, acquired during the arrhythmia, showing a wide QRS complex tachycardia with the presence of AV dissociation (manifest as an atrial rate slower than the ventricular rate). Frequently, however, it is not possible to identify P waves and the atrial rate amongst the wide QRS complexes, so other evidence of AV dissociation (ie, fusion and capture beats) is helpful in confirming the diagnosis of VT. Additional ECG features (eg, QRS axis, concordance, QRS morphology, etc) can provide additional supportive evidence for a diagnosis of VT versus supraventricular tachycardia (table 1). (See "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Evaluation of the electrocardiogram'.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis for a wide QRS complex tachycardia (WCT) includes SMVT, supraventricular tachycardia with aberrant conduction (either preexistent or rate-related), supraventricular tachycardia with preexcitation, and tachycardia with ventricular pacing (algorithm 1). Differentiating SMVT 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. The presence of a WCT in a patient with prior myocardial infarction (MI) or other structural heart disease probably represents SMVT. By contrast, a WCT in a patient without coronary heart disease (CHD) or structural heart disease more likely represents supraventricular tachycardia.

Bundle branch reentry — Bundle branch reentrant tachycardia (BBRT) should always be considered in patients presenting with SMVT in the setting of nonischemic cardiomyopathy because it is eminently curable by catheter ablation. While the most common ECG appearance is that of a left bundle branch block with left axis pattern, rarely, it may have a right bundle branch block pattern. BBRT has rarely been reported in persons without apparent structural heart disease or persons with coronary disease. These patients usually display an IVCD on the standard ECG, usually a left bundle branch block type pattern.

Supraventricular tachycardia — A patient with an underlying bundle branch block, or someone that is dependent on a ventricular pacemaker, who then develops tachycardia will, by definition, have a WCT. Review of a baseline ECG showing bundle branch block or ventricular paced rhythm with a similar QRS morphology to that seen during WCT suggests a higher likelihood of supraventricular tachycardia with aberrancy, but does not exclude ventricular tachycardia.

In patients who present with symptomatic WCT, where time may be limited, a history of prior MI or other structural heart disease (or absence thereof) is the most important piece of historical information helping the clinician to distinguish supraventricular tachycardia from SMVT. While the absence of CHD or other structural heart disease does not exclude SMVT, supraventricular tachycardia is much more likely in patients without CHD or structural heart disease. (See 'History and associated symptoms' above and "Wide QRS complex tachycardias: Approach to the diagnosis".)

Electrocardiogram artifact — ECG artifact, particularly when observed on a rhythm strip, can be misdiagnosed as VT (waveform 4). Artifact is highly probable, and a true WCT excluded, if narrow-complex beats can be identified regularly "marching" through the rhythm strip, particularly if there is a one-to-one association between P waves and QRS complexes. (See "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations", section on 'Artifact mimicking ventricular tachycardia'.)

ADDITIONAL DIAGNOSTIC EVALUATION — Following acute treatment for SMVT, reversible causes of arrhythmia should be sought. These include myocardial ischemia and adverse drug effects. Neither anemia nor electrolyte disturbances cause SMVT, hypotension, and heart failure, which may, with the appropriate substrate, facilitate the induction of SMVT or contribute to its persistence but are rarely the primary cause for the arrhythmia. Thereafter, a thorough diagnostic evaluation to exclude associated structural heart disease is warranted. Even young, otherwise healthy patients need a thorough evaluation to exclude entities such as undiagnosed cardiomyopathy, anomalous origin of a coronary artery, hypertrophic cardiomyopathy, or arrhythmogenic right ventricular cardiomyopathy. (See "Congenital and pediatric coronary artery abnormalities" and "Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac death" and "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations".)

The diagnostic evaluation to establish the presence and type of heart disease generally includes various invasive and noninvasive techniques, depending in part upon the clinical history and presentation. Cardiac imaging (with echocardiography and preferably cardiac magnetic resonance [CMR] imaging) and continuous ECG monitoring (for 24 hours or longer while hospitalized) should be performed in all patients. Invasive electrophysiology studies (EPS) can frequently be helpful but are not routinely performed in most patients, unless catheter ablation is being considered or there is persistent diagnostic uncertainty.

