Continuing Education Activity

Ventricular tachycardia is a potentially life-threatening arrhythmia characterized by rapid ventricular depolarization, leading to sustained or nonsustained elevations in heart rate. This cardiac rhythm abnormality is classified as monomorphic or polymorphic based on electrocardiographic morphology. Ventricular tachycardia arises from reentry circuits, triggered activity, or abnormal automaticity, often in the setting of myocardial scarring or fibrosis. Etiologies include structural heart disease, ischemic cardiomyopathy, myocarditis, electrolyte disturbances, and drug-induced proarrhythmia.

Risk factors comprise prior myocardial infarction, left ventricular dysfunction, heart failure, inherited channelopathies, and advanced age. Clinical presentation ranges from asymptomatic episodes and palpitations to syncope, hemodynamic compromise, and sudden cardiac death. Diagnosis relies on electrocardiography, Holter monitoring, cardiac imaging, and, in selected cases, electrophysiological studies to identify arrhythmogenic substrates. Management includes antiarrhythmic pharmacotherapy, catheter ablation, and implantable cardioverter-defibrillator placement, tailored to underlying pathology and hemodynamic status.

Complications encompass recurrent arrhythmias, heart failure exacerbation, and mortality. Prognosis depends on underlying cardiac function, ventricular tachycardia burden, and promptness of intervention, with early recognition and targeted therapy mitigating the risk of sudden cardiac death.

This activity for healthcare professionals is designed to enhance learners' competence in evaluating and managing ventricular tachycardia. Participants will advance their mastery of the condition's etiology, risk factors, pathophysiology, clinical presentation, and evidence-based diagnostic and therapeutic approaches. Improved skills will equip clinicians to collaborate with interprofessional teams providing care for individuals with this potentially fatal cardiac condition.

Objectives:

• Differentiate ventricular tachycardia from other tachyarrhythmias based on ECG analysis in a clinical context.
• Determine the underlying cause of ventricular tachycardia, guided by clinical presentation and findings from other diagnostic modalities, including echocardiography.
• Implement evidence-based, individualized strategies for managing ventricular tachycardia and mitigating serious sequelae.
• Collaborate with the interprofessional teams to facilitate prompt and thorough delivery of care to patients with ventricular tachycardia, improving outcomes.

Introduction

Ventricular tachycardia is defined as a wide complex tachycardia (WCT) consisting of 3 or more consecutive beats at a rate exceeding 100 per minute. The arrhythmia originates from specialized conducting tissue or the ventricular myocardium below the penetrating atrioventricular bundle. Ventricular tachycardia may occur in structurally normal hearts, but it is substantially more common in individuals with underlying structural heart disease.[1]

Ventricular tachycardia is classified as monomorphic or polymorphic based on QRS morphology. Monomorphic ventricular tachycardia arises from a single ventricular focus, producing uniform electrical activity (see Image. Ventricular Tachycardia with Negative Polarity). Electrocardiographic (ECG) findings demonstrate QRS complexes of consistent shape and duration (see Image. Monomorphic Ventricular Tachycardia). Polymorphic ventricular tachycardia exhibits QRS complexes with variable shape and duration. Bidirectional ventricular tachycardia, a rare form often associated with calcium overload and catecholaminergic polymorphic ventricular tachycardia (CPVT), presents with dual QRS morphologies alternating on a beat-to-beat basis.[2]

The clinical presentation of ventricular tachycardia ranges from palpitations to sudden cardiac death (SCD). Distinguishing between potential causes of this abnormal rhythm is imperative to determine the urgency and selection of treatment. Appropriate management and prevention of SCD require understanding the pathophysiology of ventricular tachycardia and underlying structural heart disease. This activity summarizes the etiology and epidemiology of ventricular tachycardia and reviews the evaluation and treatment of patients presenting with this arrhythmia.[3]

Etiology

The majority of ventricular tachycardias occur in patients with structural heart diseases, typically due to myocardial scarring or fibrosis. Myocardial fibrosis may be classified as ischemic or nonischemic. Ischemic fibrosis results from prior myocardial infarction, whereas nonischemic fibrosis is multifactorial. Although differentiating ischemic from nonischemic fibrosis may influence long-term management, the initial management of ventricular tachycardia is similar.

Reentry represents the most common mechanism of ventricular tachycardia in structural heart disease.[4] Fibrosis and scar formation create regions of heterogeneous conduction with surviving myocardial fibers embedded within nonconductive scar tissue. These surviving fibers form slow-conducting channels that permit delayed propagation of electrical impulses through scarred myocardium.

The combination of slowed conduction and regions of unidirectional block facilitates the formation of a reentrant circuit. An electrical impulse may travel around the scar through these channels, reenter previously depolarized tissue after recovery of excitability, and circulate continuously, thereby sustaining ventricular tachycardia.

The reentrant circuit often includes an isthmus of viable myocardium bounded by areas of dense scar or anatomical barriers. This substrate-dependent mechanism explains the typical monomorphic pattern and reproducibility of scar-related ventricular tachycardia during electrophysiologic testing. Understanding this mechanism provides the foundation for catheter ablation targeting critical isthmus sites within the reentry circuit.[5][6]

Approximately 10% of ventricular tachycardias occur in the absence of structural heart disease.[7] Idiopathic outflow tract tachycardia represents the most common form of ventricular tachycardia in patients with structurally normal hearts. Other causes include inherited channelopathies, such as CPVT and long QT syndrome (LQTS). These tachycardias are less likely to involve reentry mechanisms due to the absence of myocardial fibrosis. Common triggers of ventricular tachycardia include electrolyte imbalances, including hypokalemia, hypocalcemia, and hypomagnesemia; use of illicit drugs such as cocaine or methamphetamine; and intake of prescription medications, including digitalis.

