Approach Considerations
Electrocardiography (ECG) is the criterion standard for the diagnosis of ventricular tachycardia (VT). [9] In a patient who is hemodynamically unstable or unconscious, however, the diagnosis of VT is made from the physical findings and ECG rhythm strip only.
Advanced cardiac life support (ACLS) protocols should be quickly followed. Laboratory tests should be deferred until electrical cardioversion has restored sinus rhythm and the patient is stabilized. If the patient is hemodynamically stable at presentation, a 12-lead ECG and electrolyte levels may be obtained before attempted conversion with medications or direct current (DC) cardioversion. Note that if electrolyte levels are not obtained in an acute evaluation of VT post conversion, the hyperadrenergic state or hemodynamic compromise often associated with VT may affect the subsequently obtained electrolyte laboratory values.
The ECG should be repeated once sinus rhythm has been restored, or when prior VT is suspected, as in a patient who experienced syncope. The ECG may also provide clues for differentiating among potential arrhythmia mechanisms or causes of VT, such as the following:
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Acute or chronic infarction
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Ischemia
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Myocardial scar
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Ventricular preexcitation
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Hypertrophy
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Conduction disease
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QT prolongation
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Other precordial repolarization abnormalities (eg, Brugada syndrome, arrhythmogenic right ventricular dysplasia [ARVD])
Appropriate laboratory studies are indicated. In addition, a full evaluation should usually include echocardiography and coronary angiography to assess for structural and ischemic heart disease. These considerations are paramount in defining further treatment in any patient with VT. These patients often require aggressive management of the underlying ischemic heart disease and heart failure.
The 2017 American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Rhythm Society (HRS) guideline for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death includes the following recommendations [44] :
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Assessment of the risk for sudden death in patients with cardiomyopathies, particularly in those with hypertrophic cardiomyopathy, sarcoidosis, ARVD, or neuromuscular disease
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Evaluation for genetic arrhythmia syndromes in patients younger than 40 years with unexplained sudden cardiac death, unexplained near drowning, or recurrent syncope in the absence of ischemic or other structural heart disease
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Cardiac evaluation and genetic counseling and genetic testing as appropriated on the basis of clinical findings in first-degree relatives of victims of sudden cardiac death who were aged 40 years or younger
Screening of first-degree relatives should be contemplated when a patient is identified as having any of the following:
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Long QT syndrome
-
Short QT syndrome
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Hypertrophic or dilated cardiomyopathy
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Right ventricular dysplasia
Family screening typically involves the following:
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History and physical examination
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ECG
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Echocardiography
-
Treadmill testing
In some patients with spontaneous polymorphic VT, genetic studies may be helpful for family screening or for clarifying a diagnosis. Spontaneous polymorphic VT may be related to genetic mutations affecting ion channels, such as occur in long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT. Finally, some patients are predisposed to drug-induced ventricular arrhythmias by otherwise subclinical genetic ion channel defects.
Chest radiography is indicated if symptoms suggest the possibility of heart failure or other cardiopulmonary pathology as a contributing factor. Cardiac computed tomography (CT) scanning and cardiac magnetic resonance imaging (cMRI) are evolving quickly but have not yet supplanted echocardiography and nuclear imaging for quantification of ventricular function. CMRI can be especially helpful in the evaluation of uncommon myocardial infiltrative diseases, such as sarcoidosis.
Laboratory Studies
Assess electrolyte levels of all patients with ventricular tachycardia (VT), including serum potassium, magnesium, calcium, and phosphate levels. Ionized calcium levels are preferred to total serum calcium levels. Hypokalemia is a common VT trigger and is commonly seen in patients taking diuretics. Hypokalemia, hypomagnesemia, and hypocalcemia may predispose patients to either monomorphic VT or torsade de pointes.
In accordance with the clinical history, measure serum levels of therapeutic drugs (eg, digoxin, tricyclic antidepressants). Toxicology screens (eg, for methamphetamine, methadone, cocaine) may be helpful in cases related to recreational or therapeutic drug use.
Evaluate for myocardial ischemia or infarction with serum cardiac troponin I or T levels or other cardiac markers if symptoms or clinical signs of ischemia are present. Persistently elevated cardiac enzyme levels may also be an indication of ongoing myocarditis.
