Back To Search Results

Ventricular Tachycardia

Editor: Heidi Alvey Updated: 7/30/2023 2:05:23 AM

Introduction

Ventricular tachycardia (VT) is a wide complex tachycardia, defined as three or more consecutive beats at a rate of more than 100 per minute, arising from the ventricle.[1]  Ventricular tachycardia is a potentially life-threatening arrhythmia, and it is responsible for the majority of sudden cardiac deaths in the United States.[2] It is classified by duration as non-sustained or sustained ventricular tachycardia. Non-sustained ventricular tachycardia is defined as ventricular tachycardia of fewer than 30 seconds duration that does not lead to hemodynamic instability, while sustained VT lasts more than 30 seconds or requires intervention within 30 seconds due to hemodynamic compromise.[3] 

On the basis of QRS morphology, VT is divided into monomorphic and polymorphic ventricular tachycardia. Monomorphic VT is characterized by a single, stable QRS morphology with no beat-to-beat variation, while polymorphic VT has beat-to-beat variation in QRS shape and multiple QRS morphologies.[4] Torsades de Pointes is a form of polymorphic ventricular tachycardia (occurs in the setting of the long QT interval), characterized by waxing and waning of QRS amplitude, giving it the name "twisting of the points."[5] Bidirectional ventricular tachycardia is another form of polymorphic ventricular tachycardia and has a characteristic beat-to-beat change in the QRS axis. It is commonly seen in the setting of digitalis toxicity and patients with catecholaminergic polymorphic ventricular tachycardia (CPVT).[6] 

Ischemic heart disease is the most common cause of ventricular tachycardia, and 5 to 10% of patients with acute coronary syndrome are found to have ventricular arrhythmias. Ventricular tachycardia in acute coronary syndrome is usually polymorphic, while monomorphic ventricular tachycardia is a sign of a myocardial scar.[7] Accelerated atrioventricular rhythm (AIVR) is a monomorphic ventricular tachycardia, referred to as a sign of successful reperfusion, and it has a strong association with infarct size.[8][9] 

Ventricular tachycardia is a major contributor to sudden cardiac death in patients with ischemic and non-ischemic cardiomyopathy. Ventricular tachycardia in cardiomyopathy is usually monomorphic due to scar-related reentry, and its degeneration into ventricular fibrillation may result in cardiac arrest or even sudden cardiac death.[10][11] The clinical presentation of ventricular tachycardia varies from palpitation to sudden cardiac death. For appropriate management of VT and prevention of sudden cardiac death, it is essential to understand the pathophysiology of ventricular tachycardia and underlying structural heart disease. In this chapter, we summarize the etiology and epidemiology of ventricular tachycardia and discuss the evaluation and management of patients present with ventricular tachycardia.

Etiology

Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care

Etiology

Ventricular tachycardia accounts for approximately 8% of cases of wide-complex tachycardia.[12] The most common cause of ventricular tachycardia is underlying ischemic heart disease. Ventricular tachycardia in the presence of acute coronary syndrome is usually polymorphic, while the monomorphic VT is a characteristic feature of myocardial scar-related reentry. Ventricular tachycardia predicts a higher risk of death after acute myocardial infarction. [13] 

The other causes of ventricular tachycardia include ischemic or non-ischemic dilated cardiomyopathy, adult and congenital structural heart disease, inherited cardiac channelopathies, infiltrative cardiomyopathy, electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia), illicit drugs such as cocaine or methamphetamine, and digitalis toxicity.[14] Infiltrative cardiomyopathy can result from systemic lupus erythematosus, sarcoidosis, amyloidosis, rheumatoid arthritis, and hemochromatosis.[15] In the presence of a substrate, ventricular tachycardia is triggered by multiple factors; the most common triggers include myocardial ischemia, hypokalemia, hypomagnesemia, hypocalcemia, sepsis, and metabolic acidosis. 

Inherited cardiac channelopathies are more common in young individuals. The long-QT syndrome is the most common inherited cardiac channelopathy, and Torsades de Pointes is the characteristic feature of the long-QT syndrome.[16] The other inherited channelopathies responsible for ventricular tachycardia include Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome, and malignant early repolarization syndrome.[17] Hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and myocarditis are responsible for ventricular tachycardia and cardiac arrest/sudden cardiac death.

Idiopathic ventricular tachycardia is an uncommon class of ventricular tachycardia. It is usually found in younger people, with no evidence of structural heart disease. The most common idiopathic ventricular tachycardia arises from outflow tracts, mitral/tricuspid annulus, and fascicles of the left bundle branch.[18] Idiopathic VT is benign, responds really well to calcium channel blockers, and has an excellent outcome after catheter ablation.[19] 

Epidemiology

Ventricular tachycardia and ventricular fibrillation cause most cases of sudden cardiac death, with an estimated rate of 300,000 deaths each year in the United States.[2][20] Sudden cardiac deaths caused by ventricular tachyarrhythmias account for approximately half of the deaths related to cardiac causes.[20]  Ventricular tachycardia is strongly associated with coronary artery disease; around 15% of the patients with coronary artery disease are found to have ventricular tachycardia.[21] The incidence of ventricular tachycardia is relatively higher in men due to a higher incidence of coronary artery disease; however, the incidence in women is expected to increase with the rising incidence of coronary artery disease.

Ventricular tachycardia is much more common in the setting of acute coronary syndrome, and around 5 to 10% of the patients presenting with acute myocardial infarction are found to have ventricular arrhythmias within the first few days of the presentation.[22][23]  Patients with myocardial infarction, who develop ventricular tachyarrhythmias after the first two days of myocardial infarction, have an increased risk of death as compared to those having VT within the first two days.[24] Ventricular tachycardia is rare in children but can occur in the presence of inherited channelopathies or structural heart disease.

Idiopathic ventricular tachycardia is less common, and it is estimated to have an incidence of around 15 per 100,100 individuals in the general population. Its incidence increases with age, and there is no difference between men and women. The incidence of idiopathic VT has increased over the last two decades, mainly because of early diagnosis and increased awareness. The age at the diagnosis of idiopathy VT varies from 2nd decade to the 70th decade, but the mean age at the time of diagnosis is reported as 52 years in one study.[25]

Pathophysiology

Mechanism of Ventricular Tachycardia

Ventricular tachycardia is a diverse group of tachyarrhythmias, and its cellular mechanism depends on the underlying structural heart disease and channelopathy. Understanding the mechanism of ventricular tachycardia helps in the risk stratification of patients and guides appropriate management strategies. Reentry is the most common mechanism of ventricular tachycardia, followed by triggered activity and enhanced automaticity.[26] Reentry is the mechanism of scar-related ventricular tachycardia and bundle branch reentry VT.[27] Sustained reentrant ventricular tachycardia may degenerate into ventricular fibrillation, resulting in cardiac arrest or sudden cardiac death in patients with structural heart disease.[28]

The basic mechanism of ventricular tachycardia in long QT syndromes is triggered activity due to early after-depolarization. While delayed after-depolarization is the main mechanism of ventricular tachycardia in catecholaminergic polymorphic VT, verapamil-sensitive VT,  and digoxin toxicity.[6] Enhanced automaticity may also play a role in catecholaminergic VT. Although the mechanism of idiopathic ventricular tachycardia (outflow tract VT) is unclear, delayed after-depolarization is proposed as the possible mechanism. Most outflow tract VTs terminate in response to adenosine, suggesting cyclic AMP-mediated delayed after-depolarization is the main mechanism of these ventricular tachycardias.[29][30] 

Hemodynamic Consequences of Ventricular Tachycardia

The hemodynamic effects of ventricular tachycardia depend on coronary artery disease,  left ventricular systolic function, valvular heart disease, and other co-morbid conditions. The rapid ventricular rate in VT leads to low cardiac output due to a significant reduction in preload as well as stroke volume.[31] In the presence of structural heart disease, coronary artery disease, and left ventricular systolic dysfunction, the hemodynamic changes may lead to systemic hypotension, coronary and cerebral hypoperfusion, syncope, and even cardiac arrest. Coronary hypoperfusion further impairs hemodynamics, leading to ventricular fibrillation and even sudden cardiac death.[32] 

Ventricular tachycardia is relatively well tolerated in patients with a structurally normal heart, but incessant VT may lead to tachycardia-induced cardiomyopathy, hemodynamic instability, heart failure, and syncope. [33] In patients with inherited ventricular arrhythmias, including long QT syndrome, arrhythmogenic cardiomyopathy, catecholaminergic polymorphic VT, and Brugada syndrome, VT may degenerate in ventricular fibrillation and result in hemodynamic collapse, even in the presence of normal left ventricular systolic function.[34][35]