Inherited cardiac channelopathies are more prevalent in younger individuals. LQTS represents the most common inherited cardiac channelopathy, with torsades de pointes as its characteristic arrhythmia. Other inherited channelopathies associated with ventricular tachycardia include Brugada syndrome, CPVT, short QT syndrome, and malignant early repolarization syndrome.[8]

Idiopathic ventricular tachycardia is a category of ventricular tachycardia, typically occurring in younger individuals without evidence of structural heart disease. The most frequent origins of idiopathic ventricular tachycardia include the ventricular outflow tracts, mitral or tricuspid annulus, and fascicles of the left bundle branch. Idiopathic ventricular tachycardia rarely causes SCD but can negatively affect quality of life. Most cases are refractory to pharmacologic therapy, while catheter ablation demonstrates high rates of treatment success.[9]

Epidemiology

Ventricular tachycardia is a common cause of death in the US, with substantially higher rates in individuals with underlying cardiovascular disease. Between 2007 and 2020, 7,025 deaths were attributed to ventricular tachycardia in individuals with underlying heart disease in the US. Age-adjusted mortality rates per 100,000 demonstrate an increase from 0.22 in 2007 to 0.32 in 2020. Mortality was disproportionately higher in Black men (0.44) compared with all men (0.37) and women (0.20). Death rates peaked in men aged 65 to 84 (1.30) and women of the same age group (0.60), compared with younger men aged 35 to 64 (0.10) and women (0.08). Regional variation revealed higher rates in the Southern US (0.31) relative to the Northeastern (0.26) and Western (0.19) territories. No significant difference emerged between metropolitan and nonmetropolitan areas.

Overall mortality due to cardiovascular disease has declined in the US. However, increasing mortality from ventricular tachycardia may reflect the growing population of adults older than 60 and improved recognition of ventricular tachycardia as a primary cause of death. The prevalence of implanted cardiac devices, including pacemakers, defibrillators, loop recorders, and wearable cardiac monitoring devices, contributes to the detection of fatal events.[10]

Pathophysiology

Mechanisms Underlying Ventricular Tachycardia

Ventricular tachycardia encompasses a diverse group of tachyarrhythmias, with cellular mechanisms determined by underlying structural heart disease and channelopathies. Understanding the mechanisms driving ventricular tachycardia supports risk stratification and guides appropriate management strategies.

Ventricular tachycardia arises from 3 principal electrophysiologic mechanisms: reentry, triggered activity, and enhanced automaticity. Reentry represents the most common mechanism in patients with structural heart disease, particularly in association with postmyocardial infarction scarring or with cardiomyopathy. Fibrosis and scar formation generate areas of slow conduction and unidirectional block, permitting electrical impulses to circulate continuously through surviving myocardial fibers within the scar. This process forms a stable reentrant circuit that repeatedly depolarizes the ventricles, typically producing monomorphic ventricular tachycardia. Sustained reentrant ventricular tachycardia may degenerate into ventricular fibrillation, resulting in cardiac arrest or SCD in patients with structural heart disease.[11]

Triggered activity results from afterdepolarizations occurring during or immediately after repolarization. Early afterdepolarizations arise during phases 2 or 3 of the action potential and are often associated with prolonged repolarization, such as in LQTS, or with electrolyte disturbances. Delayed afterdepolarizations occur after phase 4 and typically relate to intracellular calcium overload, as seen in conditions such as digoxin toxicity or catecholaminergic states.

Enhanced automaticity originates from increased spontaneous depolarization of ventricular myocardial cells or Purkinje fibers. This mechanism occurs when the slope of phase 4 depolarization increases, allowing ectopic ventricular foci to reach threshold earlier than the normal conduction system. Enhanced automaticity is frequently observed in ischemia, electrolyte abnormalities, or heightened sympathetic stimulation.

The mechanism of idiopathic ventricular tachycardia, particularly outflow tract ventricular tachycardia, remains incompletely understood, although delayed afterdepolarization is proposed as a likely mechanism. Some outflow tract ventricular tachycardias terminate in response to adenosine, suggesting that afterdepolarization mediated by cyclic adenosine monophosphate drives these arrhythmias.[12]

Hemodynamic Consequences of Ventricular Tachycardia

The hemodynamic effects of ventricular tachycardia depend on the presence of comorbid conditions, including coronary artery disease (CAD), left ventricular systolic dysfunction (LVSD), and valvular heart disease. Rapid ventricular rates in ventricular tachycardia reduce cardiac output by decreasing both preload and stroke volume. In patients with structural heart disease, CAD, or LVSD, these hemodynamic alterations may cause systemic hypotension, coronary and cerebral hypoperfusion, syncope, and cardiac arrest. Coronary hypoperfusion further compromises hemodynamics, potentially precipitating ventricular fibrillation and SCD.