Electrocardiography
Polymorphic ventricular tachycardia
When the QRS complex varies from beat to beat, the rhythm is described as polymorphic ventricular tachycardia (VT) and suggests a variable electrical activation sequence. The most notorious, and probably the most common, form of polymorphic VT is torsade de pointes, a French term meaning “twisting of the points” and refers to the unusual shifting-axis QRS complexes that appear as if the heart is rotating upon an axis.
Torsade de pointes typically occurs during sinus rhythm and in the presence of drugs or conditions that prolong the QT interval (eg, class IA antiarrhythmics, hypomagnesemia, droperidol). The dysrhythmia may occur either in the presence or in the absence of myocardial ischemia or infarction. The term torsade de pointes is reserved for polymorphic VT observed in the setting of a prolonged QT interval (see the images below). Other polymorphic VTs are occasionally observed during ischemia or myocarditis.
The typical initiation of torsade de points occurs with a “long-short” sequence—that is, a longer RR interval resulting in further prolongation of the QT interval, followed by an early depolarization occurring at a time of heterogeneous repolarization.
Torsade de pointes. Image A: This is polymorphic ventricular tachycardia associated with resting QT-interval prolongation. In this case, it was caused by the class III antiarrhythmic agent sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels. Image B: Torsade de pointes, a form of ventricular tachycardia. Courtesy of Science Source/BSIP.
Monomorphic ventricular tachycardia
When the ventricular activation sequence is constant, the electrocardiographic (ECG) pattern remains the same, and the rhythm is called monomorphic VT (see the image below). Monomorphic VT is most commonly seen in patients with underlying structural heart disease. There is typically a zone of slow conduction, most commonly the result of scarring or fibrillar disarray. Causes include prior infarct, any primary cardiomyopathy, surgical scar, hypertrophy, and muscle degeneration.
Reentrant tachycardias occur when an electrical wavefront travels slowly through the zone of slow conduction (usually damaged muscle protected by scar tissue), allowing the rest of the circuit time to repolarize. The wavefront breaks out of the scar, activates the ventricle, and reenters the slow conduction zone.
Monomorphic VT is occasionally observed in patients with structurally normal hearts (idiopathic VT). These VTs are often exercise dependent, and their clinical behavior may be more consistent with triggered activity or abnormal automaticity.
Monomorphic VTs are typically named for their site of origin. The following are the most commonly involved sites [45] :
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Right ventricular outflow tract
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Left ventricular outflow tract
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Left ventricular septum
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Aortic root
The QRS morphology during VT can be used to predict the exit site from the zone of slow conduction [46] or the site of origin, regardless of the underlying substrate. The earliest activation is closest to the leads with QS complexes during tachycardia. [47]
Monomorphic VTs have classically been considered benign. Rarely, however, they may result in sudden death, despite the presence of a structurally normal heart. [48]
Differentiating monomorphic VT from supraventricular tachycardia
Polymorphic VT is easily diagnosed after exclusion of lead motion artifact. Monomorphic VT can be more difficult to sort out. The ECG will demonstrate a wide-complex tachycardia, representing either VT or supraventricular tachycardia (SVT) with aberrant conduction. If the patient is unstable, or if differentiation between VT and SVT is uncertain, treat the rhythm as VT; the majority of patients with wide-complex regular tachycardias will have VT. If the patient is stable, the ECG can be examined for clues to the mechanism underlying the arrhythmia.
Atrioventricular dissociation
AV dissociation (see the images below), is apparent in approximately half of VT episodes; when present, it is a hallmark of VT. [49] AV dissociation occurs because the sinus node is depolarizing the atria at a rate that is slower than the pathologic, faster ventricular rate. At times, P waves can be seen in between or embedded in the QRS complexes, but the P waves and QRS complexes have their own independent rates.
The electrocardiogram shows a form of idiopathic ventricular tachycardia (VT) seen in the absence of structural heart disease. This rhythm arises from the left ventricular septum and often responds to verapamil. Upon superficial examination, it appears to be supraventricular tachycardia with bifascicular conduction block. Closer examination of lead V1 shows narrowing of fourth QRS complex, consistent with fusion between the wide QRS complex and the conducted atrial beat, confirming atrioventricular dissociation and a VT mechanism.