History and Physical

Clinical presentation of ventricular tachycardia varies, depending on the patients` age, co-morbid conditions, underlying structural heart diseases, and mechanism of ventricular tachycardia. Although the common symptoms of ventricular tachycardia include palpitations, shortness of breath, chest pain, and syncope, the patients may present with cardiac arrest or even sudden cardiac death.[36][37] Patients with idiopathic ventricular tachycardia usually present with palpitation during exercise or emotional stress, but shortness can be the first presentation due to heart failure and tachycardia-induced cardiomyopathy. Syncope and cardiac arrest are rare clinical presentations of idiopathic ventricular tachycardia in patients with no evidence of structural heart disease.[38]

Ventricular tachycardia in the presence of coronary artery disease may present with chest pain, syncope, shortness, and cardiac arrest. Ventricular tachycardia in the presence of left ventricular systolic dysfunction is not tolerated well and results in significant hemodynamic compromise patients usually present with syncope, shortness of breath (due to pulmonary edema), cardiac arrest, and even sudden cardiac death. While those with implantable cardioverter-defibrillator (ICD) may present with ICD shocks.[36] Patients with ventricular tachycardia due to channelopathies may have syncope, cardiac arrest, and sudden cardiac death as the first presentation; that is why it is essential to have a three-generation detailed family history while evaluating a young patient with ventricular tachycardia.[39]

The clinical examination of ventricular tachycardia may include hypotension and signs of heart failure. Elevated jugular venous pressure and cannon waves can be found even in hemodynamically stable patients. The detailed precordial examination may reveal the signs of underlying structural heart disease and signs of adverse effects of antiarrhythmic drugs, e.g., amiodarone.[40]

Evaluation

History and Physical Examination

Detailed history and clinical examination are pivotal in evaluating a patient with ventricular tachycardia. All patients undergoing evaluation for ventricular tachycardia should be asked about the risk factors for atherosclerotic cardiovascular diseases, prior history of palpitations, syncope, or ventricular tachycardia, and history of inherited cardiac conditions in the first-degree relatives.[41] Clinical practice guidelines recommended a three-generation, detailed family history in patients with suspected cardiac channelopathies.[42] Although a physical examination may help identify underlying structural heart disease, it is essential for managing patients presenting with ventricular tachycardia.[43]

Electrocardiographic Evaluation

The first step in evaluating presumed ventricular tachycardia is a 12-lead electrocardiogram (ECG).[44][45] A 12-lead ECG should be done during VT (if possible) and during sinus rhythm. A 12-lead ECG in sinus rhythm helps diagnose the underlying cause of ventricular tachycardia, e.g., myocardial ischemia/infarction, long QT syndrome, hypertrophic cardiomyopathy, Brugada syndrome, and arrhythmogenic right ventricular cardiomyopathy. Patients with ventricular tachycardia having symptoms associated with exertion, ischemic heart disease, or suspected to have catecholaminergic polymorphic ventricular tachycardia should undergo further testing with a treadmill stress test.[46] Patients having syncope, presyncope, or palpitations with no arrhythmia detected on a single 12-lead ECG should undergo further evaluation with ambulatory ECG monitoring.[47] In patients with infrequent symptoms suspected to be due to ventricular tachycardia, an implantable loop recorder can be considered.

Echocardiogram and Other Non-invasive Imaging

In patients with ventricular tachycardia and possible structural heart disease, an echocardiogram is recommended to evaluate the cardiac structure and function.[48][49] An echocardiogram is an essential tool for diagnosing hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy (ARVC). Cardiac computed tomography (CT) and cardiac magnetic resonance (CMR) imaging can be considered in selected patients. Cardiac MRI not only defines the myocardial scar but also helps diagnose infiltrative heart diseases, ARVC, and myocarditis.[50]In younger patients with an episode of unexplained cardiac arrest secondary to ventricular tachyarrhythmia, CT coronary angiography can be used to confirm the presence or absence of coronary artery anomalies.[51] It is also helpful for the diagnosis of coronary artery disease. [42][52]

Invasive Evaluation

 For patients presenting with cardiac arrest due to ventricular tachycardia due to presumed myocardial ischemia, an invasive coronary angiogram is recommended to evaluate coronary artery disease and guide the revascularization strategy.[53] Although an invasive electrophysiology study is no longer recommended for diagnosing ventricular tachycardia, it can be used in selected patients to assess the risk of sudden cardiac death who do not meet the criteria of ICD implantation.[52] An endomyocardial biopsy is indicated, in selected patients, for the diagnosis of myocarditis and infiltrative cardiomyopathies when non-invasive imaging is non-diagnostic.[54]

Genetic Testing

Genetic testing is not recommended as a routine test in patients presenting with ventricular tachycardia. However, in selected patients with suspected inherited cardiac channelopathies, genetic testing can be done to confirm the diagnosis.[55]Genetic testing should also be offered to asymptomatic family members of patients with congenital long QT syndrome, hypertrophic cardiomyopathy, catecholaminergic polymorphic VT, and right ventricular dysplasia.[3]

Other Investigations

Serum levels of potassium, magnesium, and calcium are essential investigations for diagnosing and managing patients with ventricular tachycardia. High-sensitivity cardiac troponin is required for the diagnosis of myocardial infarction. While natriuretic peptide is an excellent prognostic marker in patients with structural heart disease who present with ventricular tachycardia and have the risk of sudden cardiac death.[56]

Treatment / Management

Acute Management

Cardiac arrest is the life-threatening presentation of ventricular tachycardia. Patients presenting with cardiac arrest secondary to ventricular tachycardia should be resuscitated and managed according to the advanced life support (ACLS) algorithm.[57] In the absence of a cardiac arrest, patients with hemodynamically unstable ventricular tachycardia are managed with direct current cardioversion.[58] In hemodynamically unstable patients, intravenous amiodarone should be used to maintain the sinus rhythm if ventricular tachycardia does not respond to direct current cardioversion or VT recurs after successful cardioversion.[59] All hemodynamically unstable patients with myocardial infarction/ischemia-induced ventricular tachycardia should undergo coronary angiogram followed by revascularization. (A1)

Ventricular tachycardia (VT) storm is one of the presentations of VT in patients with structural heart diseases. It is defined as three or more episodes of sustained ventricular tachycardia within 24 hours, which requires intervention in the form of antiarrhythmic drugs, anti-tachycardia pacing, or direct current cardioversion.[60] VT storm not only causes significant morbidity in the form of hospitalization and decompensated heart failure but also increases mortality. The initial management of VT storm includes intravenous antiarrhythmic drugs, intravenous beta-blockers, and direct current cardioversion along with sedation. In refractory conditions, patients may require intubation, mechanical circulatory support, and catheter ablation of ventricular tachycardia.[61](B3)

In patients with structural heart disease and hemodynamically stable ventricular tachycardia, intravenous procainamide, amiodarone, and sotalol (depending on availability) are recommended for the acute treatment of ventricular tachycardia.[62]  Intravenous lidocaine can be used as an alternative antiarrhythmic drug if the drugs mentioned above are not available. Intravenous beta-blockers can be considered in patients with ventricular tachycardia secondary to ischemia.[63](A1)

Intravenous beta-blockade and non-dihydropyridine calcium channel blockers are the first choice drugs for treating hemodynamically stable patients with idiopathic ventricular tachycardia.[64] Intravenous verapamil should be given as a bolus by using a large bore cannula. Direct current cardioversion may be considered if VT does not respond to antiarrhythmic drugs. Asymptomatic patients with non-sustained ventricular tachycardia (VT) and no underlying structural heart disease may not require any additional therapy.

Intravenous beta-blockade is the mainstay of treatment in hemodynamically stable patients with VT secondary to underlying cardiac channelopathies.[65] Intravenous magnesium and mexiletine can be considered in patients with long QT-induced stable VT.[66] Some patients with long QT syndrome may have incessant VT due to short-long sequence and R on T phenomenon; temporary pacing at a higher rate is effective in preventing Torsades de Pointes in these patients.[67] Serum potassium, magnesium, and calcium levels should be optimized in all patients presenting with ventricular tachycardia.