Ventricular tachycardia is generally well tolerated in structurally normal hearts. However, incessant ventricular tachycardia may induce tachycardia-mediated cardiomyopathy, hemodynamic instability, heart failure, and syncope. Inherited ventricular arrhythmias, including LQTS, arrhythmogenic cardiomyopathy, CPVT, and Brugada syndrome, may degenerate into ventricular fibrillation, resulting in hemodynamic collapse even when left ventricular systolic function is normal.[13]

Histopathology

Myocardial scar formation results from irreversible cardiomyocyte injury, most commonly following myocardial infarction, myocarditis, or damage from chronic cardiomyopathies. Histopathologically, scar tissue is characterized by the replacement of necrotic myocardium with dense fibrous connective tissue composed primarily of collagen types I and III.

During the healing process, inflammatory cells such as macrophages remove necrotic debris, followed by fibroblast proliferation and deposition of extracellular matrix. A mature fibrotic scar forms over time, lacking contractile cardiomyocytes and normal electrical conduction properties.

Small bundles of surviving myocardial fibers may persist within the scarred region, interspersed within fibrotic tissue. These surviving myocyte strands often demonstrate altered cellular architecture, including myocyte hypertrophy, disarray, and gap junction remodeling. The heterogeneous distribution of fibrosis and viable myocardium produces areas of slow and anisotropic conduction. This structural and electrical heterogeneity creates the substrate for reentrant ventricular arrhythmias, particularly monomorphic ventricular tachycardia in patients with ischemic or nonischemic cardiomyopathy.[14][15]

History and Physical

Characterized by a rapid heart rate originating from the ventricles, ventricular tachycardia presents with variable clinical manifestations, including both stable and unstable forms, and multiple ECG morphologies. Typical symptoms include palpitations, lightheadedness, syncope, dyspnea, chest pain, and SCD. Symptom severity and pattern depend on the underlying condition contributing to the arrhythmia.[16]

Ventricular tachycardia in the presence of CAD may manifest as chest pain, syncope, shortness of breath, hypotension, and cardiac arrest. Ventricular tachycardia in patients with LVSD is poorly tolerated, producing marked hemodynamic compromise. Presentations in this population include syncope, dyspnea due to pulmonary edema, cardiac arrest, and SCD. Patients with an implantable cardioverter-defibrillator (ICD) may present with device-delivered shocks.

Individuals with ventricular tachycardia secondary to channelopathies may present initially with syncope, cardiac arrest, or SCD. A detailed 3-generation family history is essential when evaluating young patients with ventricular tachycardia. Idiopathic ventricular tachycardia typically manifests as palpitations during exercise or emotional stress. Dyspnea may occur as the initial presentation in cases complicated by heart failure or tachycardia-induced cardiomyopathy. Syncope and cardiac arrest are uncommon in idiopathic ventricular tachycardia among patients without structural heart disease.[17]

Physical examination of patients with ventricular tachycardia may reveal a rapid heart rate, hypotension, altered mental status, jugular venous cannon waves, pulmonary congestion, and lower extremity edema. Findings vary depending on the presence of structural heart disease and the duration or severity of the arrhythmia.

Evaluation

Initial History and Physical Examination

A detailed history and clinical examination are pivotal in the evaluation of patients with ventricular tachycardia. The initial assessment should determine hemodynamic stability, including the evaluation of responsiveness, heart rate, and blood pressure. Patients identified as unstable require prompt stabilization before completing a comprehensive history and physical examination.[18] All individuals assessed for ventricular tachycardia should be investigated for risk factors for atherosclerotic cardiovascular disease, prior episodes of palpitations, syncope, or ventricular tachycardia, and a family history of inherited cardiac conditions in 1st-degree relatives. Clinical practice guidelines recommend a detailed 3-generation family history in patients with suspected cardiac channelopathies.[19]

Electrocardiogram

Obtaining a 12-lead ECG constitutes a critical first step in the evaluation of ventricular tachycardia. WCT represents ventricular tachycardia in approximately 80% of cases. Other potential causes include supraventricular tachycardia (SVT) with aberrancy, atrial fibrillation with aberrant conduction, ventricular paced rhythm, and QRS widening induced by drugs or electrolyte disturbances. Rapid recognition of the underlying rhythm can be challenging. Diagnostic algorithms, including the Brugada and Vereckei algorithms, can assist in differentiation.[20] ECG in sinus rhythm provides additional diagnostic information, helping identify underlying causes of ventricular tachycardia such as myocardial ischemia or infarction, LQTS, hypertrophic cardiomyopathy (HCM), Brugada syndrome, and arrhythmogenic right ventricular cardiomyopathy (ARVC).

Noninvasive Imaging

Transthoracic echocardiography is the gold standard for evaluating patients presenting with ventricular tachycardia. This modality provides a detailed assessment of cardiac structure and function and aids in determining the underlying etiology.

Computed tomography angiography has emerged as a noninvasive method for assessing cardiac vasculature. This technique reduces the need for invasive cardiac catheterization, particularly when ruling out CAD in low-risk populations. Cardiac magnetic resonance imaging (MRI) plays a primary role in evaluating heart structure, volume, and function. This technology also provides tissue characterization, facilitating differentiation among various cardiomyopathies. The limitations of cardiac MRI include longer acquisition times, higher costs, and a reduced ability to assess the coronary arteries.

The recent introduction of dual-modality positron emission tomography (PET) and MRI (PET/MRI) provides an additional technique for detecting coronary artery inflammation, microcalcification, and thrombus. PET/MRI generates integrated images by combining anatomical and functional assessment, with PET allowing quantification of metabolism, inflammation, and perfusion. Simultaneous evaluation of myocardial tissue and molecular characteristics has become an increasingly valuable tool in clinical practice.[21]

Invasive Testing  

Patients presenting with ventricular tachycardia secondary to presumed myocardial ischemia should undergo invasive coronary angiography. This procedure evaluates CAD and informs the revascularization strategy.