Retrograde conduction can also exist from the ventricles to the atria via the AV node. This is not AV dissociation and reveals itself on ECG as a 1:1 correlation between the wide QRS complex and an inverted P wave, which follows the QRS complex.
Fusion and capture beats
Fusion beats and capture beats can occur in the presence of VT, depending on the refractory period of the AV node and on the timing of ventricular and atrial depolarizations, respectively (see the image below). If present, they help distinguish VT from SVT with aberrant conduction.
Fusion beats, capture beats, and atrioventricular dissociation can be seen on this electrocardiogram.
A fusion beat has a mixed morphology because of normal AV node/His-Purkinje conduction occurring simultaneously with abnormal ventricular depolarization. A normally conducted impulse travels from the AV node through the normal conduction pathway (producing a narrow QRS complex), and the competing impulse originates from the abnormal ectopic ventricular focus outside of the normal conduction pathway (producing a wide QRS complex). The two impulses converge, leading to a mixed (fused) QRS.
A capture beat occurs when an atrial impulse arrives at the AV node when the node has just recovered from its refractory period. The timing must be just right, because the AV node is frequently in its refractory state as a result of depolarization caused by retrograde conduction from the rapid ventricular rhythm. When this occurs, conduction proceeds normally through the AV node/His-Purkinje system, “capturing” the ventricle and leading to a normal, narrow QRS complex.
Unfortunately, most VT tracings do not show obvious clues of AV dissociation, fusion, or capture. In such cases, the QRS morphology may often (depending on the clinical context) provide enough information to permit an accurate diagnosis. The two most commonly applied sets of ECG criteria are described below.
Brugada et al proposed ECG discrimination criteria for VT that focused primarily on the QRS morphologies in the precordial leads (V1-V6). [15] They reported a sensitivity of 98.7% and a specificity of 96.5% with the following criteria:
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Absence of RS complexes in the precordial leads
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RS duration exceeding 100 ms in any precordial lead
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Ventriculoatrial dissociation in any of 12 leads
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Certain QRS morphologies, such as QR or QS in lead V6
Vereckei et al refined a different ECG algorithm based on a single lead, aVR, and reported better accuracy than was achieved with the Brugada criteria. [16] They noted the presence of a negative QRS complex in lead aVR during right or left bundle-branch conduction of SVTs. VT was predicted by the following:
-
Presence of an initial R wave in lead aVR
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Width of an initial R or Q wave exceeding 40 ms in lead aVR
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Notching on the initial downstroke of a predominantly negative QRS complex in lead aVR
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A ventricular activation-velocity ratio (V i/V t) of 1 or less
Differentiating VT from sinus tachycardia
The image below demonstrates a tachycardia with a 1:1 atrial-to-ventricular ratio. It is not immediately clear whether the atria are driving the ventricles (sinus tachycardia) or the ventricles are driving the atria (VT).
This electrocardiogram is from a 32-year-old woman with recent-onset heart failure and syncope.
In this case, a diagnosis of sinus tachycardia would require the presence of severe conduction disease manifesting as marked first-degree AV block with left bundle-branch block. However, close inspection shows that the actual diagnosis is VT, as indicated by absence of RS complexes in the precordial leads, a QS pattern in lead V6, and an R wave in lead aVR. The patient proved to have an incessant VT associated with dilated cardiomyopathy.
Signal-averaged ECG
Signal-averaged ECG (SAECG) is a noninvasive test that often demonstrates abnormal results in patients with VT related to a prior infarct or right ventricular dysplasia. SAECG—along with heart rate variability (HRV), baroflex sensitivity, and heart rate turbulence—may be useful for refining the diagnosis and risk stratification of patients with ventricular arrhythmias or those who are at increased risk of developing life-threatening ventricular arrhythmias. [40]
Echocardiography
Echocardiography is used for patients at high risk for serious ventricular arrhythmias or sudden cardiac death. In particular, echocardiography can provide an estimate of left ventricular (LV) systolic function, and the presence or absence of associated LV wall motion abnormalities commonly indicative of a prior scar. Echocardiography may also show findings suggestive of a myocardial infiltrative process. Imaging of the right ventricle (RV) may be more limited, and other imaging techniques may be required to obtain accurate and global views of RV function. The high-risk group consists of patients with any of the following [40] :
-
Dilated, hypertrophic, or RV cardiomyopathy
-
A history of acute myocardial infarction
-
Inherited disorders associated with sudden cardiac death
Cardiac Imaging Studies
Cardiac computed tomography (CT) scanning and cardiac magnetic resonance imaging (cMRI) are evolving quickly but have not yet supplanted echocardiographic and nuclear imaging for quantification of ventricular function. CMRI can be especially helpful in the evaluation of uncommon myocardial infiltrative diseases, such as sarcoidosis.