Long-Term Management

All patients with structural heart disease and left ventricular systolic dysfunction should be offered guidelines-directed medical therapy for heart failure.[68] Patients with ischemic cardiomyopathy who survive sudden cardiac arrest due to ventricular tachycardia, or experience hemodynamically unstable or stable sustained ventricular tachycardia, should have an implantable cardiac defibrillator (ICD) placed if their estimated meaningful survival is greater than one year.[69][70][71] Patients with unexplained syncope who have ischemic cardiomyopathy, non-ischemic cardiomyopathy, or adult congenital heart disease who do not meet the criteria for an ICD can undergo an electrophysiological study to assess the risk of sustained ventricular tachycardia, however, performing the study solely for risk stratification is not indicated.[72][73][52] If a sustained VT is induced during an electrophysiology study, implantation of an ICD should be recommended for the prevention of sudden cardiac death. (A1)

In patients with ischemic cardiomyopathy who present with ventricular tachycardia, the long-term beta-blockade is recommended to prevent the recurrence of VT and reduce the risk of sudden cardiac death. If the patients present with recurrent episodes of ventricular tachycardia or ICD shocks despite being on the optimal doses of beta-blocking drugs, amiodarone, and sotalol are recommended to suppress the recurrent ventricular tachycardia.[74] Amiodarone is more effective than sotalol, and it has lower proarrhythmic properties; however, it has systemic adverse effects, which may result in the early discontinuation of therapy.(A1)

Catheter ablation has been proven as an effective treatment option for patients with drug-refractory ventricular tachycardia. It is recommended in a select group of patients with ischemic cardiomyopathy who continue to have sustained VT on antiarrhythmic drugs or are intolerant of amiodarone or other antiarrhythmic medications.[75][76][77] In VANISH trial, catheter ablation reduced the recurrence of VT, ventricular storm, and ICD shock as compared to antiarrhythmic drugs; however, it did not improve survival.[78]  The International VT Ablation Center Collaborative (IVTCC) study reveals that 70% of patients with structural heart diseases achieve freedom from VT after catheter ablation, and freedom from VT improves survival in this particular group of patients.[79] Ventricular tachycardia ablation is a relatively safe procedure in experienced centers with a procedure-related mortality of less than 1%. Vascular access-related complications are similar to other electrophysiology procedures, while stroke, tamponade, and atrioventricular blocks are rare.[78][79](A1)

Patients with non-ischemic cardiomyopathy who survive sudden cardiac death due to VT or develop sustained VT with no reversible cause should have an ICD implanted for secondary prevention of SCD if they have an expected survival of more than a year with good quality of life. While amiodarone can be considered for preventing sudden cardiac death and recurrence of VT if the expected meaningful survival is less than a year.[42] In patients with recurrent VT, despite being on optimal heart failure therapy and beta blockade, contemporary guidelines recommend amiodarone and sotalol to prevent recurrent VT episodes. Catheter ablation can be considered in selected patients with drug-refractory VT, resulting in recurrent ICD shocks.[80](A1)

In patients with ventricular tachycardia due to arrhythmogenic right ventricular cardiomyopathy (ARVC), the beta-blockade is helpful in reducing recurrent arrhythmia. All patients with ARVC who survive sudden cardiac death are recommended to have an ICD implanted for secondary prevention of sudden cardiac death.[81] While ICD can be considered in certain high-risk patients presenting with syncope and ventricular tachycardia but do not have a history of cardiac arrest.[58] In ARVC patients with recurrent VT and appropriate ICD shocks on beta blockers and antiarrhythmic drugs, catheter ablation can be considered in experienced centers where both endocardia and epicardial ablation facilities are available.[82](A1)

Beta blockade is the mainstay of treatment for patients with congenital long QT syndrome and catecholaminergic polymorphic ventricular tachycardia (CPVT).[83] For patients with cardiac channelopathies, who survived cardiac arrest, an implantable cardioverter-defibrillator is indicated for secondary prevention of sudden cardiac death. In highly symptomatic patients on the optimal dose of beta blockers, left cardiac sympathetic denervation can be considered in experienced centers.[84] Implantation of an ICD for secondary prevention of sudden cardiac death is recommended in patients with Brugada syndrome, short QT syndrome, hypertrophic cardiomyopathy, and those with idiopathic polymorphic ventricular tachycardia, who survive sudden cardiac death due to ventricular tachycardia.[3](A1)

Non-dihydropyridine calcium channel blockers and beta-blockade are effective treatment options for patients with idiopathic ventricular tachycardia. Most patients respond very well to beta-blockers and verapamil and do not require further treatment options.[85] Other antiarrhythmic drugs can be considered in patients with idiopathic VT who do not respond to beta blockers and calcium channel-blocking drugs. Catheter ablation is an effective therapy that can be considered in patients with idiopathic VT that does not respond to beta-blockers, calcium channel blockers, and other antiarrhythmic drugs.[86] (A1)

Differential Diagnosis

Ventricular tachycardia is the most common cause of broad complex tachycardia. However, there are multiple other causes of broad complex tachycardia. The common differentials of VT include supraventricular tachycardia with bundle branch aberrancy, supraventricular tachycardia with preexcitation, antidromic atrioventricular tachycardia (AVRT), pacemaker-mediated tachycardia, and metabolic derangements.[87] 

A meticulous history, clinical examination, and electrocardiogram (ECG) help differentiate ventricular tachycardia from the other causes of broad complex tachycardia.[88] Electrocardiographic algorithms can be used to differentiate ventricular tachycardia from supraventricular tachycardia with aberrancy.[89][90] Careful interpretation of ECG may help identify the origin of VT and differentiate idiopathic VT from the other forms of ventricular tachycardia.[91][92] 

Prognosis

The prognosis of VT depends on the underlying etiology and the presence of structural heart disease. As coronary artery disease is the main cause of VT, patients with ischemic cardiomyopathy-related VT have the worst prognosis. The two-year mortality in these patients has been reported to be as high as 30% if they remain untreated.[93] However, the implantation of a defibrillator significantly reduces the incidence of sudden cardiac death and improves survival in these patients.[94] 

Patients with idiopathic ventricular tachycardia have excellent prognoses in the absence of other co-morbid conditions, and they are estimated to have longevity almost equal to the general population.[95]  Patients with hypertrophic cardiomyopathy, long QT syndrome, and arrhythmogenic right ventricular cardiomyopathy have a higher risk of sudden cardiac death, even in normal left ventricular systolic function. Beta-blockers reduce the burden of ventricular tachycardia in these patients, and implantable cardioverter defibrillators prevent sudden cardiac death.[96][97]

Complications

Complications of ventricular tachycardia depend on the underlying mechanism of ventricular tachycardia. The common complications of idiopathic ventricular tachycardia include tachycardia-induced cardiomyopathy and heart failure. Tachycardia-induced cardiomyopathy is much more common in patients with incessant episodes of VT and those with a genetic predisposition and other risk factors of cardiomyopathy, e.g., alcohol intake.[98] 

Cardiac arrest and sudden cardiac death are the major complications of inherited ventricular tachycardia as well as scar-related ventricular tachycardia. However, these complications can be minimized with early recognition and implantation of implantable cardioverter-defibrillator.[42] The beta-blockade has also been reported to reduce the incidence of sudden cardiac death in patients with cardiac channelopathies and ischemic cardiomyopathy.[99][3]

Deterrence and Patient Education

Ventricular tachycardia is a potentially life-threatening condition. Although palpitation is the most common presentation of ventricular tachycardia, patients may present with syncope, cardiac arrest, and even sudden cardiac death. All patients with broad complex tachycardia should undergo detailed evaluation, including three-generation family history, transthoracic echocardiogram, and cardiac magnetic resonance imaging (if required). Patients with a family history of sudden cardiac death at a young age are recommended to consult a cardiologist to evaluate cardiac channelopathies and other inherited cardiac conditions. Asymptomatic relatives of patients with inherited channelopathies and other inherited causes of ventricular tachycardia should consult a cardiac electrophysiologic and/or a geneticist for screening and genetic counseling.[55]

Enhancing Healthcare Team Outcomes

Cardiac arrest is a fatal presentation of ventricular tachycardia. Early recognition, bystander cardiopulmonary resuscitation (CPR), and public access to defibrillation have helped improve the rate of survival for patients who have an out-of-hospital cardiac arrest due to ventricular arrhythmias. However, survival after out-of-hospital still remains low.[100][101][102] [Level 1] Patient care after the return of spontaneous circulation (ROSC), with special emphasis on targeted temperature management (TTM) and cardio-cerebral resuscitation, has further improved survival.[103] [Level 2] A dedicated resuscitation team, with no clinical responsibilities that interfere with their participation in CPR, is the basic requirement for managing cardiac arrest. Effective communication among team members has also been identified as a positive factor in improving outcomes.[104]

