Background

Ventricular tachycardia (VT) is a type of arrhythmia, or abnormal heart rhythm, characterized by a rapid and regular beating of the heart originating in the ventricles, the lower chambers of the heart. In a normal heart rhythm, electrical signals control the heartbeat, starting in the sinoatrial (SA) node, traveling through the atria, and then passing through the atrioventricular (AV) node to reach the ventricles.

Ventricular tachycardia occurs when the electrical signals in the ventricles become disorganized, leading to a rapid heartbeat. VT is caused by abnormal electrical impulses that originate in the ventricles instead of the usual pathway through the atria. This can result in a faster heartbeat and disrupt the normal coordination of the heart’s pumping action.

Ventricular tachycardia often occurs in individuals with underlying heart conditions, such as coronary artery disease, heart attacks, cardiomyopathy, heart valve disease, or inherited heart disorders. Certain medications, electrolyte imbalances, and scar tissue from previous heart surgeries can also contribute to its development. 

Epidemiology

Ventricular tachycardia and ventricular fibrillation are major contributors to sudden cardiac death, accounting for an estimated 300,000 fatalities annually in the United States.

Ventricular tachycardia exhibits a strong association with coronary artery disease, with approximately 15% of individuals diagnosed with coronary artery disease also experiencing ventricular tachycardia.

The incidence of ventricular tachycardia is notably higher in men, primarily due to an increased prevalence of coronary artery disease in this demographic. However, it is anticipated that the incidence in women will rise as the occurrence of coronary artery disease increases among them. 

Anatomy

Pathophysiology

Ventricular tachycardia (VT) is characterized by a rapid and regular heartbeat originating in the ventricles. The pathophysiology is closely tied to abnormalities in the heart’s electrical conduction system. In individuals with underlying heart disease, such as coronary artery disease (CAD) or myocardial infarction, scar tissue forms in the myocardium.

This scar tissue disrupts the normal electrical pathways, creating circuits that allow for the reentry of electrical signals, leading to the sustained and rapid firing of the ventricles. In the context of ischemic heart disease, inadequate blood supply to the heart muscle can result in tissue damage, and subsequent scar formation can create a substrate for reentrant circuits.

This abnormal electrical activity can trigger VT. In non-ischemic cardiomyopathies, such as dilated cardiomyopathy or hypertrophic cardiomyopathy, structural abnormalities and remodeling of the heart muscle can also contribute to the development of VT. Furthermore, electrolyte imbalances, particularly disruptions in potassium levels, can affect the excitability of cardiac cells and increase the risk of ventricular arrhythmias.

Other factors, such as certain medications or genetic conditions, may also influence the susceptibility to VT. Ventricular tachycardia often presents as a monomorphic or polymorphic rhythm on an ECG, with the ventricles beating at a rate exceeding 100 beats per minute. The sustained nature of VT can compromise cardiac output, leading to symptoms such as dizziness, palpitations, chest discomfort, or, in severe cases, loss of consciousness. 

Etiology

Electrolyte Imbalances: Disturbances in electrolyte levels, particularly potassium, can affect the electrical properties of cardiac cells. Abnormalities in electrolyte concentrations may increase the susceptibility to ventricular arrhythmias, including VT. 

Inherited Arrhythmia Syndromes: Certain genetic conditions, such as long QT syndrome, Brugada syndrome, or arrhythmogenic right ventricular dysplasia (ARVD), can predispose individuals to VT. These conditions often involve mutations in genes responsible for cardiac ion channels or structural proteins. 

Age and Gender: The incidence of VT increases with age, and men tend to have a higher prevalence of VT, primarily due to a higher incidence of coronary artery disease. However, as the prevalence of coronary artery disease rises in women, the incidence of VT in women is also expected to increase. 

Genetics

Prognostic Factors

The presence of other medical conditions, such as diabetes, hypertension, or renal dysfunction, can impact the overall prognosis. Age and general health status are important prognostic factors.

Elderly individuals and those with multiple comorbidities may have a higher risk of complications and a potentially less favorable prognosis. In cases where ventricular tachycardia is associated with inherited arrhythmia syndromes, the specific genetic factors involved can impact the long-term prognosis. 