Genetic Testing 

Channelopathies are inherited genetic electrical heart disorders that affect cardiac myocyte function in the absence of structural heart defects. Undiagnosed channelopathies can cause SCD in young individuals. Advances in genetic research have elucidated underlying mutations and complex pathophysiology in nonischemic cardiomyopathies. Comprehensive clinical evaluations, detailed family histories, and genetic testing have significantly improved diagnostic accuracy and risk stratification.[22]

Other Investigations

Assessment of serum potassium, magnesium, and calcium levels is essential for the diagnosis and management of ventricular tachycardia. Measurement of high-sensitivity cardiac troponin is required for the diagnosis of myocardial infarction. Natriuretic peptides provide valuable prognostic information in patients with structural heart disease who present with ventricular tachycardia and are at risk for SCD.

Treatment / Management

Acute Management

Cardiac arrest constitutes the life-threatening presentation of ventricular tachycardia. Patients presenting with cardiac arrest secondary to ventricular tachycardia should be resuscitated and treated according to the Advanced Cardiac Life Support (ACLS) algorithm.[23] In the absence of cardiac arrest, hemodynamically unstable ventricular tachycardia is managed with direct current cardioversion.[24] If ventricular tachycardia persists or recurs after successful cardioversion, intravenous amiodarone should be administered to maintain sinus rhythm.[25] All patients with hemodynamically unstable ventricular tachycardia secondary to myocardial infarction or ischemia should undergo coronary angiography, followed by revascularization.

Ventricular tachycardia storm is a severe presentation of ventricular tachycardia in patients with structural heart disease. The condition is defined as 3 or more episodes of sustained ventricular tachycardia within 24 hours, requiring intervention with antiarrhythmic drugs, antitachycardia pacing, or direct current cardioversion.[26] Ventricular tachycardia storm causes substantial morbidity, including hospitalization and decompensated heart failure, and is associated with increased mortality. Initial management of ventricular tachycardia storm includes intravenous administration of antiarrhythmic drugs and β-blockers, direct current cardioversion, and sedation. Refractory cases may necessitate intubation, mechanical circulatory support, and catheter ablation of ventricular tachycardia.[27][28]

Intravenous procainamide, amiodarone, or sotalol (depending on availability) is recommended for the acute treatment of patients with structural heart disease who have hemodynamically stable ventricular tachycardia.[29] Intravenous lidocaine serves as an alternative if the preferred antiarrhythmic agents are unavailable. Intravenous β-blockers may be considered in ventricular tachycardia secondary to ischemia.[30]

Intravenous β-blockers and nondihydropyridine calcium channel blockers (CCBs) are 1st-line agents for the treatment of hemodynamically stable idiopathic ventricular tachycardia.[31] Intravenous verapamil should be administered as a bolus using a large-bore cannula. Direct current cardioversion may be considered if ventricular tachycardia does not respond to antiarrhythmic therapy.

Asymptomatic patients with nonsustained ventricular tachycardia and no underlying structural heart disease may not require additional therapy. Intravenous β-blocker administration remains the mainstay of treatment in hemodynamically stable ventricular tachycardia secondary to cardiac channelopathies.[32] Intravenous infusion of magnesium and mexiletine may be considered in patients with long-QT–induced stable ventricular tachycardia.[33] Some patients with LQTS may experience incessant ventricular tachycardia due to short–long sequences or the R-on-T phenomenon. Temporary pacing at a higher rate effectively prevents torsades de pointes in these cases.[34]

Serum potassium, magnesium, and calcium levels should be optimized in all patients presenting with ventricular tachycardia. Correction of electrolyte abnormalities is critical to stabilize cardiac membrane potential and prevent torsadogenic events.

Long-Term Management

All patients with structural heart disease and LVSD should receive guideline-directed medical therapy for heart failure.[35] Patients with ischemic cardiomyopathy who survive SCD due to ventricular tachycardia or experience hemodynamically unstable or stable sustained ventricular tachycardia should undergo ICD placement if estimated meaningful survival exceeds 1 year.[36][37][38] Individuals with unexplained syncope and underlying ischemic cardiomyopathy, nonischemic cardiomyopathy, or adult congenital heart disease who do not meet ICD criteria may undergo an electrophysiological study to assess the risk of sustained ventricular tachycardia. Performing the study solely for risk stratification without a clinical indication is not recommended.[39][40][41]

ICD implantation should be recommended for the prevention of SCD if sustained ventricular tachycardia is induced during an electrophysiology study. Long-term β-blocker therapy is recommended in patients with ischemic cardiomyopathy presenting with ventricular tachycardia to prevent recurrence and reduce the risk of SCD. Recurrent episodes of ventricular tachycardia or ICD shocks despite optimal β-blocker therapy warrant the use of amiodarone or sotalol to suppress arrhythmias.[42] Amiodarone demonstrates greater efficacy and lower proarrhythmic potential than sotalol, but systemic adverse effects may lead to early discontinuation.