In-hospital cardiac arrest shares a similarity with out-of-hospital cardiac arrest in that early cardiopulmonary resuscitation (CPR), and defibrillation are important factors in survival. [Level 1] Every minute treatment is delayed reduces survival by approximately 10%.[105] This makes the resuscitation team an essential part of ventricular tachycardia management. Resuscitation teams universally consist of physicians, nurses, anesthesiologists, and respiratory therapists coordinating their efforts. Hospitals that are high performing include more support staff (pharmacy, clerical, security, spiritual staff).[104] 

Management of a patient with ventricular tachycardia requires an interprofessional team. A cardiac electrophysiologic and a cardiac critical care nurse are essential to the team. Diabetic patients with ischemic heart disease should be seen by an endocrinologist to manage it properly. Strenuous exercise should be avoided as it may precipitate VT in some patients. All patients should be strongly encouraged to discontinue smoking. Patients presenting with VT secondary to (suspected) inherited cardiac conditions require a geneticist for genetic counseling and testing. The pharmacist should educate the patient on medication compliance and the need to follow up with the cardiologist, as well as perform medication reconciliation and contact the prescriber if they have any concerns about the patient's medication regimen. They can assist the clinical team in managing drug-drug interactions and making appropriate drug treatment selections. Nurses often coordinate activities between various providers, counsel patients, and assist in assessments and procedures. This interprofessional model will help drive optimal patient results in VT cases. [Level 5]

Media


(Click Image to Enlarge)
Ventricular Tachycardia rhythm example
Ventricular Tachycardia rhythm example
Contributed by Tammy J. Toney-Butler, AS, RN, CEN, TCRN, CPEN

(Click Image to Enlarge)
Ventricular Tachycardia, [SATA]
Ventricular Tachycardia, [SATA]
Contributed by Steve Bhmji, MS, MD, PhD

References


[1]

Nikolic G. Definition of ventricular tachycardia. The American journal of cardiology. 1982 Nov:50(5):1197-8     [PubMed PMID: 7137043]

Level 3 (low-level) evidence

[2]

Tang PT, Shenasa M, Boyle NG. Ventricular Arrhythmias and Sudden Cardiac Death. Cardiac electrophysiology clinics. 2017 Dec:9(4):693-708. doi: 10.1016/j.ccep.2017.08.004. Epub     [PubMed PMID: 29173411]


[3]

Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology. 2018 Oct 2:72(14):e91-e220. doi: 10.1016/j.jacc.2017.10.054. Epub 2018 Aug 16     [PubMed PMID: 29097296]

Level 1 (high-level) evidence

[4]

Buxton AE,Calkins H,Callans DJ,DiMarco JP,Fisher JD,Greene HL,Haines DE,Hayes DL,Heidenreich PA,Miller JM,Poppas A,Prystowsky EN,Schoenfeld MH,Zimetbaum PJ,Heidenreich PA,Goff DC,Grover FL,Malenka DJ,Peterson ED,Radford MJ,Redberg RF,American College of Cardiology,American Heart Association Task Force on Clinical Data Standards,(ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology), 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). Journal of the American College of Cardiology. 2006 Dec 5     [PubMed PMID: 17161282]


[5]

Buca S,McKinney J,Brywczynski J,Slovis C, A twisting of points: recognize the signs of Torsades de Pointes. JEMS : a journal of emergency medical services. 2011 Jul     [PubMed PMID: 21807276]


[6]

Kim CW, Aronow WS, Dutta T, Frenkel D, Frishman WH. Catecholaminergic Polymorphic Ventricular Tachycardia. Cardiology in review. 2020 Nov/Dec:28(6):325-331. doi: 10.1097/CRD.0000000000000302. Epub     [PubMed PMID: 31934898]


[7]

Gupta S, Pressman GS, Figueredo VM. Incidence of, predictors for, and mortality associated with malignant ventricular arrhythmias in non-ST elevation myocardial infarction patients. Coronary artery disease. 2010 Dec:21(8):460-5. doi: 10.1097/MCA.0b013e32834022fa. Epub     [PubMed PMID: 20881482]

Level 2 (mid-level) evidence

[8]

Jakkoju A, Jakkoju R, Subramaniam PN, Glancy DL. Accelerated idioventricular rhythm. Proceedings (Baylor University. Medical Center). 2018 Oct:31(4):506-507. doi: 10.1080/08998280.2018.1493323. Epub 2018 Oct 2     [PubMed PMID: 31080367]


[9]

Terkelsen CJ,Sørensen JT,Kaltoft AK,Nielsen SS,Thuesen L,Bøtker HE,Lassen JF, Prevalence and significance of accelerated idioventricular rhythm in patients with ST-elevation myocardial infarction treated with primary percutaneous coronary intervention. The American journal of cardiology. 2009 Dec 15     [PubMed PMID: 19962468]


[10]

Pandozi C,Lavalle C,Russo M,Galeazzi M,Ficili S,Malacrida M,Centurion Aznaran C,Colivicchi F, Mapping of ventricular tachycardia in patients with ischemic cardiomyopathy: Current approaches and future perspectives. Clinical cardiology. 2019 Oct     [PubMed PMID: 31411347]

Level 3 (low-level) evidence

[11]

Balaban G, Costa CM, Porter B, Halliday B, Rinaldi CA, Prasad S, Plank G, Ismail TF, Bishop MJ. 3D Electrophysiological Modeling of Interstitial Fibrosis Networks and Their Role in Ventricular Arrhythmias in Non-Ischemic Cardiomyopathy. IEEE transactions on bio-medical engineering. 2020 Nov:67(11):3125-3133. doi: 10.1109/TBME.2020.2976924. Epub 2020 Apr 3     [PubMed PMID: 32275581]


[12]

Alzand BS, Crijns HJ. Diagnostic criteria of broad QRS complex tachycardia: decades of evolution. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. 2011 Apr:13(4):465-72. doi: 10.1093/europace/euq430. Epub 2010 Dec 3     [PubMed PMID: 21131372]


[13]

Jabbari R, Engstrøm T, Glinge C, Risgaard B, Jabbari J, Winkel BG, Terkelsen CJ, Tilsted HH, Jensen LO, Hougaard M, Chiuve SE, Pedersen F, Svendsen JH, Haunsø S, Albert CM, Tfelt-Hansen J. Incidence and risk factors of ventricular fibrillation before primary angioplasty in patients with first ST-elevation myocardial infarction: a nationwide study in Denmark. Journal of the American Heart Association. 2015 Jan 5:4(1):e001399. doi: 10.1161/JAHA.114.001399. Epub 2015 Jan 5     [PubMed PMID: 25559012]

Level 2 (mid-level) evidence

[14]

Koplan BA,Stevenson WG, Ventricular tachycardia and sudden cardiac death. Mayo Clinic proceedings. 2009 Mar     [PubMed PMID: 19252119]


[15]

Bejar D,Colombo PC,Latif F,Yuzefpolskaya M, Infiltrative Cardiomyopathies. Clinical Medicine Insights. Cardiology. 2015     [PubMed PMID: 26244036]


[16]

Lankaputhra M, Voskoboinik A. Congenital long QT syndrome: a clinician's guide. Internal medicine journal. 2021 Dec:51(12):1999-2011. doi: 10.1111/imj.15437. Epub     [PubMed PMID: 34151491]


[17]

Skinner JR, Winbo A, Abrams D, Vohra J, Wilde AA. Channelopathies That Lead to Sudden Cardiac Death: Clinical and Genetic Aspects. Heart, lung & circulation. 2019 Jan:28(1):22-30. doi: 10.1016/j.hlc.2018.09.007. Epub 2018 Oct 4     [PubMed PMID: 30389366]


[18]

Kobayashi Y. Idiopathic Ventricular Premature Contraction and Ventricular Tachycardia: Distribution of the Origin, Diagnostic Algorithm, and Catheter Ablation. Journal of Nippon Medical School = Nippon Ika Daigaku zasshi. 2018:85(2):87-94. doi: 10.1272/jnms.2018_85-14. Epub     [PubMed PMID: 29731502]


[19]

Tondo C,Carbucicchio C,Dello Russo A,Majocchi B,Zucchetti M,Pizzamiglio F,Bologna F,Cattaneo F,Colombo D,Russo E,Casella M, Idiopathic Ventricular Tachycardia: Transcatheter Ablation or Antiarrhythmic Drugs? Journal of atrial fibrillation. 2015 Feb-Mar     [PubMed PMID: 27957145]

Level 3 (low-level) evidence

[20]