Clinical History

The clinical presentation of ventricular tachycardia (VT) exhibits variability, contingent on factors such as the patient’s age, underlying structural heart diseases, comorbidities, and the specific mechanism of VT. While common symptoms encompass palpitations, chest pain, shortness of breath, and syncope, the manifestation can range from milder symptoms to severe outcomes such as sudden cardiac arrest.

In instances of idiopathic ventricular tachycardia, patients typically experience palpitations, particularly during exertion or emotional stress. However, the initial presentation may involve shortness of breath, reflecting heart failure or tachycardia-induced cardiomyopathy.

Cardiac arrest and syncope are uncommon presentations of idiopathic ventricular tachycardia in individuals lacking evidence of structural heart disease. It is noteworthy that the clinical spectrum of VT underscores the importance of considering various factors when assessing and managing patients with this arrhythmia. 

Physical Examination

Clinical assessment may involve the identification of hypotension and signs indicative of heart failure. Even in hemodynamically stable patients, elevated jugular venous pressure and cannon waves may be observed. A meticulous precordial examination can reveal signs of underlying structural heart disease and manifestations of adverse effects resulting from antiarrhythmic drugs, such as amiodarone.

In cases where ventricular tachycardia coexists with coronary artery disease, patients may present with syncope, chest pain, shortness of breath, and cardiac arrest. The tolerance of ventricular tachycardia is notably lower in the presence of left ventricular systolic dysfunction, leading to significant hemodynamic compromise. Patients often present with syncope, shortness of breath (attributed to pulmonary edema), cardiac arrest, and even sudden cardiac death.

Those equipped with an implantable cardioverter-defibrillator may present with ICD shocks. Individuals experiencing ventricular tachycardia due to channelopathies may have syncope, cardiac arrest, and sudden cardiac death as initial presentations. This underscores the importance of obtaining a comprehensive three-generation family history when evaluating young patients with ventricular tachycardia. 

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

• Antidromic atrioventricular tachycardia 
• Supraventricular tachycardia 
• Supraventricular tachycardia with preexcitation 
• Pacemaker-mediated tachycardia 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

The treatment paradigm for ventricular tachycardia (VT) involves a multifaceted approach tailored to the specific characteristics and underlying conditions of each patient. In cases of drug-refractory VT, catheter ablation has emerged as an effective intervention, particularly recommended for select individuals with ischemic cardiomyopathy who continue to experience sustained VT despite antiarrhythmic drug therapy or are intolerant to medications like amiodarone.

Trials like VANISH have shown that catheter ablation reduces the recurrence of VT, ventricular storm, and implantable cardiac defibrillator (ICD) shocks, although it may not necessarily improve overall survival. The International VT Ablation Center Collaborative (IVTCC) study demonstrates that approximately 70% of patients with structural heart diseases achieve freedom from VT after catheter ablation, leading to enhanced survival in this specific patient group.

Medical therapy, adhering to guidelines for heart failure, is crucial for managing patients with structural heart disease and left ventricular systolic dysfunction. Additionally, the implantation of ICDs is recommended for those with ischemic cardiomyopathy surviving sudden cardiac arrest or experiencing sustained VT. In the presence of a VT storm, interventions include antiarrhythmic drugs, beta-blockers, and direct current cardioversion, with considerations for advanced measures like intubation, mechanical circulatory support, and catheter ablation in refractory cases.

It is imperative to conduct risk assessments, such as electrophysiological studies, for patients with unexplained syncope to determine the necessity of ICD placement for preventing sudden cardiac death. While catheter ablation is generally safe in experienced centers, vascular access-related complications are comparable to other electrophysiology procedures, and serious complications such as stroke or tamponade are rare. Overall, the comprehensive treatment strategy for VT involves a combination of pharmacological and interventional approaches, emphasizing individualized care and close monitoring to optimize outcomes and enhance patient survival. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

intervention-with-a-procedure

Catheter Ablation 

Catheter ablation has demonstrated efficacy as a viable treatment option for individuals experiencing drug-refractory ventricular tachycardia. It is explicitly recommended for a carefully selected subset of patients with ischemic cardiomyopathy who persist in having sustained ventricular tachycardia despite antiarrhythmic drug therapy or are unable to tolerate medications such as amiodarone.