Catheter ablation is an effective treatment option for patients with drug-refractory ventricular tachycardia. This intervention is indicated for select patients with ischemic cardiomyopathy who continue to experience sustained ventricular tachycardia despite antiarrhythmic therapy or are intolerant of antiarrhythmic agents like amiodarone.[43][44][45]

The VANISH (Ventricular Tachycardia Ablation in Ischemic Heart Disease) trial demonstrated that catheter ablation reduced the recurrence of ventricular tachycardia, ventricular storm, and ICD shocks compared with antiarrhythmic drug therapy. However, survival did not improve.[46] The IVTCC (International Ventricular Tachycardia Ablation Center Collaborative) study reported that 70% of patients with structural heart disease achieve freedom from ventricular tachycardia after catheter ablation, and achieving freedom from ventricular tachycardia in this group is associated with improved survival.

Ventricular tachycardia ablation is relatively safe in experienced centers, with procedure-related mortality below 1%. Vascular access–related complications are comparable to other electrophysiology procedures, while stroke, tamponade, and atrioventricular blocks are rare.[47]

Patients with nonischemic cardiomyopathy who survive SCD due to ventricular tachycardia or develop sustained ventricular tachycardia without a reversible cause should undergo ICD implantation for secondary prevention of SCD if expected survival exceeds 1 year with good quality of life. Amiodarone may be considered for preventing SCD and recurrence of ventricular tachycardia in patients with expected survival of less than 1 year.[48]

In individuals with recurrent ventricular tachycardia despite optimal heart failure therapy and β-blocker treatment, contemporary guidelines recommend amiodarone or sotalol to prevent recurrent ventricular tachycardia episodes. Catheter ablation may be considered in select patients with drug-refractory ventricular tachycardia who experience recurrent ICD shocks.[49]

β-blocker therapy reduces recurrent arrhythmias in patients with ventricular tachycardia due to ARVC. All individuals with ARVC who survive SCD should undergo ICD implantation for secondary prevention of further life-threatening arrhythmic events.[50] ICD placement may be considered in high-risk patients presenting with syncope and ventricular tachycardia who have no prior history of cardiac arrest. Patients with ARVC who experience recurrent ventricular tachycardia and appropriate ICD shocks despite β-blocker and antiarrhythmic therapy may undergo catheter ablation in experienced centers equipped with both endocardial and epicardial ablation capabilities.[51] β-blocker therapy remains the mainstay of treatment for individuals with congenital LQTS and CPVT.[52]

ICD placement is indicated for secondary prevention of SCD in patients with cardiac channelopathies who survive cardiac arrest. Left cardiac sympathetic denervation may be considered in experienced centers in highly symptomatic patients on optimal β-blocker therapy.[53] ICD implantation is recommended for secondary prevention of SCD in individuals with Brugada syndrome, short QT syndrome, HCM, and idiopathic polymorphic ventricular tachycardia who survive SCD due to ventricular tachycardia.[54]

Nondihydropyridine CCBs and β-blockers are effective treatments for patients with idiopathic ventricular tachycardia. Most patients respond well to β-blockers and verapamil, without requiring additional therapy.[55] Other antiarrhythmic agents may be considered in patients with idiopathic ventricular tachycardia who do not respond to β-blockers or CCBs. Catheter ablation is an effective option for patients with idiopathic ventricular tachycardia refractory to antiarrhythmic drugs, including β-blockers and CCBs.[56]

Differential Diagnosis

WCT most commonly arises from ventricular tachycardia, accounting for approximately 70% to 80% of cases. Other causes include SVT with aberrant conduction, such as bundle branch block; atrial fibrillation with aberrancy; ventricular paced rhythms; and preexcited tachycardias associated with accessory pathways. QRS widening during tachycardia may also occur due to drug toxicity, particularly sodium channel–blocking agents, or metabolic and electrolyte disturbances, including hyperkalemia.

Accurate and rapid identification of the underlying rhythm in WCT remains challenging but is essential for appropriate management. Several ECG diagnostic algorithms facilitate differentiation of ventricular tachycardia from SVT with aberrancy. Widely used approaches include the Brugada and Vereckei algorithms, both of which analyze specific ECG features to improve diagnostic accuracy.[57][58]

A 12-lead ECG obtained during sinus rhythm also aids identification of substrates predisposing to ventricular tachycardia. Common etiologies include prior myocardial infarction or ischemia; inherited channelopathies, such as LQTS; and structural heart diseases, including HCM, Brugada syndrome, and ARVC.

Prognosis

The prognosis of ventricular tachycardia depends on the underlying etiology and the presence of structural heart disease. CAD is the most common cause of ventricular tachycardia, and patients with ischemic cardiomyopathy–related ventricular tachycardia have the worst prognosis. Two-year mortality in untreated patients has been reported to reach 30%.[59]

ICD implantation significantly reduces the incidence of SCD.[60] Although ICDs protect against sudden death, they do not effectively prevent the recurrence of ventricular tachycardia. Multiple studies demonstrate that catheter ablation is required to reduce recurrent ventricular tachycardia and ICD therapies. Catheter ablation combined with ICD placement may decrease ICD shocks and ventricular tachycardia storm in patients with underlying ischemic heart disease, although overall mortality remains unaffected.