McNally B,Robb R,Mehta M,Vellano K,Valderrama AL,Yoon PW,Sasson C,Crouch A,Perez AB,Merritt R,Kellermann A,Centers for Disease Control and Prevention., Out-of-hospital cardiac arrest surveillance --- Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005--December 31, 2010. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002). 2011 Jul 29     [PubMed PMID: 21796098]


[21]

Aronow WS, Ahn C, Mercando AD, Epstein S, Kronzon I. Prevalence and association of ventricular tachycardia and complex ventricular arrhythmias with new coronary events in older men and women with and without cardiovascular disease. The journals of gerontology. Series A, Biological sciences and medical sciences. 2002 Mar:57(3):M178-80     [PubMed PMID: 11867655]


[22]

American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology), Buxton AE, Calkins H, Callans DJ, DiMarco JP, Fisher JD, Greene HL, Haines DE, Hayes DL, Heidenreich PA, Miller JM, Poppas A, Prystowsky EN, Schoenfeld MH, Zimetbaum PJ, Goff DC, Grover FL, Malenka DJ, Peterson ED, Radford MJ, Redberg RF. 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 Dec 5:114(23):2534-70     [PubMed PMID: 17130345]


[23]

Dumas F, Cariou A, Manzo-Silberman S, Grimaldi D, Vivien B, Rosencher J, Empana JP, Carli P, Mira JP, Jouven X, Spaulding C. Immediate percutaneous coronary intervention is associated with better survival after out-of-hospital cardiac arrest: insights from the PROCAT (Parisian Region Out of hospital Cardiac ArresT) registry. Circulation. Cardiovascular interventions. 2010 Jun 1:3(3):200-7. doi: 10.1161/CIRCINTERVENTIONS.109.913665. Epub 2010 May 18     [PubMed PMID: 20484098]


[24]

Volpi A,Cavalli A,Franzosi MG,Maggioni A,Mauri F,Santoro E,Tognoni G, One-year prognosis of primary ventricular fibrillation complicating acute myocardial infarction. The GISSI (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto miocardico) investigators. The American journal of cardiology. 1989 May 15     [PubMed PMID: 2565684]


[25]

Sirichand S, Killu AM, Padmanabhan D, Hodge DO, Chamberlain AM, Brady PA, Kapa S, Noseworthy PA, Packer DL, Munger TM, Gersh BJ, McLeod CJ, Shen WK, Cha YM, Asirvatham SJ, Friedman PA, Mulpuru SK. Incidence of Idiopathic Ventricular Arrhythmias: A Population-Based Study. Circulation. Arrhythmia and electrophysiology. 2017 Feb:10(2):. doi: 10.1161/CIRCEP.116.004662. Epub     [PubMed PMID: 28183845]


[26]

Clémenty J, Cheradame I, Bordier P, Gosse P, Poquet F. [Mechanisms of ventricular tachycardia]. Archives des maladies du coeur et des vaisseaux. 1993 May:86(5 Suppl):705-13     [PubMed PMID: 8267497]


[27]

Lopez EM, Malhotra R. Ventricular Tachycardia in Structural Heart Disease. The Journal of innovations in cardiac rhythm management. 2019 Aug:10(8):3762-3773. doi: 10.19102/icrm.2019.100801. Epub 2019 Aug 15     [PubMed PMID: 32477742]


[28]

Zipes DP,Wellens HJ, Sudden cardiac death. Circulation. 1998 Nov 24;     [PubMed PMID: 9826323]


[29]

Lerman BB, Belardinelli L, West GA, Berne RM, DiMarco JP. Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activity. Circulation. 1986 Aug:74(2):270-80     [PubMed PMID: 3015453]


[30]

Lerman BB, Stein K, Engelstein ED, Battleman DS, Lippman N, Bei D, Catanzaro D. Mechanism of repetitive monomorphic ventricular tachycardia. Circulation. 1995 Aug 1:92(3):421-9     [PubMed PMID: 7634458]


[31]

Kanagasundram AN, Richardson TD, Stevenson WG. The Heart Rate of Ventricular Tachycardia. Circulation. 2021 Jan 19:143(3):227-229. doi: 10.1161/CIRCULATIONAHA.120.051941. Epub 2021 Jan 19     [PubMed PMID: 33464966]


[32]

Zeppenfeld K, Wijnmaalen AP, Ebert M, Baldinger SH, Berruezo A, Catto V, Vaseghi M, Arya A, Kumar S, de Riva M, Deneke T, Gaspar T, Soejima K, van Rein N, Tedrow UB, Piorkowski C, Shivkumar K, Carbucicchio C, Hindricks G, Stevenson WG. Clinical Outcomes in Patients With Dilated Cardiomyopathy and Ventricular Tachycardia. Journal of the American College of Cardiology. 2022 Sep 13:80(11):1045-1056. doi: 10.1016/j.jacc.2022.06.035. Epub     [PubMed PMID: 36075673]

Level 2 (mid-level) evidence

[33]

Ohe T, Aihara N, Kamakura S, Kurita T, Shimizu W, Shimomura K. Long-term outcome of verapamil-sensitive sustained left ventricular tachycardia in patients without structural heart disease. Journal of the American College of Cardiology. 1995 Jan:25(1):54-8     [PubMed PMID: 7798526]


[34]

Locati ET,Bagliani G,Cecchi F,Johny H,Lunati M,Pappone C, Arrhythmias due to Inherited and Acquired Abnormalities of Ventricular Repolarization. Cardiac electrophysiology clinics. 2019 Jun     [PubMed PMID: 31084855]


[35]

Corrado D, Basso C, Judge DP. Arrhythmogenic Cardiomyopathy. Circulation research. 2017 Sep 15:121(7):784-802. doi: 10.1161/CIRCRESAHA.117.309345. Epub     [PubMed PMID: 28912183]


[36]

Havakuk O, Viskin D, Viskin S, Adler A, Rozenbaum Z, Elbaz Zuzut M, Borohovitz A, Chorin E, Rosso R. Clinical Presentation of Sustained Monomorphic Ventricular Tachycardia Without Cardiac Arrest. Journal of the American Heart Association. 2020 Nov 17:9(22):e016673. doi: 10.1161/JAHA.120.016673. Epub 2020 Nov 4     [PubMed PMID: 33146061]


[37]

Morady F, Shen EN, Bhandari A, Schwartz AB, Scheinman MM. Clinical symptoms in patients with sustained ventricular tachycardia. The Western journal of medicine. 1985 Mar:142(3):341-4     [PubMed PMID: 3993009]

Level 3 (low-level) evidence

[38]

Durin O,Pedrinazzi C,Agricola P,Romagnoli G,Donato G,Inama G, [Idiopathic ventricular tachycardia: clinical characteristics and management]. Giornale italiano di cardiologia (2006). 2010 Oct     [PubMed PMID: 21416823]


[39]

Kaufman ES. Mechanisms and clinical management of inherited channelopathies: long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, and short QT syndrome. Heart rhythm. 2009 Aug:6(8 Suppl):S51-5. doi: 10.1016/j.hrthm.2009.02.009. Epub 2009 Feb 12     [PubMed PMID: 19631908]


[40]

Hadid C. Sustained ventricular tachycardia in structural heart disease. Cardiology journal. 2015:22(1):12-24. doi: 10.5603/CJ.a2014.0069. Epub 2014 Oct 9     [PubMed PMID: 25299497]


[41]

Behere SP, Weindling SN. Inherited arrhythmias: The cardiac channelopathies. Annals of pediatric cardiology. 2015 Sep-Dec:8(3):210-20. doi: 10.4103/0974-2069.164695. Epub     [PubMed PMID: 26556967]


[42]

Al-Khatib SM,Stevenson WG,Ackerman MJ,Bryant WJ,Callans DJ,Curtis AB,Deal BJ,Dickfeld T,Field ME,Fonarow GC,Gillis AM,Granger CB,Hammill SC,Hlatky MA,Joglar JA,Kay GN,Matlock DD,Myerburg RJ,Page RL, 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: Executive summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart rhythm. 2018 Oct     [PubMed PMID: 29097320]

Level 1 (high-level) evidence

[43]

Steinbach KK, Merl O, Frohner K, Hief C, Nürnberg M, Kaltenbrunner W, Podczeck A, Wessely E. Hemodynamics during ventricular tachyarrhythmias. American heart journal. 1994 Apr:127(4 Pt 2):1102-6     [PubMed PMID: 8160588]

Level 3 (low-level) evidence

[44]

Wellens HJ, Bär FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. The American journal of medicine. 1978 Jan:64(1):27-33     [PubMed PMID: 623134]