Signal-averaged ECG (SAECG) is rarely helpful in evaluating patients with SMVT. In patients presenting with SMVT without known structural heart disease, stress testing can be helpful as a screen for coronary heart disease (CHD), and may help elicit VT in patients with idiopathic VT, arrhythmogenic right ventricular cardiomyopathy, or other unusual structural abnormalities. In patients with SMVT and history of prior myocardial infarction [MI], revascularization is rarely adequate as monotherapy to prevent recurrent VT, as SMVT is usually due to a reentrant circuit emanating from a prior infarct scar. CPVT is classically triggered by exertion, but condition is usually associated with frequent PVCs and PMVT on stress testing, not SMVT.

Cardiac imaging — All patients with SMVT should undergo cardiac imaging to evaluate for structural heart disease [10-12]. Echocardiography has long been the preferred method for evaluation of structural heart disease because of its widespread availability, accuracy in diagnosing a variety of structural cardiac defects (myocardial, valvular, congenital), safety to the patients, and relatively low expense. However, CMR imaging generally provides superior image quality and also allows for tissue characterization, making it an important imaging option for certain diagnoses (eg, arrhythmogenic right ventricular cardiomyopathy, cardiac sarcoidosis, other infiltrative cardiomyopathies, etc) and for patients with poor quality or nondiagnostic echocardiographic images [13-15]. In addition, if ablation is contemplated, CMR findings (areas of delayed gadolinium enhancement) may help guide ablation. (See "Tests to evaluate left ventricular systolic function" and "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis".)

Continuous ECG monitoring — Following acute treatment for SMVT, hospitalized patients should have continuous ECG monitoring while any potential reversible causes are identified and corrected. Typically the duration of continuous ECG monitoring should be at least 24 hours following the last episode of SMVT, but additional monitoring may be useful if patients have reversible causes that have not been fully remedied (eg, ongoing myocardial ischemia, heart failure, hypokalemia, etc).

Since SMVT generally occurs infrequently and sporadically, we do not routinely perform outpatient ambulatory ECG monitoring [16,17]. However, in patients with syncope suspected of having SMVT, but in whom the diagnosis has not been, extended ambulatory ECG monitoring with an event (loop) monitor, extended Holter monitor, or insertable cardiac monitor (also sometimes referred to as an implantable cardiac monitor or implantable loop recorder) can successfully aid in establishing the diagnosis [18-20]. (See "Ambulatory ECG monitoring".)

Signal-averaged electrocardiogram — We do not routinely perform a signal-averaged ECG (SAECG) for diagnostic purposes in patients with documented SMVT. The rationale for not routinely obtaining a SAECG is that, while the SAECG often demonstrates late potentials (low amplitude oscillations occurring after the QRS complex) in patients with SMVT and ischemic heart disease, the presence of late potentials provides only indirect data that are suggestive, but not diagnostic, of SMVT [21-23]. Although the SAECG has a prognostic role for predicting the risk of SMVT in patients with ischemic heart disease, it has a limited role in the evaluation of patients who have already experienced SMVT and is rarely used in current cardiology practice [24-26]. (See "Signal-averaged electrocardiogram: Overview of technical aspects and clinical applications".)

The rare patients in whom the SAECG can aid in the diagnosis of underlying heart disease include patients with suspected arrhythmogenic right ventricular cardiomyopathy, in whom the SAECG findings are part of the diagnostic criteria for the disorder, as well as patients with suspected Brugada syndrome. The diagnostic approaches to these conditions are discussed in detail separately. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation", section on 'Diagnostic evaluation' and "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis", section on 'Diagnostic evaluation'.)

Exercise testing — Exercise stress testing, or pharmacologic stress testing if the patient cannot exercise, is an important component of the diagnostic approach in patients presenting with SMVT and suspected myocardial ischemia.

●For patients with SMVT and evidence of an acute coronary syndrome, stress testing is typically deferred in favor of prompt coronary angiography (with or without revascularization as indicated). (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes".)

●For patients with SMVT in whom CHD is a possible contributing factor to SMVT (eg, patients with numerous risk factors for atherosclerotic cardiovascular disease, patients with cardiac imaging findings suggesting CHD, etc), we proceed with stress testing primarily for prognostic purposes. The choice of the optimal stress test should be based upon the patient's ability to exercise, the ability to interpret the patient's baseline ECG, and the pre-test probability of CHD [27]. (See "Selecting the optimal cardiac stress test".)