Individuals with idiopathic ventricular tachycardia have an excellent prognosis in the absence of other comorbidities, with life expectancy approximating that of the general population.[61] Patients with HCM, LQTS, and ARVC remain at higher risk of SCD, even with preserved left ventricular systolic function. β-blockers reduce the burden of ventricular tachycardia in these populations, and ICDs provide protection against SCD.[62][63]

Complications

The complications of ventricular tachycardia depend on the underlying mechanism. Common ones include tachycardia-induced cardiomyopathy and heart failure. Tachycardia-induced cardiomyopathy occurs more frequently in patients with incessant ventricular tachycardia episodes and individuals with genetic predisposition or additional cardiomyopathy risk factors, such as alcohol use.[64] Cardiac arrest and SCD represent major complications of inherited ventricular tachycardia and scar-related ventricular tachycardia. Early recognition and ICD implantation can substantially reduce these risks. β-blocker therapy also decreases the incidence of SCD in patients with cardiac channelopathies and ischemic cardiomyopathy.[65]

Deterrence and Patient Education

Ventricular tachycardia is a potentially life-threatening arrhythmia. Although palpitations represent the most common presentation, syncope, cardiac arrest, and SCD can also occur. All patients presenting with WCT should undergo a comprehensive evaluation, including a 3-generation family history, transthoracic echocardiography, and cardiac MRI. Patients with a family history of SCD at a young age should consult a cardiologist for evaluation of inherited cardiac conditions, including cardiac channelopathies. Asymptomatic relatives of patients with such genetic causes of ventricular tachycardia should be referred to a cardiac electrophysiologist or geneticist for screening and genetic counseling.

Enhancing Healthcare Team Outcomes

Cardiac arrest represents a fatal presentation of ventricular tachycardia. Early recognition, bystander cardiopulmonary resuscitation (CPR), and public access to defibrillation have improved survival rates for patients experiencing out-of-hospital cardiac arrest (OHCA) due to ventricular arrhythmias. Overall survival after OHCA remains low despite these advances.[66][67][68] Postresuscitation care following the return of spontaneous circulation, with emphasis on targeted temperature management and cardio-cerebral resuscitation, has further improved outcomes.[69]

A dedicated resuscitation team, free from clinical responsibilities that could interfere with CPR, is essential for managing cardiac arrest. Effective communication among team members contributes positively to patient outcomes. In-hospital cardiac arrest parallels OHCA in that early CPR and defibrillation are critical for survival. Each minute of delay in treatment reduces survival by approximately 10%.[70] High-performing resuscitation teams typically include physicians, nurses, anesthesiologists, and respiratory therapists, with additional support from pharmacy, clerical, security, and spiritual staff in some hospitals.[71]

Management of ventricular tachycardia requires an interprofessional team. Core members include a cardiac electrophysiologist and a cardiac critical care nurse. Patients with ischemic heart disease and diabetes benefit from endocrinology consultation. Strenuous exercise should be avoided, and smoking cessation must be strongly encouraged. Patients with suspected inherited cardiac conditions require a geneticist for counseling and testing. Pharmacists provide medication education, reconciliation, guidance on drug interactions, and coordination with prescribers. Nurses coordinate provider activities, counsel patients, and assist with assessments and procedures. This interprofessional model supports optimal patient outcomes in ventricular tachycardia management.

Review Questions

• Access free multiple choice questions on this topic.
• Click here for a simplified version.
• Comment on this article.

References

1.

Whitaker J, Wright MJ, Tedrow U. Diagnosis and management of ventricular tachycardia. Clin Med (Lond). 2023 Sep;23(5):442-448. [PMC free article: PMC10541285] [PubMed: 37775174]

2.

Almarzuqi A, Kimber S, Quadros K, Senaratne J. Bidirectional Ventricular Tachycardia: Challenges and Solutions. Vasc Health Risk Manag. 2022;18:397-406. [PMC free article: PMC9188370] [PubMed: 35698640]

3.

Ding WY, Mahida S. Wide complex tachycardia: differentiating ventricular tachycardia from supraventricular tachycardia. Heart. 2021 Dec;107(24):1995-2003. [PubMed: 34035115]

4.

Donahue JK, Chrispin J, Ajijola OA. Mechanism of Ventricular Tachycardia Occurring in Chronic Myocardial Infarction Scar. Circ Res. 2024 Feb 02;134(3):328-342. [PMC free article: PMC10836816] [PubMed: 38300981]

5.

Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity. A mechanism of recurrent ventricular tachycardia. Circulation. 1978 Apr;57(4):659-65. [PubMed: 630672]

6.

Stevenson WG, Friedman PL, Sager PT, Saxon LA, Kocovic D, Harada T, Wiener I, Khan H. Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping. J Am Coll Cardiol. 1997 May;29(6):1180-9. [PubMed: 9137211]

7.

Sohinki DA, Mathew ST. Ventricular Arrhythmias in the Patient with a Structurally Normal Heart. J Innov Card Rhythm Manag. 2018 Oct;9(10):3338-3353. [PMC free article: PMC7252725] [PubMed: 32477784]

8.

Barwad P. Cardiac sympathetic denervation: A wonder solution to channelopathy-related ventricular tachycardia and much more. J Postgrad Med. 2022 Jan-Mar;68(1):10-11. [PMC free article: PMC8860114] [PubMed: 35073682]

9.

Velázquez-Rodríguez E, García-Hernández N, Silva-Oropeza E, Jiménez-Arteaga S, Martínez-Sánchez A, Alva-Espinoza C, David-Gómez F, Yáñez-Gutiérrez L. Idiopathic left fascicular ventricular tachycardia in children and adolescents. Bol Med Hosp Infant Mex. 2022;79(4):248-258. [PubMed: 36100212]

10.