Notably, findings from the VANISH trial indicate that catheter ablation, when compared to antiarrhythmic drugs, results in reduced recurrence of ventricular tachycardia, ventricular storm, and implantable cardiac defibrillator (ICD) shocks. However, it does not demonstrate a significant improvement in overall survival.

According to the International VT Ablation Center Collaborative (IVTCC) study, approximately 70% of patients with structural heart diseases achieve freedom from ventricular tachycardia following catheter ablation, and this freedom from ventricular tachycardia contributes to improved survival in this specific patient cohort. 

In experienced centers, VT ablation is considered a relatively safe procedure, with a procedure-related mortality of less than 1%. Vascular access-related complications are comparable to those observed in other electrophysiology procedures, while occurrences of tamponade, stroke, and atrioventricular blocks are infrequent.

These insights underscore the importance of considering catheter ablation as a therapeutic avenue in the management of ventricular tachycardia, particularly in cases where traditional pharmacological approaches prove insufficient or intolerable. 

phases-of-management

Acute Phase of Management 

Patients who present with cardiac arrest resulting from ventricular tachycardia necessitate immediate resuscitation and should be managed in accordance with the advanced life support (ACLS) algorithm. In cases where cardiac arrest is absent but ventricular tachycardia causes hemodynamic instability, direct current cardioversion is the preferred management approach.

For hemodynamically unstable patients not responding to direct current cardioversion or experiencing recurrent ventricular tachycardia, intravenous amiodarone is recommended to restore and maintain sinus rhythm. Unstable patients with ventricular tachycardia induced by myocardial infarction or ischemia should undergo coronary angiogram followed by revascularization. 

Ventricular tachycardia storm represents a specific presentation in patients with structural heart diseases. It is defined by three or more sustained ventricular tachycardia episodes within 24 hours, requiring intervention such as anti-tachycardia pacing, antiarrhythmic drugs, or direct current cardioversion. VT storm not only leads to substantial morbidity, including hospitalization and decompensated heart failure but also escalates mortality rates.

Initial management of VT storm involves the administration of intravenous beta-blockers, antiarrhythmic drugs, and direct current cardioversion with sedation. In cases resistant to these measures, patients may necessitate intubation, catheter ablation, and mechanical circulatory support of ventricular tachycardia.  

Long-term Phase of Management 

Patients diagnosed with left ventricular systolic dysfunction and structural heart disease should be offered medical therapy following established guidelines for heart failure management.

In the case of ischemic cardiomyopathy, individuals who survive sudden cardiac arrest resulting from ventricular tachycardia or experience hemodynamically stable or unstable sustained ventricular tachycardia should undergo implantation of an implantable cardiac defibrillator if their anticipated meaningful survival exceeds one year.

For individuals with unexplained syncope and concurrent ischemic cardiomyopathy, adult congenital heart disease or non-ischemic cardiomyopathy, an electrophysiological study may be conducted to assess the risk of sustained ventricular tachycardia.

However, performing the study solely for risk stratification is not deemed appropriate. If an electrophysiology study induces sustained ventricular tachycardia, the recommendation is to proceed with the implantation of an ICD to prevent sudden cardiac death. 

In Patients with Structural Heart Disease 

For individuals experiencing hemodynamically stable ventricular tachycardia and concurrent structural heart disease, the recommended acute treatment options include intravenous administration of amiodarone, procainamide, and sotalol (if available).

In cases where these specific drugs are not accessible, intravenous lidocaine can be employed as an alternative antiarrhythmic agent. Additionally, intravenous beta-blockers may be considered in situations where ventricular tachycardia is secondary to ischemia. 

In Patients with Idiopathic Ventricular Tachycardia 

For hemodynamically stable individuals with idiopathic ventricular tachycardia, the primary pharmacological options include intravenous beta-blockers and non-dihydropyridine calcium channel blockers.

Verapamil administered intravenously should be delivered as a bolus using a large bore cannula. In cases where ventricular tachycardia does not respond to antiarrhythmic drugs, consideration may be given to direct current cardioversion. Asymptomatic patients with non-sustained ventricular tachycardia (VT) and no underlying structural heart disease may not necessitate additional therapy. 

Medication

Future Trends

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References