The use of late gadolinium enhancement (LGE) and extracellular volume (ECV) cMRI appear to have the potential to predict the estimated 5-year risk of sudden death and syncope or nonsustained ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM). [50] In a study of 73 German patients with HCM and 16 control subjects, investigators found that not only was global ECV was the best predictor of an increased risk of sudden death but that when used in conjunction with the sudden cardiac risk score, the diagnostic accuracy to identify HCM patients with syncope or nonsustained VT was significantly improved. These findings may have implications for improved patient selection of HCM patients for ICD implantation. [50]
Although cMRI is often used for the evaluation of arrhythmogenic right ventricular dysplasia, the diagnostic yield of this test has yet to be clearly defined. Right ventricular angiography may still be the criterion standard imaging study for this disorder.
MRI, cardiac CT scanning, or radionuclide angiography can be useful in patients with ventricular arrhythmias when echocardiography fails to provide accurate evaluation of left or right ventricular function. These studies may also be useful for assessment of structural changes in the heart. [40]
Assessment of Recurrent Syncope or Palpitations
Occasionally, patients present with recurrent syncope or palpitations. In this setting, an arrhythmic cause of syncope may be sought. Options include Holter monitoring, which has a low yield, and event recording. The goal is to document the patient’s rhythm during symptoms. Individuals with infrequent symptoms are best served by the implantation of a loop recorder, which may have a battery life of 2-4 years.
If such techniques are not practical, a provocative electrophysiologic study can be performed.
Genetic Testing
Genetic testing is now feasible for a variety of inherited disorders that may cause long QT syndrome, arrhythmogenic right ventricular dysplasia, or dilated or hypertrophic cardiomyopathy. However, the absence of a defined genomic mutation does not exclude these abnormalities, and interpretation of mutations, especially those resulting in a noncoding alteration is presently difficult.
The current approach is not exhaustive and is focused on established monogenic germline abnormalities and tracking these abnormalities in a defined family.
Myocardial Biopsy
The advent of cardiac magnetic resonance imaging (cMRI) has facilitated the diagnosis of infiltrative cardiomyopathies but, occasionally, myocardial biopsy with special histologic processing may be useful in the diagnosis of arrhythmogenic right ventricular dysplasia or a hypertrophic or infiltrative myopathy. Most reentrant ventricular tachycardias (VTs) are related to myocardial scarring from ischemic or dilated cardiomyopathy. Fibrotic replacement of myocytes and interweaving of scar tissue with functional myocytes is common along slow conduction zones of VT circuits.
Pacemaker and Other Cardiac Devices
The presence of a dual-chamber pacemaker or implantable cardioverter-defibrillator (ICD) can occasionally simplify the diagnosis. Most contemporary devices are capable of recording and logging tachyarrhythmias for subsequent analysis during interrogation of the implanted device, as well as providing real-time telemetry of intracardiac signals.
Analysis may reveal the disease process underlying the ventricular tachycardia (VT). However, the episode may prove to have been triggered by the device itself. Possibilities include the following:
-
Tracking of an atrial tachyarrhythmia in a dual-mode, dual-pacing, dual-sensing (DDD) device or an atrial-triggered, ventricular-inhibited (VDD) device
-
Endless loop tachycardia
-
Inappropriate rate-responsive pacing due to sensor problems or incorrect sensor programming
-
Overt pacemaker failure (runaway pacer)
The most common problem involves the patient whose device is tracking atrial fibrillation or atrial flutter. In the absence of a mode-switching algorithm, a DDD or VDD pacer responds by pacing the ventricle at the programmed upper rate limit of the device. Application of a magnet to the pacer generator may terminate endless loop tachycardia or drop the paced rate enough to allow diagnosis of the underlying atrial tachyarrhythmia.