In patients in whom significant myocardial ischemia is identified, the decision to proceed with revascularization should primarily be based on the presence or absence of symptoms attributable to the ischemia. However, treatment of myocardial ischemia does not eliminate the risk of recurrent SMVT, particularly in patients with prior MI and the presence of myocardial scar.

Electrophysiologic studies — EPS is the most definitive means of establishing the diagnosis of SMVT [28]. (See "Invasive diagnostic cardiac electrophysiology studies".)

There are a number of potential uses for EPS in the evaluation of patients with SMVT:

●To establish the diagnosis of SMVT when the diagnosis is uncertain.

●To establish the mechanism of the SMVT. When combined with mapping, the location of the arrhythmogenic focus can be identified, which is useful in cases where ablation is being considered. (See "Invasive diagnostic cardiac electrophysiology studies", section on 'Mapping and ablation'.)

●Prior to catheter ablation of SMVT, EPS should be performed to assess whether the clinical VT is inducible and also to assess the extensiveness of scar tissue.

●When BBRT is suspected, EPS can confirm the diagnosis, and ablation is highly effective.

While EPS can be helpful in the diagnosis of VT, it is not without limitations:

●Patients with a prior MI and a history of SMVT almost always (90+ percent) have inducible SMVT with EPS. However, in some studies of patients with ischemic heart disease, up to 5 percent of patients with clinically documented SMVT are not inducible; thus, noninducibility does not exclude this diagnosis [28,29].

●The clinically occurring morphology of SMVT is frequently not the same as the morphology of the induced VT during EPS and may have consequences for eventual catheter ablation. This is in part related to the limited number of induction attempts during routine diagnostic studies.

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 5^th to 6^th 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 10^th to 12^th 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 for "patient info" and the keyword[s] of interest.)

●Basics topics (see "Patient education: Ventricular tachycardia (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Background – Sustained monomorphic ventricular tachycardia (SMVT) is a potentially life-threatening arrhythmia which requires urgent attention and evaluation.

●Clinical manifestations – Patients with structural heart disease, especially coronary artery disease and a prior myocardial infarction, who present with a wide QRS complex tachycardia (WCT) should be presumed to have VT. All available telemetry recordings and surface electrocardiograms (ECGs), including prior ECGs, should be reviewed for clues to the diagnosis of VT which include (see 'Electrocardiogram' above and "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Evaluation of the electrocardiogram'):

•Atrioventricular (AV) dissociation with P waves appearing independently of the QRS complexes. If not obvious, AV dissociation is suggested by the presence of fusion or captured complexes.

•Variability of ST and T waves from superimposed P waves or from changes in repolarization.

•QRS axis shift from baseline ECG axis.

•Morphology of QRS complex, especially in leads V1-V6.

●Differential diagnosis – The differential diagnosis of SMVT includes supraventricular tachycardia with aberrant conduction (preexisting or rate-related), supraventricular tachycardia with preexcitation, supraventricular tachycardia in a pacemaker dependent patient, and ECG artifact (waveform 4). (See 'Differential diagnosis' above.)

●Cardiac imaging – Echocardiography should be performed to evaluate for structural heart disease. If the echocardiographic evaluation is inconclusive, cardiac computed tomography (CT) or magnetic resonance imaging (MRI) should be performed. (See 'Cardiac imaging' above.)

●Exercise testing – All patients should be evaluated for ischemic heart disease. We typically proceed with exercise stress testing (or pharmacologic stress testing if the patient is unable to exercise) with or without cardiac imaging, as clinically appropriate, and coronary angiography when indicated. (See 'Exercise testing' above.)

●Electrophysiologic studies – Invasive electrophysiologic studies can provide a more definitive diagnosis in instances where the diagnosis of ventricular tachycardia (VT) remains uncertain, or in cases where catheter ablation is being considered. However, if the diagnosis of VT is certain, and therapy with an implantable cardiac defibrillator (ICD) placement is planned, electrophysiologic studies are unlikely to affect further management and are not recommended unless catheter ablation is also being planned. (See 'Electrophysiologic studies' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Philip J. Podrid, MD, FACC and Leonard Ganz, MD, FHRS, FACC, who contributed to an earlier version of this topic review.