Ibrahim R, Sroubek J, Nakhla S, Lee JZ. Trends and disparities in ventricular tachycardia mortality in the United States. J Cardiovasc Electrophysiol. 2023 Feb;34(2):465-467. [PMC free article: PMC10107254] [PubMed: 36640434]

11.

Muser D, Santangeli P, Liang JJ. Mechanisms of Ventricular Arrhythmias and Implications for Catheter Ablation. Card Electrophysiol Clin. 2022 Dec;14(4):547-558. [PubMed: 36396177]

12.

Belhassen B, Scheinman M, Nogami A. Verapamil-Sensitive Idiopathic Left Ventricular Tachycardia Alongside Atrial Flutter. JACC Clin Electrophysiol. 2024 Aug;10(8):1935-1936. [PubMed: 39197971]

13.

Könemann H, Dagres N, Merino JL, Sticherling C, Zeppenfeld K, Tfelt-Hansen J, Eckardt L. Spotlight on the 2022 ESC guideline management of ventricular arrhythmias and prevention of sudden cardiac death: 10 novel key aspects. Europace. 2023 May 19;25(5) [PMC free article: PMC10228619] [PubMed: 37102266]

14.

Ghafoor M, Kamal M, Nadeem U, Husain AN. Educational Case: Myocardial Infarction: Histopathology and Timing of Changes. Acad Pathol. 2020 Jan-Dec;7:2374289520976639. [PMC free article: PMC7750744] [PubMed: 33415186]

15.

De Silva K, Campbell T, Bennett RG, Anderson RD, Davey C, O'Donohue AK, Schindeler A, Turnbull S, Selvakumar D, Bhaskaran A, Kotake Y, Hsu CJ, Chong JJH, Kizana E, Kumar S. Whole-Heart Histological and Electroanatomic Assessment of Postinfarction Cardiac Magnetic Resonance Imaging Scar and Conducting Channels. Circ Arrhythm Electrophysiol. 2024 Sep;17(9):e012922. [PubMed: 39193754]

16.

Menon R, Emerson G, Yee J. Ventricular Tachycardia. J Educ Teach Emerg Med. 2023 Oct;8(4):S25-S48. [PMC free article: PMC10631810] [PubMed: 37969159]

17.

Moore BM, Roston TM, Laksman Z, Krahn AD. Updates on inherited arrhythmia syndromes (Brugada syndrome, long QT syndrome, CPVT, ARVC). Prog Cardiovasc Dis. 2025 Jul-Aug;91:130-143. [PubMed: 40505939]

18.

Angelow AM, Coates J. Evaluation of Wide Complex Tachycardia. Nurs Clin North Am. 2023 Sep;58(3):325-336. [PubMed: 37536784]

19.

Finocchiaro G, Westaby J, Sheppard MN, Papadakis M, Sharma S. Sudden Cardiac Death in Young Athletes: JACC State-of-the-Art Review. J Am Coll Cardiol. 2024 Jan 16;83(2):350-370. [PubMed: 38199713]

20.

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 Clin Electrophysiol. 2022 Jul;8(7):831-839. [PubMed: 35863808]

21.

Kazimierczyk R, Kaminski KA, Nekolla SG. Cardiac PET/MRI: Recent Developments and Future Aspects. Semin Nucl Med. 2024 Sep;54(5):733-746. [PubMed: 38853039]

22.

Dib Nehme R, Sinno L, Shouman W, Ziade JA, Ammar LA, Amin G, Booz GW, Zouein FA. Cardiac Channelopathies: Clinical Diagnosis and Promising Therapeutics. J Am Heart Assoc. 2025 May 06;14(9):e040072. [PMC free article: PMC12184234] [PubMed: 40281647]

23.

Craig-Brangan KJ, Day MP. Update: 2017/2018 AHA BLS, ACLS, and PALS guidelines. Nursing. 2019 Feb;49(2):46-49. [PubMed: 30676559]

24.

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. J Am Coll Cardiol. 2018 Oct 02;72(14):1677-1749. [PubMed: 29097294]

25.

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? Rev Cardiovasc Med. 2021 Dec 22;22(4):1383-1392. [PubMed: 34957778]

26.

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, 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. [PMC free article: PMC8453449] [PubMed: 31085023]

27.

Zaman J, Agarwal S. Management of ventricular tachycardia storm. Heart. 2021 Oct;107(20):1671-1677. [PubMed: 34257075]

28.

Lenarczyk R, Zeppenfeld K, Tfelt-Hansen J, Heinzel FR, Deneke T, Ene E, Meyer C, Wilde A, Arbelo E, Jędrzejczyk-Patej E, Sabbag A, Stühlinger M, di Biase L, Vaseghi M, Ziv O, Bautista-Vargas WF, Kumar S, Namboodiri N, Henz BD, Montero-Cabezas J, Dagres N, Peichl P, Frontera A, Tzeis S, Merino JL, Soejima K, de Chillou C, Tung R, Eckardt L, Maury P, Hlivak P, Tereshchenko LG, Kojodjojo P, Atié J. Management of patients with an electrical storm or clustered ventricular arrhythmias: a clinical consensus statement of the European Heart Rhythm Association of the ESC-endorsed by the Asia-Pacific Heart Rhythm Society, Heart Rhythm Society, and Latin-American Heart Rhythm Society. Europace. 2024 Mar 30;26(4) [PMC free article: PMC10999775] [PubMed: 38584423]

29.