Electrophysiologic Study
Diagnostic electrophysiologic study (EPS) requires placement of electrode catheters in the ventricle, followed by programmed ventricular stimulation using progressive pacing protocols. Premature ventricular beats are induced after conditioning pacing drives in an attempt to induce reentrant arrhythmia. [51] The response of the arrhythmia to pharmacologic agents can be assessed (eg, beta adrenergic stimulation or blockage, adenosine, calcium blockers).
In patients with symptoms suggestive of ventricular tachycardia (VT), this kind of provocative testing can be used to assess whether the ventricles can sustain a reentrant tachyarrhythmia. The diagnostic yield of EPS is highest in patients with reentrant VT circuits.
EPS is particularly relevant in patients considered to be at high risk for sudden death due to significant underlying structural heart disease. EPS may be useful in demonstrating whether the substrate for sustained VT is present in a patient presenting with syncope or ischemic, nonsustained VT. In patients with recurrent symptoms related to VT, programmed electrical stimulation can generally reproduce clinically relevant VT circuits.
If the diagnosis of right ventricular dysplasia is being considered, many laboratories perform right ventricular angiography at the time of the EPS. Diagnostic abnormalities include right ventricular dilatation, dyskinesis, and aneurysms.
EPS is recommended for diagnostic assessment of patients with a remote history of myocardial infarction and symptoms related to ventricular tachyarrhythmias, including palpitations, presyncope, and syncope, and in patients with coronary heart disease to guide and measure the efficacy of VT ablation. EPS is reasonable for diagnostic evaluation in patients with palpitations or suspected outflow tract VT. [40]
-
This electrocardiogram (ECG) shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. The tracing was obtained from a patient with severe ischemic cardiomyopathy during an electrophysiologic study. A single external shock subsequently converted VT to sinus rhythm. The patient had an atrial rate of 72 beats/min (measured with intracardiac electrodes; not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, surface ECG findings (dissociated P waves, fusion or capture beats) are present in only about 20% of cases. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.
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This electrocardiogram shows slow monomorphic ventricular tachycardia (VT), 121 beats/min, from a patient with an old inferior wall myocardial infarction and well-preserved left ventricular (LV) function (ejection fraction, 55%). The patient presented with symptoms of palpitation and neck fullness. Note the ventriculoatrial dissociation, which is most obvious in leads V2 and V3. Slower VT rates and preserved LV function are associated with better long-term prognosis.
-
At first glance, this tracing suggests rapid polymorphic ventricular tachycardia. It is actually sinus rhythm with premature atrial complex and a superimposed lead motion artifact. Hidden sinus beats can be observed by using calipers to march backward from the final two QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
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Torsade de pointes. Image A: This is polymorphic ventricular tachycardia associated with resting QT-interval prolongation. In this case, it was caused by the class III antiarrhythmic agent sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels. Image B: Torsade de pointes, a form of ventricular tachycardia. Courtesy of Science Source/BSIP.
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Preexcited atrial fibrillation. The patient has an accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over an accessory pathway results in a wide QRS complex, mimicking ventricular tachycardia.
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Curative ablation of ventricular tachycardia (VT). The patient had VT in the setting of ischemic cardiomyopathy. VT was induced in an electrophysiology laboratory, and an ablation catheter was placed at the critical zone of slow conduction within the VT circuit. Radiofrequency (RF) energy was applied to tissue through the catheter tip, and VT was terminated when the critical conducting tissue was destroyed.
-
Ventricular pacing at 120 beats/min. Newer pacemakers use bipolar pacing. If a smaller pacing stimulus artifact is overlooked, an erroneous diagnosis of ventricular tachycardia may result. Because leads are most commonly placed in the right ventricular apex, paced beats will have a left bundle-branch block morphology with inferior axis. Causes of rapid pacing include (1) tracking of atrial tachycardia in DDD mode, (2) rapid pacing due to the rate response being activated, and (3) endless loop tachycardia. Application of a magnet to the pacemaker will disable sensing and allow further diagnosis. Sometimes “pacing spike detection” must be programmed “ON” in the electrocardiographic system to make the spike apparent.