[45]

Pérez-Rodon J, Martínez-Alday J, Barón-Esquivias G, Martín A, García-Civera R, Del Arco C, Cano-Gonzalez A, Moya-Mitjans A. Prognostic value of the electrocardiogram in patients with syncope: data from the group for syncope study in the emergency room (GESINUR). Heart rhythm. 2014 Nov:11(11):2035-44. doi: 10.1016/j.hrthm.2014.06.037. Epub 2014 Jun 30     [PubMed PMID: 24993462]

Level 2 (mid-level) evidence

[46]

Elhendy A,Chandrasekaran K,Gersh BJ,Mahoney D,Burger KN,Pellikka PA, Functional and prognostic significance of exercise-induced ventricular arrhythmias in patients with suspected coronary artery disease. The American journal of cardiology. 2002 Jul 15     [PubMed PMID: 12106835]


[47]

Barrett PM, Komatireddy R, Haaser S, Topol S, Sheard J, Encinas J, Fought AJ, Topol EJ. Comparison of 24-hour Holter monitoring with 14-day novel adhesive patch electrocardiographic monitoring. The American journal of medicine. 2014 Jan:127(1):95.e11-7. doi: 10.1016/j.amjmed.2013.10.003. Epub 2013 Oct 15     [PubMed PMID: 24384108]


[48]

Solomon SD, Zelenkofske S, McMurray JJ, Finn PV, Velazquez E, Ertl G, Harsanyi A, Rouleau JL, Maggioni A, Kober L, White H, Van de Werf F, Pieper K, Califf RM, Pfeffer MA, Valsartan in Acute Myocardial Infarction Trial (VALIANT) Investigators. Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. The New England journal of medicine. 2005 Jun 23:352(25):2581-8     [PubMed PMID: 15972864]


[49]

Gula LJ, Klein GJ, Hellkamp AS, Massel D, Krahn AD, Skanes AC, Yee R, Anderson J, Johnson GW, Poole JE, Mark DB, Lee KL, Bardy GH. Ejection fraction assessment and survival: an analysis of the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT). American heart journal. 2008 Dec:156(6):1196-200. doi: 10.1016/j.ahj.2008.08.007. Epub 2008 Nov 6     [PubMed PMID: 19033019]

Level 1 (high-level) evidence

[50]

Mahida S,Sacher F,Dubois R,Sermesant M,Bogun F,Haïssaguerre M,Jaïs P,Cochet H, Cardiac Imaging in Patients With Ventricular Tachycardia. Circulation. 2017 Dec 19     [PubMed PMID: 29255125]


[51]

Sdiri W, Ben Slima H, Mizouni H, Ben Ahmed H, Menif E, Boujnah MR. [Role of multidetector CT scan in the diagnosis of congenital coronary artery anomalies with inter-aortopulmonary course: about two cases and literature review]. Annales de cardiologie et d'angeiologie. 2013 Aug:62(4):273-7. doi: 10.1016/j.ancard.2012.04.002. Epub 2012 May 3     [PubMed PMID: 22621848]

Level 3 (low-level) evidence

[52]

Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2018 Sep 25:138(13):e272-e391. doi: 10.1161/CIR.0000000000000549. Epub     [PubMed PMID: 29084731]

Level 1 (high-level) evidence

[53]

Yannopoulos D, Bartos JA, Raveendran G, Conterato M, Frascone RJ, Trembley A, John R, Connett J, Benditt DG, Lurie KG, Wilson RF, Aufderheide TP. Coronary Artery Disease in Patients With Out-of-Hospital Refractory Ventricular Fibrillation Cardiac Arrest. Journal of the American College of Cardiology. 2017 Aug 29:70(9):1109-1117. doi: 10.1016/j.jacc.2017.06.059. Epub     [PubMed PMID: 28838358]


[54]

Ammirati E,Buono A,Moroni F,Gigli L,Power JR,Ciabatti M,Garascia A,Adler ED,Pieroni M, State-of-the-Art of Endomyocardial Biopsy on Acute Myocarditis and Chronic Inflammatory Cardiomyopathy. Current cardiology reports. 2022 May;     [PubMed PMID: 35201561]


[55]

Musunuru K, Hershberger RE, Day SM, Klinedinst NJ, Landstrom AP, Parikh VN, Prakash S, Semsarian C, Sturm AC, American Heart Association Council on Genomic and Precision Medicine; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; and Council on Clinical Cardiology. Genetic Testing for Inherited Cardiovascular Diseases: A Scientific Statement From the American Heart Association. Circulation. Genomic and precision medicine. 2020 Aug:13(4):e000067. doi: 10.1161/HCG.0000000000000067. Epub 2020 Jul 23     [PubMed PMID: 32698598]


[56]

Deng Y, Cheng SJ, Hua W, Cai MS, Zhang NX, Niu HX, Chen XH, Gu M, Cai C, Liu X, Huang H, Zhang S. N-Terminal Pro-B-Type Natriuretic Peptide in Risk Stratification of Heart Failure Patients With Implantable Cardioverter-Defibrillator. Frontiers in cardiovascular medicine. 2022:9():823076. doi: 10.3389/fcvm.2022.823076. Epub 2022 Mar 1     [PubMed PMID: 35299981]


[57]

Craig-Brangan KJ, Day MP. Update: 2017/2018 AHA BLS, ACLS, and PALS guidelines. Nursing. 2019 Feb:49(2):46-49. doi: 10.1097/01.NURSE.0000552705.65749.a0. Epub     [PubMed PMID: 30676559]


[58]

Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology. 2018 Oct 2:72(14):1677-1749. doi: 10.1016/j.jacc.2017.10.053. Epub 2017 Oct 30     [PubMed PMID: 29097294]

Level 1 (high-level) evidence

[59]

Pannone L,D'Angelo G,Gulletta S,Falasconi G,Brugliera L,Frontera A,Cianfanelli L,Baldetti L,Ossola P,Melillo F,De Blasi G,Malatino L,Landoni G,Margonato A,Della Bella P,Zacchetti D,Vergara P, Amiodarone in ventricular arrhythmias: still a valuable resource? Reviews in cardiovascular medicine. 2021 Dec 22     [PubMed PMID: 34957778]


[60]

Cronin EM, Bogun FM, Maury P, Peichl P, Chen M, Namboodiri N, Aguinaga L, Leite LR, Al-Khatib SM, Anter E, Berruezo A, Callans DJ, Chung MK, Cuculich P, d'Avila A, Deal BJ, Della Bella P, Deneke T, Dickfeld TM, Hadid C, Haqqani HM, Kay GN, Latchamsetty R, Marchlinski F, Miller JM, Nogami A, Patel AR, Pathak RK, Saenz Morales LC, Santangeli P, Sapp JL Jr, Sarkozy A, Soejima K, Stevenson WG, Tedrow UB, Tzou WS, Varma N, Zeppenfeld K. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. Heart rhythm. 2020 Jan:17(1):e2-e154. doi: 10.1016/j.hrthm.2019.03.002. Epub 2019 May 10     [PubMed PMID: 31085023]

Level 3 (low-level) evidence

[61]

Zaman J, Agarwal S. Management of ventricular tachycardia storm. Heart (British Cardiac Society). 2021 Oct:107(20):1671-1677. doi: 10.1136/heartjnl-2019-316192. Epub 2021 Jul 13     [PubMed PMID: 34257075]


[62]

Gorgels AP, van den Dool A, Hofs A, Mulleneers R, Smeets JL, Vos MA, Wellens HJ. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. The American journal of cardiology. 1996 Jul 1:78(1):43-6     [PubMed PMID: 8712116]

Level 1 (high-level) evidence

[63]

Piccini JP,Hranitzky PM,Kilaru R,Rouleau JL,White HD,Aylward PE,Van de Werf F,Solomon SD,Califf RM,Velazquez EJ, Relation of mortality to failure to prescribe beta blockers acutely in patients with sustained ventricular tachycardia and ventricular fibrillation following acute myocardial infarction (from the VALsartan In Acute myocardial iNfarcTion trial [VALIANT] Registry). The American journal of cardiology. 2008 Dec 1     [PubMed PMID: 19026290]

Level 2 (mid-level) evidence

[64]

Belhassen B,Horowitz LN, Use of intravenous verapamil for ventricular tachycardia. The American journal of cardiology. 1984 Nov 1     [PubMed PMID: 6496334]


[65]