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. Am J Cardiol. 1996 Jul 01;78(1):43-6. [PubMed: 8712116]

30.

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). Am J Cardiol. 2008 Dec 01;102(11):1427-32. [PubMed: 19026290]

31.

Belhassen B, Horowitz LN. Use of intravenous verapamil for ventricular tachycardia. Am J Cardiol. 1984 Nov 01;54(8):1131-3. [PubMed: 6496334]

32.

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 Cardiovasc Med. 2021 Jul;31(5):290-302. [PubMed: 32434043]

33.

Thomas SH, Behr ER. Pharmacological treatment of acquired QT prolongation and torsades de pointes. Br J Clin Pharmacol. 2016 Mar;81(3):420-7. [PMC free article: PMC4767204] [PubMed: 26183037]

34.

Viskin S. Long QT syndromes and torsade de pointes. Lancet. 1999 Nov 06;354(9190):1625-33. [PubMed: 10560690]

35.

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., ACC/AHA Joint Committee Members. 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 03;145(18):e895-e1032. [PubMed: 35363499]

36.

Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997 Nov 27;337(22):1576-83. [PubMed: 9411221]

37.

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. Eur Heart J. 2000 Dec;21(24):2071-8. [PubMed: 11102258]

38.

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: 10942742]

39.

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. N Engl J Med. 1999 Dec 16;341(25):1882-90. [PubMed: 10601507]

40.

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. N Engl J Med. 2002 Mar 21;346(12):877-83. [PubMed: 11907286]

41.

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. [PubMed: 29084731]

42.

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: 16403928]

43.

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, Stevenson WG, Tomaselli GF, Antman EM, Smith SC, Alpert JS, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Hiratzka LF, Hunt SA, Jacobs AK, Russell RO, 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: 14557344]

44.

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. J Cardiovasc Electrophysiol. 2015 Feb;26(2):151-7. [PubMed: 25332150]

45.

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. 2010 Jan 02;375(9708):31-40. [PubMed: 20109864]

46.

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. N Engl J Med. 2016 Jul 14;375(2):111-21. [PubMed: 27149033]

47.

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. [PMC free article: PMC4549209] [PubMed: 26031376]

48.

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;15(10):e190-e252. [PubMed: 29097320]

49.

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;129(7):728-36. [PubMed: 24211823]

50.

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, McKenna WJ, Thiene G, Marcus FI, Calkins H. Treatment of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia: An International Task Force Consensus Statement. Circulation. 2015 Aug 04;132(5):441-53. [PMC free article: PMC4521905] [PubMed: 26216213]

51.

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. [PubMed: 25530221]

52.

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: 10673253]

53.

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 Clin Electrophysiol. 2022 Mar;8(3):281-294. [PubMed: 35331422]

54.

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. J Am Coll Cardiol. 2018 Oct 02;72(14):e91-e220. [PubMed: 29097296]

55.

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

56.

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. Circ Arrhythm Electrophysiol. 2014 Apr;7(2):237-43. [PubMed: 24523413]

57.

Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991 May;83(5):1649-59. [PubMed: 2022022]

58.

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. [PubMed: 18180024]

59.

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;57(5):890-7. [PubMed: 639211]

60.

Prystowsky EN, Nisam S. Prophylactic implantable cardioverter defibrillator trials: MUSTT, MADIT, and beyond. Multicenter Unsustained Tachycardia Trial. Multicenter Automatic Defibrillator Implantation Trial. Am J Cardiol. 2000 Dec 01;86(11):1214-5, A5. [PubMed: 11090794]

61.

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

62.

Turakhia M, Tseng ZH. Sudden cardiac death: epidemiology, mechanisms, and therapy. Curr Probl Cardiol. 2007 Sep;32(9):501-46. [PubMed: 17723906]

63.

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. J Am Coll Cardiol. 2018 Oct 02;72(14):1653-1676. [PubMed: 29097297]

64.

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. [PMC free article: PMC7821765] [PubMed: 33552729]

65.

Grandi E, Ripplinger CM. Antiarrhythmic mechanisms of beta blocker therapy. Pharmacol Res. 2019 Aug;146:104274. [PMC free article: PMC6679787] [PubMed: 31100336]

66.

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. J Am Heart Assoc. 2017 Sep 22;6(9) [PMC free article: PMC5634254] [PubMed: 28939711]

67.

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., Rescu Investigators. Improving Temporal Trends in Survival and Neurological Outcomes After Out-of-Hospital Cardiac Arrest. Circ Cardiovasc Qual Outcomes. 2018 Jan;11(1):e003561. [PMC free article: PMC5791528] [PubMed: 29317455]

68.

Sasson C, Rogers MA, Dahl J, Kellermann AL. Predictors of survival from out-of-hospital cardiac arrest: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes. 2010 Jan;3(1):63-81. [PubMed: 20123673]

69.

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;79(2):198-204. [PMC free article: PMC2590640] [PubMed: 18951113]

70.

Ali B, Zafari AM. Narrative review: cardiopulmonary resuscitation and emergency cardiovascular care: review of the current guidelines. Ann Intern Med. 2007 Aug 07;147(3):171-9. [PubMed: 17679705]

71.

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. [PMC free article: PMC6245659] [PubMed: 29986959]

Disclosure: Kimberly Lovik declares no relevant financial relationships with ineligible companies.

Disclosure: Intisar Ahmed declares no relevant financial relationships with ineligible companies.