-
Supraventricular tachycardia with aberrancy. This tracing is from a patient with a structurally normal heart who has a normal resting electrocardiogram. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note the relatively narrow RS intervals in the precordial leads.
-
Termination of ventricular tachycardia (VT) with overdrive pacing. This patient has reentrant VT, which is terminated automatically by pacing from an implantable cardioverter-defibrillator.
-
Posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. The earliest activation is recorded in red, and late activation as blue to magenta. Fragmented low-amplitude diastolic local electrograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
-
This tracing depicts monomorphic ventricular tachycardia.
-
This image demonstrates polymorphic ventricular tachycardia.
-
This electrocardiogram is from a 32-year-old woman with recent-onset heart failure and syncope.
-
This electrocardiogram is from a 48-year-old man with wide-complex tachycardia during a treadmill stress test. Any wide-complex tachycardia tracing should raise the possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of a supraventricular rhythm. By Brugada criteria, RS complexes are apparent in the precordium (V2-V4), and the interval from R-wave onset to the deepest part of the S wave is shorter than 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon lead aVR, which shows no R wave, an initial q wave width shorter than 40 ms, and no initial notching in the q wave. The last Vereckei criterion examines the slope of the initial 40 ms of the QRS versus the terminal 40 ms of the QRS complex in lead aVR. In this case, the initial downward deflection in lead aVR is steeper than the terminal upward deflection, yielding Vi/Vt ratio above 1. All of these criteria are consistent with an aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with a sinus tachycardia mechanism.
-
The electrocardiogram shows a form of idiopathic ventricular tachycardia (VT) seen in the absence of structural heart disease. This rhythm arises from the left ventricular septum and often responds to verapamil. Upon superficial examination, it appears to be supraventricular tachycardia with bifascicular conduction block. Closer examination of lead V1 shows narrowing of fourth QRS complex, consistent with fusion between the wide QRS complex and the conducted atrial beat, confirming atrioventricular dissociation and a VT mechanism.
-
A wide QRS complex tachycardia is evident on this electrocardiogram from a 64-year-old man with history of previous myocardial infarction (MI) and syncope. In patients with a prior MI, the most common mechanism of wide QRS complex tachycardia is ventricular tachycardia.
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This tracing depicts atrioventricular dissociation.
-
Fusion beats, capture beats, and atrioventricular dissociation can be seen on this electrocardiogram.
-
Note the retrograde P waves in this electrocardiogram.
-
Retrograde P waves are also observed in this electrocardiogram.
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This electrocardiogram reveals torsade de pointes.
-
Hematoxylin and eosin stain; intermediate power of a healed myocardial infarct. Note the areas of fibrosis (pale pink) dissecting between the myocytes (red).
Tables
| Recommendation | Class |
|---|---|
| Resting 12-lead electrocardiography (ECG) in all patients | Class I |
12-lead ambulatory ECG to evaluate QT-interval changes or ST changes |
Class I |
| Cardiac event recorders when symptoms are sporadic to rule out transient arrhythmias | Class I |
Implantable loop recorders when symptoms are sporadic and suspected to be related to arrhythmias and when a symptom–rhythm correlation cannot be established by conventional diagnostic techniques |
Class I |
Exercise stress testing in adult patients who have an intermediate or greater probability of having coronary artery disease (CAD) to provoke ischemic changes or ventricular arrhythmia (VA) |
Class I |
| Exercise stress testing in patients with known or suspected exercise-induced VA | Class I |
| Echocardiography in all patients | Class I |
Pharmacologic stress testing plus imaging modality study to detect silent ischemia in patients with VAs who have an intermediate probability of having CAD and are physically unable to perform a symptom-limited exercise test |
Class I |
Cardiac magnetic resonance imaging (cMRI) or computed tomography (CT) scanning in patients with VAs when echocardiography does not provide accurate assessment of left- and right-ventricular function and/or evaluation of structural changes |
Class IIa |
Electrophysiologic study in patients with CAD with remote myocardial infarction with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. |
Class I |
Coronary angiography to establish or exclude significant obstructive CAD in patients with life-threatening VAs or in survivors of sudden cardiac death, who have an intermediate or greater probability of having CAD by age and symptoms |
Class IIa |