Manolis AA, Manolis TA, Apostolopoulos EJ, Apostolaki NE, Melita H, Manolis AS. The role of the autonomic nervous system in cardiac arrhythmias: The neuro-cardiac axis, more foe than friend? Trends in cardiovascular medicine. 2021 Jul:31(5):290-302. doi: 10.1016/j.tcm.2020.04.011. Epub 2020 May 17     [PubMed PMID: 32434043]


[66]

Thomas SH, Behr ER. Pharmacological treatment of acquired QT prolongation and torsades de pointes. British journal of clinical pharmacology. 2016 Mar:81(3):420-7. doi: 10.1111/bcp.12726. Epub 2015 Oct 26     [PubMed PMID: 26183037]


[67]

Viskin S. Long QT syndromes and torsade de pointes. Lancet (London, England). 1999 Nov 6:354(9190):1625-33     [PubMed PMID: 10560690]


[68]

Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, Deswal A, Drazner MH, Dunlay SM, Evers LR, Fang JC, Fedson SE, Fonarow GC, Hayek SS, Hernandez AF, Khazanie P, Kittleson MM, Lee CS, Link MS, Milano CA, Nnacheta LC, Sandhu AT, Stevenson LW, Vardeny O, Vest AR, Yancy CW. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022 May 3:145(18):e895-e1032. doi: 10.1161/CIR.0000000000001063. Epub 2022 Apr 1     [PubMed PMID: 35363499]

Level 1 (high-level) evidence

[69]

Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. The New England journal of medicine. 1997 Nov 27:337(22):1576-83     [PubMed PMID: 9411221]

Level 1 (high-level) evidence

[70]

Connolly SJ, Hallstrom AP, Cappato R, Schron EB, Kuck KH, Zipes DP, Greene HL, Boczor S, Domanski M, Follmann D, Gent M, Roberts RS. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg . Canadian Implantable Defibrillator Study. European heart journal. 2000 Dec:21(24):2071-8     [PubMed PMID: 11102258]

Level 1 (high-level) evidence

[71]

Kuck KH, Cappato R, Siebels J, Rüppel R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest : the Cardiac Arrest Study Hamburg (CASH). Circulation. 2000 Aug 15:102(7):748-54     [PubMed PMID: 10942742]

Level 1 (high-level) evidence

[72]

Buxton AE,Lee KL,Fisher JD,Josephson ME,Prystowsky EN,Hafley G, A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. The New England journal of medicine. 1999 Dec 16     [PubMed PMID: 10601507]

Level 1 (high-level) evidence

[73]

Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ, Cannom DS, Daubert JP, Higgins SL, Brown MW, Andrews ML, Multicenter Automatic Defibrillator Implantation Trial II Investigators. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. The New England journal of medicine. 2002 Mar 21:346(12):877-83     [PubMed PMID: 11907286]

Level 1 (high-level) evidence

[74]

Connolly SJ, Dorian P, Roberts RS, Gent M, Bailin S, Fain ES, Thorpe K, Champagne J, Talajic M, Coutu B, Gronefeld GC, Hohnloser SH, Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients (OPTIC) Investigators. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial. JAMA. 2006 Jan 11:295(2):165-71     [PubMed PMID: 16403928]

Level 1 (high-level) evidence

[75]

Blomström-Lundqvist C, Scheinman MM, Aliot EM, Alpert JS, Calkins H, Camm AJ, Campbell WB, Haines DE, Kuck KH, Lerman BB, Miller DD, Shaeffer CW Jr, Stevenson WG, Tomaselli GF, Antman EM, Smith SC Jr, Alpert JS, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Hiratzka LF, Hunt SA, Jacobs AK, Russell RO Jr, Priori SG, Blanc JJ, Budaj A, Burgos EF, Cowie M, Deckers JW, Garcia MA, Klein WW, Lekakis J, Lindahl B, Mazzotta G, Morais JC, Oto A, Smiseth O, Trappe HJ, American College of Cardiology, American Heart Association Task Force on Practice Guidelines, European Society of Cardiology Committee for Practice Guidelines. Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation. 2003 Oct 14:108(15):1871-909     [PubMed PMID: 14557344]

Level 1 (high-level) evidence

[76]

Al-Khatib SM,Daubert JP,Anstrom KJ,Daoud EG,Gonzalez M,Saba S,Jackson KP,Reece T,Gu J,Pokorney SD,Granger CB,Hess PL,Mark DB,Stevenson WG, Catheter ablation for ventricular tachycardia in patients with an implantable cardioverter defibrillator (CALYPSO) pilot trial. Journal of cardiovascular electrophysiology. 2015 Feb     [PubMed PMID: 25332150]

Level 3 (low-level) evidence

[77]

Kuck KH, Schaumann A, Eckardt L, Willems S, Ventura R, Delacrétaz E, Pitschner HF, Kautzner J, Schumacher B, Hansen PS, VTACH study group. Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet (London, England). 2010 Jan 2:375(9708):31-40. doi: 10.1016/S0140-6736(09)61755-4. Epub     [PubMed PMID: 20109864]

Level 1 (high-level) evidence

[78]

Sapp JL, Wells GA, Parkash R, Stevenson WG, Blier L, Sarrazin JF, Thibault B, Rivard L, Gula L, Leong-Sit P, Essebag V, Nery PB, Tung SK, Raymond JM, Sterns LD, Veenhuyzen GD, Healey JS, Redfearn D, Roux JF, Tang AS. Ventricular Tachycardia Ablation versus Escalation of Antiarrhythmic Drugs. The New England journal of medicine. 2016 Jul 14:375(2):111-21. doi: 10.1056/NEJMoa1513614. Epub 2016 May 5     [PubMed PMID: 27149033]


[79]

Tung R, Vaseghi M, Frankel DS, Vergara P, Di Biase L, Nagashima K, Yu R, Vangala S, Tseng CH, Choi EK, Khurshid S, Patel M, Mathuria N, Nakahara S, Tzou WS, Sauer WH, Vakil K, Tedrow U, Burkhardt JD, Tholakanahalli VN, Saliaris A, Dickfeld T, Weiss JP, Bunch TJ, Reddy M, Kanmanthareddy A, Callans DJ, Lakkireddy D, Natale A, Marchlinski F, Stevenson WG, Della Bella P, Shivkumar K. Freedom from recurrent ventricular tachycardia after catheter ablation is associated with improved survival in patients with structural heart disease: An International VT Ablation Center Collaborative Group study. Heart rhythm. 2015 Sep:12(9):1997-2007. doi: 10.1016/j.hrthm.2015.05.036. Epub 2015 May 30     [PubMed PMID: 26031376]


[80]

Dinov B,Fiedler L,Schönbauer R,Bollmann A,Rolf S,Piorkowski C,Hindricks G,Arya A, Outcomes in catheter ablation of ventricular tachycardia in dilated nonischemic cardiomyopathy compared with ischemic cardiomyopathy: results from the Prospective Heart Centre of Leipzig VT (HELP-VT) Study. Circulation. 2014 Feb 18     [PubMed PMID: 24211823]


[81]

Corrado D, Wichter T, Link MS, Hauer RN, Marchlinski FE, Anastasakis A, Bauce B, Basso C, Brunckhorst C, Tsatsopoulou A, Tandri H, Paul M, Schmied C, Pelliccia A, Duru F, Protonotarios N, Estes NM 3rd, McKenna WJ, Thiene G, Marcus FI, Calkins H. Treatment of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia: An International Task Force Consensus Statement. Circulation. 2015 Aug 4:132(5):441-53. doi: 10.1161/CIRCULATIONAHA.115.017944. Epub 2015 Jul 27     [PubMed PMID: 26216213]

Level 3 (low-level) evidence

[82]

Philips B, te Riele AS, Sawant A, Kareddy V, James CA, Murray B, Tichnell C, Kassamali B, Nazarian S, Judge DP, Calkins H, Tandri H. Outcomes and ventricular tachycardia recurrence characteristics after epicardial ablation of ventricular tachycardia in arrhythmogenic right ventricular dysplasia/cardiomyopathy. Heart rhythm. 2015 Apr:12(4):716-25. doi: 10.1016/j.hrthm.2014.12.018. Epub 2014 Dec 18     [PubMed PMID: 25530221]


[83]

Moss AJ, Zareba W, Hall WJ, Schwartz PJ, Crampton RS, Benhorin J, Vincent GM, Locati EH, Priori SG, Napolitano C, Medina A, Zhang L, Robinson JL, Timothy K, Towbin JA, Andrews ML. Effectiveness and limitations of beta-blocker therapy in congenital long-QT syndrome. Circulation. 2000 Feb 15:101(6):616-23     [PubMed PMID: 10673253]

Level 1 (high-level) evidence

[84]

Dusi V,Pugliese L,De Ferrari GM,Odero A,Crotti L,Dagradi F,Castelletti S,Vicentini A,Rordorf R,Li C,Shkolnikova M,Spazzolini C,Schwartz PJ, Left Cardiac Sympathetic Denervation for Long QT Syndrome: 50 Years' Experience Provides Guidance for Management. JACC. Clinical electrophysiology. 2022 Mar     [PubMed PMID: 35331422]


[85]

Gill JS, Blaszyk K, Ward DE, Camm AJ. Verapamil for the suppression of idiopathic ventricular tachycardia of left bundle branch block-like morphology. American heart journal. 1993 Nov:126(5):1126-33     [PubMed PMID: 8237755]


[86]

Ling Z, Liu Z, Su L, Zipunnikov V, Wu J, Du H, Woo K, Chen S, Zhong B, Lan X, Fan J, Xu Y, Chen W, Yin Y, Nazarian S, Zrenner B. Radiofrequency ablation versus antiarrhythmic medication for treatment of ventricular premature beats from the right ventricular outflow tract: prospective randomized study. Circulation. Arrhythmia and electrophysiology. 2014 Apr:7(2):237-43. doi: 10.1161/CIRCEP.113.000805. Epub 2014 Feb 12     [PubMed PMID: 24523413]

Level 1 (high-level) evidence

[87]

Deneke T, Mügge A, Kerber S, Nentwich K, Fochler F, Müller P, Grewe P, Halbfass P. [Differential diagnosis of tachycardia with a broad QRS-complex]. Herzschrittmachertherapie & Elektrophysiologie. 2015 Sep:26(3):214-26. doi: 10.1007/s00399-015-0387-1. Epub 2015 Sep 1     [PubMed PMID: 26323810]


[88]

Moccetti F,Yadava M,Latifi Y,Strebel I,Pavlovic N,Knecht S,Asatryan B,Schaer B,Kühne M,Henrikson CA,Stephan FP,Osswald S,Sticherling C,Reichlin T, Simplified Integrated Clinical and Electrocardiographic Algorithm for Differentiation of Wide QRS Complex Tachycardia: The Basel Algorithm. JACC. Clinical electrophysiology. 2022 Jul     [PubMed PMID: 35863808]


[89]

Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart rhythm. 2008 Jan:5(1):89-98. doi: 10.1016/j.hrthm.2007.09.020. Epub 2007 Sep 20     [PubMed PMID: 18180024]


[90]

Chen Q, Xu J, Gianni C, Trivedi C, Della Rocca DG, Bassiouny M, Canpolat U, Tapia AC, Burkhardt JD, Sanchez JE, Hranitzky P, Gallinghouse GJ, Al-Ahmad A, Horton R, Di Biase L, Mohanty S, Natale A. Simple electrocardiographic criteria for rapid identification of wide QRS complex tachycardia: The new limb lead algorithm. Heart rhythm. 2020 Mar:17(3):431-438. doi: 10.1016/j.hrthm.2019.09.021. Epub 2019 Sep 20     [PubMed PMID: 31546028]


[91]

Ushijima S, Kamata E, Saito H, Mitsui T, Kobayashi H, Iwa T. [Diagnosis of the origin of ventricular tachycardia by 12-lead electrocardiogram--evaluation of ECG of clinical cases of VT]. Kokyu to junkan. Respiration & circulation. 1984 Jun:32(6):619-25     [PubMed PMID: 6473942]

Level 3 (low-level) evidence

[92]

Xiong Y,Zhu H, Electrocardiographic characteristics of idiopathic ventricular arrhythmias based on anatomy. Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc. 2020 Nov;     [PubMed PMID: 32592448]


[93]

Anderson KP,DeCamilla J,Moss AJ, Clinical significance of ventricular tachycardia (3 beats or longer) detected during ambulatory monitoring after myocardial infarction. Circulation. 1978 May     [PubMed PMID: 639211]


[94]

Prystowsky EN, Nisam S. Prophylactic implantable cardioverter defibrillator trials: MUSTT, MADIT, and beyond. Multicenter Unsustained Tachycardia Trial. Multicenter Automatic Defibrillator Implantation Trial. The American journal of cardiology. 2000 Dec 1:86(11):1214-5, A5     [PubMed PMID: 11090794]


[95]

Chiu C, Sequeira IB. Diagnosis and treatment of idiopathic ventricular tachycardia. AACN clinical issues. 2004 Jul-Sep:15(3):449-61     [PubMed PMID: 15475817]


[96]

Turakhia M, Tseng ZH. Sudden cardiac death: epidemiology, mechanisms, and therapy. Current problems in cardiology. 2007 Sep:32(9):501-46     [PubMed PMID: 17723906]


[97]

Kusumoto FM,Bailey KR,Chaouki AS,Deshmukh AJ,Gautam S,Kim RJ,Kramer DB,Lambrakos LK,Nasser NH,Sorajja D, Systematic Review for the 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology. 2018 Oct 2     [PubMed PMID: 29097297]

Level 1 (high-level) evidence

[98]

Guelly C, Abilova Z, Nuralinov O, Panzitt K, Akhmetova A, Rakhimova S, Kozhamkulov U, Kairov U, Molkenov A, Seisenova A, Trajanoski S, Abildinova Rashbayeva G, Kaussova G, Windpassinger C, Lee JH, Zhumadilov Z, Bekbossynova M, Akilzhanova A. Patients with coronary heart disease, dilated cardiomyopathy and idiopathic ventricular tachycardia share overlapping patterns of pathogenic variation in cardiac risk genes. PeerJ. 2021:9():e10711. doi: 10.7717/peerj.10711. Epub 2021 Jan 19     [PubMed PMID: 33552729]


[99]

Grandi E, Ripplinger CM. Antiarrhythmic mechanisms of beta blocker therapy. Pharmacological research. 2019 Aug:146():104274. doi: 10.1016/j.phrs.2019.104274. Epub 2019 May 14     [PubMed PMID: 31100336]


[100]

van Diepen S, Girotra S, Abella BS, Becker LB, Bobrow BJ, Chan PS, Fahrenbruch C, Granger CB, Jollis JG, McNally B, White L, Yannopoulos D, Rea TD. Multistate 5-Year Initiative to Improve Care for Out-of-Hospital Cardiac Arrest: Primary Results From the HeartRescue Project. Journal of the American Heart Association. 2017 Sep 22:6(9):. doi: 10.1161/JAHA.117.005716. Epub 2017 Sep 22     [PubMed PMID: 28939711]


[101]

Buick JE,Drennan IR,Scales DC,Brooks SC,Byers A,Cheskes S,Dainty KN,Feldman M,Verbeek PR,Zhan C,Kiss A,Morrison LJ,Lin S, Improving Temporal Trends in Survival and Neurological Outcomes After Out-of-Hospital Cardiac Arrest. Circulation. Cardiovascular quality and outcomes. 2018 Jan     [PubMed PMID: 29317455]

Level 2 (mid-level) evidence

[102]

Sasson C, Rogers MA, Dahl J, Kellermann AL. Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis. Circulation. Cardiovascular quality and outcomes. 2010 Jan:3(1):63-81. doi: 10.1161/CIRCOUTCOMES.109.889576. Epub 2009 Nov 10     [PubMed PMID: 20123673]

Level 1 (high-level) evidence

[103]

Rittenberger JC,Guyette FX,Tisherman SA,DeVita MA,Alvarez RJ,Callaway CW, Outcomes of a hospital-wide plan to improve care of comatose survivors of cardiac arrest. Resuscitation. 2008 Nov     [PubMed PMID: 18951113]

Level 2 (mid-level) evidence

[104]

Nallamothu BK, Guetterman TC, Harrod M, Kellenberg JE, Lehrich JL, Kronick SL, Krein SL, Iwashyna TJ, Saint S, Chan PS. How Do Resuscitation Teams at Top-Performing Hospitals for In-Hospital Cardiac Arrest Succeed? A Qualitative Study. Circulation. 2018 Jul 10:138(2):154-163. doi: 10.1161/CIRCULATIONAHA.118.033674. Epub     [PubMed PMID: 29986959]

Level 2 (mid-level) evidence

[105]

Ali B, Zafari AM. Narrative review: cardiopulmonary resuscitation and emergency cardiovascular care: review of the current guidelines. Annals of internal medicine. 2007 Aug 7:147(3):171-9     [PubMed PMID: 17679705]

Level 3 (low-level) evidence